Academic literature on the topic '1-adrenergic receptors'
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Journal articles on the topic "1-adrenergic receptors"
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Kiely, J., J. R. Hadcock, S. W. Bahouth та C. C. Malbon. "Glucocorticoids down-regulate β1-adrenergic-receptor expression by suppressing transcription of the receptor gene". Biochemical Journal 302, № 2 (1994): 397–403. http://dx.doi.org/10.1042/bj3020397.
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The expression of beta 2-adrenergic receptors is up-regulated by glucocorticoids. In contrast, beta 1-adrenergic receptors display glucocorticoid-induced down-regulation. In rat C6 glioma cells, which express both of these subtypes of beta-adrenergic receptors, the synthetic glucocorticoid dexamethasone stimulates no change in the total beta-adrenergic receptor content, but rather shifts the beta 1:beta 2 ratio from 80:20 to 50:50. Radioligand binding and immunoblotting demonstrate a sharp decline in beta 1-adrenergic receptor expression. Metabolic labelling of cells with [35S]-methionine in tandem with immunoprecipitation by beta 1-adrenergic-receptor-specific antibodies reveals a sharp decline in the synthesis of the receptor within 48 h for cells challenged with glucocorticoid. Steady-state levels of beta 1-adrenergic-receptor mRNA declined from 0.47 to 0.26 amol/microgram of total cellular RNA within 2 h of dexamethasone challenge, as measured by DNA-excess solution hybridization. The stability of receptor mRNA was not influenced by glucocorticoid; the half-lives of the beta 1- and beta 2-subtype mRNAs were 1.7 and 1.5 h respectively. Nuclear run-on assays revealed the basis for the down-regulation of receptor expression, i.e. a sharp decline in the relative rate of transcription for the beta 1-adrenergic-receptor gene in nuclei from dexamethasone-treated as compared with vehicle-treated cells. These data demonstrate transcriptional suppression as a molecular explanation for glucocorticoid-induced down-regulation of beta 1-adrenergic receptors.
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Gesek, F. A., and K. E. White. "Molecular and functional identification of beta-adrenergic receptors in distal convoluted tubule cells." American Journal of Physiology-Renal Physiology 272, no. 6 (1997): F712—F720. http://dx.doi.org/10.1152/ajprenal.1997.272.6.f712.
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Renal nerve stimulation or circulating catecholamines activate the beta-adrenergic receptors that mediate direct effects on tubular transport. Three subtypes of beta-adrenergic receptors have been characterized: beta 1, beta 2, and beta 3. beta-Adrenergic-receptor effects on Na+ and Ca2+ transport in distal convoluted tubules (DCT) have not been established. The focus of this study was to 1) identify the subtypes of beta-adrenergic receptors in DCT cells and 2) examine functional responses to beta-receptor activation on adenosine 3',5'-cyclic monophosphate (cAMP) formation and Na+ and Ca2+ entry. To determine the subtypes of beta-receptors present, RNA isolated from immortalized mouse DCT cells was reverse transcribed, and the cDNA was amplified using primers designed to reported sequences for beta 1-, beta 2-, and beta 3-receptor subtypes. Products of the appropriate sizes were obtained with beta 1- and beta 2-primers. No product was observed with primers to the beta 3 sequence. Receptor products were confirmed by sequencing and are identical to reported mouse beta 1- and beta 2-receptor sequence. Receptor binding of[3H]dihydroalprenolol was 123 +/- 13 fmol/mg protein, and a 3:1 ratio of beta 1- to beta 2-receptors was observed with DCT cell membranes. Isoproterenol, a beta-receptor agonist, increased cAMP formation 8.5-fold. Pretreatment with the antagonist propranolol abolished agonist-induced cAMP accumulation. Isoproterenol significantly increased 22Na+ uptake to 345 +/- 23 compared with a basal rate of 256 +/- 12 nmol.min-1.mg protein-1 and was blocked with propranolol and beta 1- and beta 2-selective antagonists. Isoproterenol had no effect on 45Ca2+ entry into DCT cells. In summary, DCT cells express three times more beta 1- than beta 2-receptors and express no detectable beta 3-adrenergic receptors. beta-Receptors couple to adenylyl cyclase, and activation of beta-adrenergic receptors increases Na+ but not Ca2+ entry in DCT cells.
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Maisel, A. S., H. J. Motulsky, M. G. Ziegler, and P. A. Insel. "Ischemia- and agonist-induced changes in alpha- and beta-adrenergic receptor traffic in guinea pig hearts." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 5 (1987): H1159—H1166. http://dx.doi.org/10.1152/ajpheart.1987.253.5.h1159.
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We have used radioligand binding techniques and subcellular fractionation to assess whether changes in expression of myocardial alpha 1- and beta-adrenergic receptors are mediated by a redistribution of receptors between various membrane fractions. Three fractions were prepared from the left ventricles of guinea pigs that underwent either 1 h of ischemia or injection of epinephrine (0.25 mg/kg ip): a crude membrane, a purified sarcolemma, and a light vesicle fraction. In control animals alpha 1-adrenergic receptors ([3H]prazosin binding) in light vesicles was only 25% of the total alpha 1-receptor density found in sarcolemmal and light vesicle fractions as compared with 50% for beta-adrenergic receptors ([125I]iodocyanopindolol binding sites). Although ischemia was associated with a 53% decrease in the number of light vesicle beta-adrenergic receptors and a 42% increase in the number of sarcolemma beta-receptors (P less than 0.05), there was no change in the number of light vesicle alpha 1-receptors, even though the number of sarcolemmal alpha 1-receptors increased 34%. Epinephrine treatment promoted internalization of beta-adrenergic receptors; sarcolemma beta-receptors decreased 37% and light vesicle beta-receptors increased 28% (P less than 0.025). For alpha 1-receptors, epinephrine treatment decreased the number of sarcolemmal receptors 41% (P less than 0.025) but failed to increase the number of receptors in the light vesicle fraction. The changes in receptor binding to beta-adrenergic receptors in sarcolemmal fractions were mirrored by parallel changes in isoproterenol-stimulated adenylate cyclase activity. These results indicate that alpha 1- and beta-adrenergic receptors may undergo a different cellular itinerary in guinea pig myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
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Lechsner, Patrick, and Erika-Gyongyi Ban. "Alpha adrenergic receptors in clinical practice – Present and future." Acta Marisiensis - Seria Medica 68, no. 4 (2022): 145–49. http://dx.doi.org/10.2478/amma-2022-0030.
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Abstract In this review we discuss the adrenergic pathways for alpha 1 and alpha 2 receptors and the current as well as potential future medication targeting these receptors. Overall, there is ongoing research into a multitude of directions with a promising outlook for alpha 1 and alpha 2 adrenergic receptors. The alpha 1-adrenergic receptor subfamily is currently modulating only a modest number of nervous system functions due the fact, that only a relatively small number of selective commercial products are available. Chronic stress can affect the long-term depression of alpha 1 receptors. Recent studies are searching for new molecular targets which might act on these receptors. Presynaptic alpha 2 receptors play an important role in modulating release of several neurotransmitters in the central nervous system. The future of alpha 2 adrenergic receptors in clinical practice looks even more promising and versatile than that of alpha 1 adrenergic receptors. Alpha 2 adrenergic receptors show different responses, especially regarding hypertension and heart failure treatment, and current research suggests a genetic component as a cause, which is being explored further.
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Bahouth, S. W., та C. C. Malbon. "Human β-adrenergic receptors. Simultaneous purification of β1- and β2-adrenergic-receptor peptides". Biochemical Journal 248, № 2 (1987): 557–66. http://dx.doi.org/10.1042/bj2480557.
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Beta-Adrenergic receptors from basal membranes of human placenta were purified from digitonin extracts by sequential rounds of affinity chromatography, hydrophobic chromatography, ion-exchange chromatography and steric-exclusion h.p.l.c. Basal membranes display both beta 1- and beta 2-adrenergic receptors, in the ratio 65:35. Affinity chromatography, hydrophobic chromatography on heptylamine-Sepharose and ion-exchange chromatography on DEAE-Sephacel removed most of the contaminating proteins, and final purification of the receptor to apparent homogeneity was achieved by steric-exclusion h.p.l.c. The purified receptors showed Mr 67000 on SDS/polyacrylamide-gel electrophoresis under reducing conditions. Specific binding of radioligand to the purified beta-adrenergic receptors displayed stereoselectivity, and the agonist competition profiles demonstrated the presence of both beta 1- and beta 2-receptors. By using the subtype-selective ligands CGP-20712A (beta 1-selective) and ICI-118,551 (beta 2-selective), the purified Mr-67000 species was shown to be composed of equivalent amounts of beta 1- and beta 2-adrenergic receptors. Affinity chromatography on Sepharose-alprenolol and sequential elution with 1 microM-CGP-20712A followed by 100 microM(-)-alprenolol permitted beta 1-adrenergic receptors to be resolved from the mixture of beta 1-/beta 2-adrenergic receptors. The pharmacologically distinct human beta 1 and beta 2-adrenergic receptors are shown to be structurally very similar peptides.
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Struthers, Allan D. "The alpha 1 adrenergic receptors." Clinica Chimica Acta 180, no. 1 (1989): 110. http://dx.doi.org/10.1016/0009-8981(89)90307-0.
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Docherty, Jim. "The Alpha-1 adrenergic receptors." Trends in Pharmacological Sciences 9, no. 7 (1988): 266–67. http://dx.doi.org/10.1016/0165-6147(88)90161-7.
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Raasmaja, A., та D. A. York. "α1- and β-adrenergic receptors in brown adipose tissue of lean (Fa/?) and obese (fa/fa) Zucker rats. Effects of cold-acclimation, sucrose feeding and adrenalectomy". Biochemical Journal 249, № 3 (1988): 831–38. http://dx.doi.org/10.1042/bj2490831.
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1. The populations of alpha 1- and beta-adrenergic receptors in brown adipose tissue (BAT) of genetically obese Zucker rats (fa/fa) were studied with [3H]prazosin and [3H]CGP-12177 respectively. 2. The density of alpha 1-adrenergic receptors in BAT was significantly lower in obese than in lean Zucker rats, both at 2-4 months of age and at 6 weeks of age. The density of beta-adrenergic receptors was identical in BAT of lean and obese 6-week-old Zucker rats. 3. Cold-acclimation increased the alpha 1-receptor density significantly in BAT of both lean and obese Zucker rats, and the number of beta-receptors was also somewhat increased. 4. Sucrose feeding did not affect the density of alpha 1-receptors in BAT of lean or obese Zucker rats, but it increased beta-receptor density. 5. Adrenalectomy restored the density of alpha 1-adrenergic receptors in BAT of obese Zucker rats to the value observed in lean rats. 6. It is concluded that there is a direct correlation between alpha 1-receptor density and tissue recruitment, and that alpha 1-receptor density is thus positively correlated with sympathetic activity. beta-Receptor density is apparently better correlated with feeding conditions.
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Scarpace, P. J., L. A. Baresi, and J. E. Morley. "Modulation of receptors and adenylate cyclase activity during sucrose feeding, food deprivation, and cold exposure." American Journal of Physiology-Endocrinology and Metabolism 253, no. 6 (1987): E629—E635. http://dx.doi.org/10.1152/ajpendo.1987.253.6.e629.
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Thermogenesis in brown adipose tissue (BAT) serves as a regulator of body temperature and weight maintenance. Thermogenesis can be stimulated by catecholamine activation of adenylate cyclase through the beta-adrenergic receptor. To investigate the effects of sucrose feeding, food deprivation, and cold exposure on the beta-adrenergic pathway, adenylate cyclase activity and beta-adrenergic receptors were assessed in rat BAT after 2 wk of sucrose feeding, 2 days of food deprivation, or 2 days of cold exposure. beta-Adrenergic receptors were identified in BAT using [125I]iodocyanopindolol. Binding sites had the characteristics of mixed beta 1- and beta 2-type adrenergic receptors at a ratio of 60/40. After sucrose feeding or cold exposure, there was the expected increase in BAT mitochondrial mass as measured by total cytochrome-c oxidase activity but a decrease in beta-adrenergic receptor density due to a loss of the beta 1-adrenergic subtype. This BAT beta-adrenergic receptor downregulation was tissue specific, since myocardial beta-adrenergic receptors were unchanged with either sucrose feeding or cold exposure. In contrast, food deprivation did not alter BAT beta-adrenergic receptor density. Forskolin-stimulated adenylate cyclase activity increased in BAT after sucrose feeding or cold exposure but not after food deprivation. The ratio of isoproterenol-stimulated to forskolin-stimulated adenylate cyclase activity decreased in the sucrose-fed and cold-exposed rats but not in the food-deprived rats. These data suggest that in BAT, sucrose feeding or cold exposure result in downregulation of beta-adrenergic receptors and that isoproterenol-stimulated adenylate cyclase activity was limited by receptor availability.
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Yoshizumi, Masaru, Kazumasa Matsumoto-Miyai, Akihiko Yonezawa та Masahito Kawatani. "Role of supraspinal and spinal α1-adrenergic receptor subtypes in micturition reflex in conscious rats". American Journal of Physiology-Renal Physiology 299, № 4 (2010): F785—F791. http://dx.doi.org/10.1152/ajprenal.00553.2009.
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α1-Adrenergic receptor subtypes are widely distributed in the central nervous system and are involved in autonomic functions such as micturition. We investigated the presence and the role of supraspinal and/or spinal α1-adrenergic receptors in modulating the micturition reflex in conscious female Wistar rats. The expression of α1-adrenergic receptor subtypes in rat brain and lumbosacral spinal cord was studied using RT-PCR. Continuous-infusion cystometrograms were obtained in conscious rats, and α1-adrenergic receptor antagonists were administered via intracerebroventricular or intrathecal routes. The mRNA expression of α1A-, α1B-, and α1D-adrenergic receptors was detected in rat brain (midbrain and pons) and lumbosacral spinal cord (dorsal and ventral parts of spinal cord). In addition, intracerebroventricular injection of the α1-adrenergic receptor antagonist tamsulosin (1–10 μg), the selective α1A-adrenergic receptor antagonist silodosin (1–10 μg), and the selective α1D-adrenergic receptor antagonist BMY 7378 (1–10 μg) significantly prolonged the intercontraction interval (ICI) but did not alter maximum voiding pressure (MVP). Although intrathecal injection of BMY 7378 (0.0001–10 μg) did not affect ICI, tamsulosin and silodosin prolonged ICI in a dose-dependent manner. MVP was significantly reduced by intrathecal injection of tamsulosin (10 μg) but not by silodosin or BMY 7378 (0.0001–10 μg). Supraspinal α1A- and α1D-adrenergic receptors are apparently important for the regulation of reflex-bladder activity in conscious rats. Noradrenergic projection from the brain stem to the lumbosacral spinal cord may promote the afferent limb rather than the efferent limb of the micturition reflex pathway via α1A-adrenergic receptors.
Dissertations / Theses on the topic "1-adrenergic receptors"
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Broso, Francesca. "Alpha-1-Adrenergic receptors as new targets in Neuroblastoma." Doctoral thesis, Università degli studi di Trento, 2021. http://hdl.handle.net/11572/318323.
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High-risk neuroblastoma (NB) is an aggressive childhood tumor that originates from progenitor neural crest cells. Even if the therapeutic protocol for NB is articulate and aggressive, the outcome remains dismal, with the 5-year disease-free overall survival below rating 50%. A novel drug combination strategy can possibly provide a new solution to this unmet therapeutic need. 13-cis retinoic acid (13-cis-RA, isotretinoin) is an anti-proliferative and pro-differentiative agent currently used in the post-consolidation phase of NB therapy. To identify molecules able to potentiate the anti-proliferative activity of 13-cis-RA, NB cells were treated with a library of 169 naturally occurring polyphenols in combination with the retinoid. This in vitro screen led to the identification of isorhamnetin as a synergistic partner of 13-cis-RA, producing an 80% reduction in cell viability. At the molecular level, this synergistic effect is followed by a marked increase in the expression of a member of the catecholamine receptor superfamily: the adrenergic receptor alpha-1B (ADRA1B) suggesting that this receptor might represent a key mediator of the synergistic effect of 13-cis-RA and isorhamnetin observed in vitro. This finding redirected our attention to the class of adrenergic receptors (ARs) as novel targets in NB. To investigate the role of ADRA1B in the synergism, we generated CHP134 NB cell lines knocked-out (KO) for the receptor and observed that exposure of CHP134 KO cell to 13-cis-RA leads to a reduction of cell viability and neural differentiation. We, therefore, substituted the genetic KO strategy with the alpha-1B adrenergic antagonist, L765,314, obtaining the same results. Subsequently, we extended the analysis on the role of adrenergic receptors (AR) performing a biased screen using two libraries of AR-ligands. The screen results confirm that the molecules working as alpha-1-ARs antagonists are those that greatly increase cell sensitivity to 13-cis-RA with reduction of cell viability and increase in differentiation. We confirmed our observation in NB xenograft mice models in vivo, treating mice with a combination of 13-cis-RA and the FDA approved alpha-1 AR antagonist doxazosin. The proposed pharmacological treatment was effective in slowing tumor growth, leading to tumors of smaller size. From our results, we can conclude that the deletion or inhibition of alpha-1-AR sensitizes NB cells to 13-Cis-RA, both in terms of induction of apoptosis and neural differentiation. Since NB is a catecholamine-rich tumor, we propose that antagonization of alpha-1-AR disrupts the established autocrine pro-survival circuit generated by catecholamines in NB and restores the ability of the cells to follow the pro-differentiative and pro-apoptotic programs endorsed by 13-cis-RA. Considering the druggable nature of the alpha-1-AR receptors, we indicate this class of receptors as a novel pharmacological target for the treatment of neuroblastoma.
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Broso, Francesca. "Alpha-1-Adrenergic receptors as new targets in Neuroblastoma." Doctoral thesis, Università degli studi di Trento, 2021. http://hdl.handle.net/11572/318323.
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High-risk neuroblastoma (NB) is an aggressive childhood tumor that originates from progenitor neural crest cells. Even if the therapeutic protocol for NB is articulate and aggressive, the outcome remains dismal, with the 5-year disease-free overall survival below rating 50%. A novel drug combination strategy can possibly provide a new solution to this unmet therapeutic need. 13-cis retinoic acid (13-cis-RA, isotretinoin) is an anti-proliferative and pro-differentiative agent currently used in the post-consolidation phase of NB therapy. To identify molecules able to potentiate the anti-proliferative activity of 13-cis-RA, NB cells were treated with a library of 169 naturally occurring polyphenols in combination with the retinoid. This in vitro screen led to the identification of isorhamnetin as a synergistic partner of 13-cis-RA, producing an 80% reduction in cell viability. At the molecular level, this synergistic effect is followed by a marked increase in the expression of a member of the catecholamine receptor superfamily: the adrenergic receptor alpha-1B (ADRA1B) suggesting that this receptor might represent a key mediator of the synergistic effect of 13-cis-RA and isorhamnetin observed in vitro. This finding redirected our attention to the class of adrenergic receptors (ARs) as novel targets in NB. To investigate the role of ADRA1B in the synergism, we generated CHP134 NB cell lines knocked-out (KO) for the receptor and observed that exposure of CHP134 KO cell to 13-cis-RA leads to a reduction of cell viability and neural differentiation. We, therefore, substituted the genetic KO strategy with the alpha-1B adrenergic antagonist, L765,314, obtaining the same results. Subsequently, we extended the analysis on the role of adrenergic receptors (AR) performing a biased screen using two libraries of AR-ligands. The screen results confirm that the molecules working as alpha-1-ARs antagonists are those that greatly increase cell sensitivity to 13-cis-RA with reduction of cell viability and increase in differentiation. We confirmed our observation in NB xenograft mice models in vivo, treating mice with a combination of 13-cis-RA and the FDA approved alpha-1 AR antagonist doxazosin. The proposed pharmacological treatment was effective in slowing tumor growth, leading to tumors of smaller size. From our results, we can conclude that the deletion or inhibition of alpha-1-AR sensitizes NB cells to 13-Cis-RA, both in terms of induction of apoptosis and neural differentiation.
Since NB is a catecholamine-rich tumor, we propose that antagonization of alpha-1-AR disrupts the established autocrine pro-survival circuit generated by catecholamines in NB and restores the ability of the cells to follow the pro-differentiative and pro-apoptotic programs endorsed by 13-cis-RA. Considering the druggable nature of the alpha-1-AR receptors, we indicate this class of receptors as a novel pharmacological target for the treatment of neuroblastoma.
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Zolty, Ronald. "Beta 1 and Alpha 2C adrenergic receptor polymorphisms and response to beta blockers in heart failure patients /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.
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Thesis (Ph.D. in Clinical Science) -- University of Colorado Denver, 2007.<br>Typescript. Includes bibliographical references (leaves 130-142). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
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Stamer, William Daniel 1964. "Characterization of alpha(2)-adrenergic receptors and aquaporin-1 water channels in the human eye." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/282123.
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In most cells, water moves across the plasma membrane by simple diffusion. However, there are specialized epithelia, such as the kidney proximal tubules, that secrete or absorb water faster than simple diffusion predicts. While the identification of a proteinacious pore that transports water was elusive for many years, the recent discovery of aquaporin-1 (AQP-1) provides a molecular mechanism for the extraordinarily high permeability to water of epithelial cells in these tissues. Like the kidney, the human eye has several epithelial-lined structures that have a high permeability to water. One of these structures, the ciliary process, secretes aqueous humor (comprised mostly of water) into the eye and is regulated therapeutically by activating α₂-adrenergic receptors (α₂-AR) on its plasma membrane. The studies presented in this dissertation are structured to address four specific aims that were designed to test the hypothesis that the AQP-1 water channels are present in the human eye and are functionally regulated by α₂-ARs. Specific aim 1 characterized the distribution of AQP-1 in the human eye by immunofluorescence microscopy using affinity purified antibodies against purified AQP-1 protein. Using standard techniques in molecular biology, specific aim 2 generated antibodies to three fusion proteins; each containing a specific region of AQP-1. After screening several cell lines from the eye and the kidney with anti-AQP-1 and anti-α₂-AR IgY, specific aim 3 identified a cell line, human trabecular meshwork (HTM) cells, that contains both the AQP-1 water channels and α₂-ARs. Lastly, specific aim 4 investigated the functional relationship between the α₂-ARs and AQP-1 water channels. Using HTM cells as a model, the activation of α₂-ARs did not measurably affect AQP-1 messenger RNA or AQP-1 protein levels as compared to control. However, since the α₂-ARs primarily couple to cyclic AMP (cAMP) and several other aquaporins are regulated by cAMP, the effect of cAMP on AQP-1 was investigated. Using Xenopus oocytes expressing AQP-1 as a model, stimulation of oocytes with forskolin, a drug which increases intracellular cAMP, increased the permeability of AQP-1 to water. This observation provided evidence that is consistent with the general hypothesis that AQP-1 water channels and α₂-ARs are functionally coupled.
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Al-Khairi, Irina. "Characterization of signal transduction pathways of alpha-1 adrenergic receptors in neonatal ventral hippocampus lesion rat model." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112374.
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Neonatal ventral hippocampus (nVH) lesioned animals show molecular and behavioral abnormalities analogous to those described in schizophrenia. As an extension to previous studies that showed an increase in ligand binding of cortical alpha-1 adrenergic receptors (AR) and a dysfunction in alpha-1 AR regulation of mesolimbic dopamine functions in post-pubertal nVH lesioned rats, we investigated the subcellular expression and activity of protein kinase C (PKC)---a second messenger in alpha-1 AR signaling---in the prefrontal cortex (PFC) and nucleus accumbens (NAcc) of post-pubertal nVH lesioned rats. Western blot analysis of membrane and cytosolic fractions showed complex changes in lesioned animals in the expression of different PKC subtypes following saline or alpha-1 AR agonist (cirazoline i.p.) injection. Among these changes, nVH lesioned animals showed a significant increase in membrane bound PKC alpha and phospho-PKC, and a decrease in cytosolic PKC gamma and PKC betaII in the PFC in comparison to sham-lesioned controls following saline. Cirazoline increased membrane bound PKC alpha in controls but decreased it in lesioned animals. In the NAcc, lesioned animals showed an increase in membrane bound and cytosolic PKC epsilon and PKC lambda levels following saline. Following cirazoline, lesioned animals showed a decrease in membrane bound PKC epsilon and PKC lambda, while controls showed an increase in cytosolic and membrane fractions of PKC epsilon with no change in PKC lambda. In vitro PKC activity assays showed increased basal activity in PFC slices of lesioned animals compared to controls, with no difference in NAcc slices. alpha-1 AR stimulation by the agonist phenylephrine (PE) increased PKC activity in PFC of controls while decreasing activity substantially in lesioned animals. In the NAcc, high concentrations of PE increased activity in controls, but decreased activity in lesioned animals. This abnormal expression and activity of PKC in the PFC and NAcc of nVH lesioned animals may be related to abnormal alpha-1 AR functions and may modulate some of the abnormal neuronal functions in these animals, such as working memory deficits and hyper neuronal excitability of the PFC and the NAcc.
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Raji, Ismaila. "Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive wistar rats." Thesis, University of the Western Cape, 2011. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_5212_1367481132.
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<p>Tulbaghia violacea Harv. (Alliaceae) is a small bulbous herb which belongs to the family, Alliaceae, most commonly associated with onions and garlic. In South Africa (SA), this <br>herb has been traditionally used in the treatment of various ailments, including fever, colds, asthma, paralysis, hypertension (HTN) and stomach problems. The aim of this study <br>was to evaluate the effect of methanol leaf extracts (MLE) of T. violacea on the blood pressure (BP) and heart rate (HR) in anaesthetized male spontaneously hypertensive rats<br> <br>and to find out the mechanism(s) by which it acts. The MLE of T. violacea (5 - 150 mg/kg), angiotensin I (ang I, 3.1 - 100 &mu<br>g/kg), captopril (10 mg/kg), angiotensin II (ang II, 3.1 - 50 <br>g/kg), losartan (30 mg/kg), phenylephrine (0.01 &ndash<br>0.16 mg/kg), prazosin (1 mg/kg), dobutamine (0.2 &ndash<br>10.0 &mu<br>g/kg), propranolol (0.1 - 12.8 mg/kg), muscarine (0.16 -10 &mu<br>g/kg), <br>and atropine (0.02 - 20.48 mg/kg) were administered intravenously into male spontaneously hypertensive rats (SHR) weighing between 300 g and 350 g and aged less than 5 <br>months. The MLE of T. violacea and/or the standard drugs were infused alone, simultaneously, or separately into each animal. The BP and HR were measured via a pressure <br>transducer connecting the femoral artery and the Powerlab. The vehicle (0.2 mls of a mixture of dimethylsulfoxide and normal saline), T. violacea (60 mg/kg) and captopril (10 <br>mg/kg) were injected intraperitoneally into some SHR for 21 days to investigate the chronic effect of these agents on plasma levels of aldosterone. The mean change, the mean <br>of the individual percentage changes and the percentage difference (in mean) observed with each intervention was calculated and statistically analyzed using the Student&rsquo<br>s t test <br>for significant difference (p <<br>0.05). The Microsoft Excel software was used for statistical analysis. T. violacea significantly (p <<br>0.05) reduced the systolic, diastolic, and mean <br>arterial BP<br>and HR dose-dependently. In a dose-dependent manner, ang I, ang II, phenylephrine significantly (p <<br>0.05) increased the BP, while propranolol, muscarine and <br>atropine reduced the BP. The increases in BP due to dobutamine were not dose-dependent. In a dose dependent manner, phenylephrine and propranolol reduced the HR, while dobutamine increased the HR. The effect of ang I, ang II, muscarine and atropine on HR were not dose-dependent<br>with both increases as well as decreases observed with ang <br>I, and II and atropine, while decreases were seen with muscarine. Captopril produced <br>significant (p <<br>0.05) reduction in BP which were not associated with any change in HR. The co-infusion of ang I with the MLE produced significant (p <<br>0.05) reduction in BP, which were not associated with significant changes in HR. The co-infusion of ang II with the <br>MLE did not produce any significant changes in BP or HR when compared to the infusion of the standard drug alone. The co-infusion of phenylephrine with the MLE did not <br>produce any significant change in BP or HR when compared to the values obtained with the infusion of the standard drug alone, in both the absence and presence of prazosin. <br>The co-infusion of dobutamine with T. violacea produced siginificant (p <<br>0.05) increases in DBP which were associated with significant (p <<br>0.05) reductions in HR, when <br>compared to the values obtained with the infusion of the standard drug alone. Theco-infusion of atropine with the MLE did not produce any significant change in BP or HR when <br>compared to the values obtained with the infusion of atropine alone. However, the infusion of T. violacea, 20 minutes after pre-treating animals with atropine (5.12 mg/kg) lead to <br>dose dependent significant (p <<br>0.05) increases in BP, which were associated with dose-dependent increases in HR. The chronic treatment of animals with T. violacea or <br>captropril produced (a) signicant (p <<br>0.05) reductions in the plasma levels of aldosterone when compared to the values obtained in the vehicle-treated group, (b) produced <br>signifiant (p <<br>0.05) reduction in BP in the captopril treated group when compared to the vehicle-treated, (c) did not produce any signficant change in BP in the T. violacea-treated <br>group when compared to the vehicle-treated group and (d) did not produce any signifiant change in HR or body weight in any of the groups. The result obtained in this study <br>suggests that T. violacea reduced BP and HR in the SHR. Secondly, the BP and HR reducing effect of the MLE may involve a) the inhibition of the ACE, b) the inhibition of the &beta<br>1 <br>adrenoceptors, c) the stimulation of the muscarinic receptors and d) the reduction of the levels of aldosternone in plasma. The results also <br>suggest that the MLE may not act <br>through the angiotensin II receptors or the &alpha<br>1 adrenergic receptors. <br></p>
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Walker, Mollie. "Characterisation of α-1 adrenergic receptors in peripheral blood mononuclear cells of complex regional pain syndrome". Thesis, Walker, Mollie (2017) Characterisation of α-1 adrenergic receptors in peripheral blood mononuclear cells of complex regional pain syndrome. Honours thesis, Murdoch University, 2017. https://researchrepository.murdoch.edu.au/id/eprint/38078/.
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Complex regional pain syndrome (CRPS) is a chronic pain condition that may occur after injury or trauma to a limb. The underlying pathophysiology of CRPS is largely undetermined, although CRPS patients commonly present with a persisting inflammatory response in the early stage of the condition and overexpress the α-1 adrenergic receptor (α-1AR) on nociceptors and keratinocytes in the affected limb. In other chronic inflammatory conditions, increased α-1AR mRNA expression in peripheral blood mononuclear cells (PBMCs) has been shown, and is thought to contribute to persisting inflammation. The α-1AR are expressed on a range of cells, including nerve, smooth muscle, skin and immune cells, and bind to adrenaline and noradrenaline released after activation of the sympathetic nervous system. The aims of this project were to examine the mRNA expression of α-1AR subtypes (α-1A, α-1B and α-1D) by qPCR in PBMCs isolated from fractionated blood of CRPS patients, and to quantify the percentages of various PBMC subpopulations compared to healthy controls. Subpopulations of PBMCs were determined by flow cytometry using a panel of fluorescent antibodies that identified CD4+ T cells, CD8+ T cells, CD4+ CD8+ T cells, CD4+ CD25+ T cells, CD8+ CD25+ T cells, B cells, natural killer (NK) cells, NKT cells, and subsets of monocytes. No differences in expression of α- 1AR subtypes in PBMCs of CRPS patients were found when compared to healthy controls. However, a significant increase in the concentration of total PBMCs isolated per mL of blood in CRPS patients and a shift from CD16- to CD16+ monocyte subpopulations was identified when compared to healthy controls. These results show there is an inflammatory component to CRPS and provide preliminary evidence that the persisting inflammation in CRPS patients may originate from over-proliferation of PBMC progenitors in the bone marrow, which is sympathetically modulated by α-1AR, and/or an expansion of other PBMC cell types that were not examined in this project.
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Kamath, Aarthi. "Alterations in responsiveness and mRNA expression of alpha-1 adrenergic receptors in neonatal ventral hippocampus lesioned rats." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18675.
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Neonatal ventral hippocampus (nVH) lesion in rats is a widely accepted animal model of schizophrenia due to the exclusively post-pubertal emergence of many schizophrenia-like abnormalities. Previous studies have shown increased ligand binding of a-1 adrenergic receptors (AR) in the frontal cortex of post-pubertal nVH lesioned rats, compared to sham-operated control rats. Also, pretreatment with a-1 AR antagonist prazosin reversed amphetamine-induced hyperlocomotion in controls, but failed to do so in lesioned animals. In order to investigate the hypothesis that nVH lesions may lead to hyperactivity of a-1 AR, we studied locomotor behavior and prepulse inhibition (PPI) in post-pubertal (PD56-90) sham and lesioned animals in response to different doses of a-1 AR agonist cirazoline. Results showed that 0.6 mg/kg cirazoline significantly increased locomotor activity in both groups of animals, without any differential effect on nVH lesioned animals. However, lesioned animals showed a substantial decrease in PPI in response to an intermediate dose of 0.45 mg/kg cirazoline that did not significantly reduce PPI in control animals. This deficit was blocked by pretreatment with prazosin, demonstrating that the effect of cirazoline was through activation of a-1 ARs. Together, these results suggest that nVH lesioned animals show a hyperactive a-1 AR system that may regulate at least some behaviors that are abnormal in these animals. In situ hybridization using digoxigenin-labeled, subtype-specific oligonucleotide probes for a-1 AR mRNA revealed a significantly higher number of cells labeled for a-1A AR mRNA, a lower number of cells labeled for a-1D AR mRNA, and no difference in the number of cells labeled for a-1B AR mRNA in the medial prefrontal cortex of nVH lesioned rats. These results suggest that alterations at the level of transcription of genes encoding for some a-1 AR subtypes may be responsible for the abnormal adrenergic system in nVH lesioned animals.<br>La lésion ventrale néonatale de l'hippocampe (nVH) chez les rats est largement admise comme modèle animal de la schizophrénie. Des études antérieures ont montré une augmentation de liaison aux récepteurs adrénergiques (AR) a-1 dans le cortex frontal des rats post-pubères ayant des lésions au niveau du nVH (nVHL) comparativement aux rats contrôles. De plus, l'hyperlocomotion normalement induite chez les rats contrôles par l'amphétamine est abolit par le prétraitement de ces rats avec le prazosin, un antagoniste du AR a-1, alors que ce dernier est sans effet sur les rats avec lésions.. Afin d'investiguer l'hypothèse que des lésions au niveau du nVH peuvent mener à l'hyperactivité du AR a-1, nous avons étudié les comportements locomoteurs et la «prepulse inhibition» (PPI) chez les rats contrôles (PD56-90) et les nVHL, en réponse à différentes doses de l'agoniste adrénergique a-1 cirazoline. Les résultats montrent qu'une dose de 0.6 mg/kg de cirazoline augmente significativement l'activité motrice dans les deux groupes d'animaux, sans effet différentiel chez les nVHL. Cependant, les nVHL présentent une diminution substantielle du PPI suite à l'administration de 0.45 mg/kg de cirazoline, laquelle dose ne réduit pas de manière significative la PPI chez les contrôles. Ce déficit a été bloqué par le prétraitement avec le prazosin, démontrant que les effets de la cirazoline sont médiés via l'activation du AR a-1. Ensemble, ces résultats suggèrent que les nVHL ont une hyperactivité du système adrénergique a-1, laquelle peut mener à certains comportements anormaux chez ces animaux. Nous avons utilisé des sondes marquées avec digoxigenin pour faire de l'hybridation in situ. Les sondes étaient spécifiques pour différents sous-types d'oligonucléotides d'ARNm de AR a-1. Les resultats ont indiqué un nombre sensiblement plus élevé de cellules marquées par l'ARNm a-1A, un nombre inférieur de cellules marquées par l'ARN
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McLean, Alison Jane. "Ligand regulation of #beta#â†1- and #beta#â†2- adrenergic receptors and their GFP-tagged forms." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323436.
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Manion, Sean T. "Amygdala, anxiety & alpha-1 adrenoreceptors : investigations utilizing a rodent model of traumatic stress /." Download the thesis in PDF, 2006. http://www.lrc.usuhs.mil/dissertations/pdf/Manion2006.pdf.
Full textBooks on the topic "1-adrenergic receptors"
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Ruffolo, Robert R., ed. The alpha-1 Adrenergic Receptors. Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4582-7.
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Perkins, John P., ed. The Beta-Adrenergic Receptors. Humana Press, 1991. http://dx.doi.org/10.1007/978-1-4612-0463-3.
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Limbird, Lee E., ed. The alpha-2 Adrenergic Receptors. Humana Press, 1988. http://dx.doi.org/10.1007/978-1-4612-4596-4.
Full textBook chapters on the topic "1-adrenergic receptors"
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Pettinger, William A., and Donald D. Smyth. "alpha-1 Adrenergic Receptors." In The alpha-1 Adrenergic Receptors. Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4582-7_1.
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Bylund, David B., and Robert R. Ruffolo. "alpha-1 Adrenergic Receptors." In The alpha-1 Adrenergic Receptors. Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4582-7_13.
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Szabadi, E., and C. M. Bradshaw. "alpha-1 Adrenergic Receptors in the Central Nervous System." In The alpha-1 Adrenergic Receptors. Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4582-7_10.
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Hoffman, Brian B. "Regulation of alpha-1 Adrenergic Receptors." In The alpha-1 Adrenergic Receptors. Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4582-7_11.
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Hieble, J. Paul, and Robert R. Ruffolo. "Therapeutic Applications of Agents Interacting with alpha-1 Adrenergic Receptors." In The alpha-1 Adrenergic Receptors. Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4582-7_12.
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Bylund, David B. "Biochemistry and Pharmacology of the alpha-1 Adrenergic Receptor." In The alpha-1 Adrenergic Receptors. Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4582-7_2.
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Unnerstall, James R. "Localizing the alpha-1 Adrenergic Receptor in the Central Nervous System." In The alpha-1 Adrenergic Receptors. Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4582-7_3.
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Timmermans, Pieter B. M. W. M., and Martin J. M. G. Thoolen. "Ca2+ Utilization in Signal Transformation of alpha-1 Adrenergic Receptors." In The alpha-1 Adrenergic Receptors. Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4582-7_4.
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Putney, James W. "Phosphoinositides and alpha-1 Adrenergic Receptors." In The alpha-1 Adrenergic Receptors. Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4582-7_5.
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DeMarinis, Robert M., Margaret Wise, J. Paul Hieble, and Robert R. Ruffolo. "Structure—Activity Relationships for alpha-1 Adrenergic Receptor Agonists and Antagonists." In The alpha-1 Adrenergic Receptors. Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4582-7_6.
Full textConference papers on the topic "1-adrenergic receptors"
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Maciaszek, J. L., B. Andemariam, and G. Lykotrafitis. "Red Blood Cell Surface Receptor Expression of BCAM/Lu is Regulated by Protein Kinase A Activity." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14311.
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Irregular sickle red blood cells (RBCs) can contribute to the pathogenesis of vasoocclusion and other complications of sickle cell disease (SCD) via abnormal adherence to the vascular endothelium. It has previously been demonstrated that epinephrine enhances SCD RBC adhesion by activating the BCAM/Lu and ICAM-4 surface receptors [1–2]. Epinephrine acts on the RBC β2-adrenergic receptor, thereby activating Gas proteins that stimulate adenylyl cyclase (AC). This enzyme catalyzes the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP), leading to protein kinase A (PKA) activation, an intermediate step in the upregulation of BCAM/Lu and ICAM-4 mediated adhesion. The interaction of BCAM/Lu with the α5 chain of laminin may contribute to vaso-occlusive events in SCD due to overexpression of BCAM on SCD RBCs.
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Lande, K., I. O. S. S. E. Kieldsen, A. Westheim, et al. "PATIENTS WITH MILD ESSENTIAL HYPERTENSION HAVE INCREASED PLATELET SIZE AND RELEASE REACTION ANO SHOW INCREASED RECEPTOR RESPONSE TO INFUSED ADRENALINE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644261.
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Hypertensive (n = 35) and normotensive {n = 44) men all 42 years old were studied. The hypertensive (HT) had larger venous platelets than the normotensive (HT) (7.46 ± 0.10 vs 7.12 ± 0.09 10-15 1, p = 0.01). Plasma concentration of |3-thromboglobulin (BTG) was increased in arterial blood in hypertensive (40 ± 8 vs 21 ± 2 ug/1, p=0.02) while the venous values were similar in the two groups. Despite similar sampling procedure, the normotensive subjects had markedly higher BTGconcentration in venous compared to arterial blood (p≺0.01) at variance from thehypertensive where the arteriovenous difference in plasma BTG concentration was not present. Adrenaline was infused to 13 hypertensive and 12 normotensive subjects with dose gradually increasing to 0.04 pg/kg/min. Forearm blood flow was measured by strain gauge technique and relative forearm resistance calculated as mean blood pressure divided by flow. Twelve normotensive subjects (control group) received saline infusion.Change in forearm resistance reflectsβ2- activation of smooth vascular cells, change in platelet count reflects splenic liberation of platelets in response to adrenergic stimulation while change in BTG may reflect platelet release upon stimulation of α2 -receptors. Thus, middle aged men with essential hypertension show increased sensitivity to adrenaline infusion in vascular smooth muscle, spleen and platelets.
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Lanza, M., A. Beretz, A. Stierlé, D. Hanau, M. Kubina, and J. P. Cazenave. "ADRENALINE ACTIVATES HUMAN PLATELETS BUT IS NOT PER SE AN AGGREGATING AGENT. EFFECTS ON PLATELET MORPHOLOGY, MEMBRANEFLUIDITY, FIBRINOGEN BINDING, CYTOPLASMIC FREE CALCIUM AND PROTEIN PHOSPHORYLATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643762.
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Adrenaline (Adr) is generally considered as a full agonist able to induce in vitro the aggregation of human platelets and could play an important role in vivo in the appearance of thrombotic disorders when catecholamine levels are increased. Adr 2.5 M) induces the aggregation and secretion of 41 % of preloaded 3H-serotonin in human platelets in citrated plasma. This effect is not seen in plasma collected on 50 ATU/ml hirudin, and is due to the generation of traces of thrombin during blood collection and not to a direct effect of citrate itself, such asthe lowering of plasma free calcium. With washed human platelets suspended in Tyrode's buffer containing 2 mM Ca2+, 0.35 %albumin and apyrase, Adr (0.1 -100 M) doesnot cause shape change, aggregation or secretion of serotonin and does not modify platelet ultrastructure as judged by electron microscopy. Adr (1-100 M) does not change platelet membrane fluidity, as studied with the lipophilic fluorescent probe TMA-DPH. Adr has no direct effect on fibrinogen binding to intact platelets, intracellular Ca2+levels measured with quin2, or phosphorylation of 20 KDa or 47 KDapolypeptides, whereas all these parameters are modified after stimulation with ADP orthrombin. Adr potentiates the action of all types of aggregating agents on aggregation, secretion, intracellular Ca2+ levels,membrane fluidity, fibrinogen binding or protein phosphorylation. This effect is also seen with alpha2-adrenergic agonists (noradrenaline, alpha-methyl noradrenaline, clonidine) and is inhibited by alpha2-adrenergicantagonists such as yohimbine. The potentiation of platelet aggregation by Adr is not modified by prior incubation of the platelets with1mM aspirin for 15 min. This study shows that Adr alone does not induce modifications ofmorphology, metabolism or function of intactand functional washed human plateletsand that Adr cannot be considered per se as an aggregating agent. However, Adr interactswith alpha2-adrenergic receptors on human plateletsand potentiates biochemical and aggregatory responses induced by other platelet agonists.
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Wachtfogel, Yanina T., Peter C. Harpel, L. Henry Edmunds, and Robert W. Colman. "FORMATION OF Cl -Cl INHIBITOR AND KALLIKREIN-Cl INHIBITOR COMPLEXES DURING CARDIOPULMONARY BYPASS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642900.
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Cardiopulmonary bypass prolongs bleeding time and increases postoperative blood loss. Contact of blood with synthetic surfaces during extracorporeal circulation leads to major qualitative and quantitative alterations in both platelets and neutrophils. Activation of platelets results in thrombocytopenia, decreased sensitivity of platelets to aggregating agents, decreased alpha2-adrenergic and fibrinogen receptors, secretion of thromboxane B2, and depletion of alpha-granule protein contents. Neutrophils,under similar conditions, have also been shown to release their specific granule protein, lactoferrin, and their azurophilic granule enzyme, elastase.We now investigate whether the classical complement, contact, or fibrinolytic pathways have been activated as potential sources of neutrophil agonists. Employing enzyme-linked immunosorbent “sandwich” assays specific for Cl -Cl inhibitor and kalli-krein-Cl inhibitor complexes respectively, we found that plasma levels of both of these formed complexes increased 2fold after clinical cardiopulmonary bypass was completed and reverted to baseline within 24 hours post-operatively. Since these complexes are cleared iji vivo, we investigated their plasma levels during jLn vitro simulated extracorporeal circulation. Over a period of 2 hours, Cl -Cl inhibitor complexes rose from a baseline of 2 + InM to 21 + 2 nM and kalli-krein-Cl inhibitor complexes rose from 2+1 nM to 25 + 5 nM. However, there was no evidence of either in vivo or vitro plasmin-alpha plasmin inhibitor complex formation. These results indicate that activation of the classical pathway of complement and the contact system in plasma may be associated with neutrophil activation seen during clinical cardiopulmonary bypass.
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Cocchi, M., M. C. Menziani, F. Fanelli та P. G. de Benedetti. "Theoretical QSAR and QSSR analyses of 5-HT1A serotonin and α1-adrenergic receptors ligands". У The first European conference on computational chemistry (E.C.C.C.1). AIP, 1995. http://dx.doi.org/10.1063/1.47824.
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McConnaha, Elizabeth, Eric Wauson, Jennifer Giles та Kim Tran. "Regulation of myocardial autophagy by the G protein-coupled estrogen receptor 1 in basal and β adrenergic activated states". У ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.273.130382.
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Pineda, Joseba, Irati Rodilla, and Aitziber Mendiguren. "Functional characterization of α1 adrenergic receptor in the rat locus coeruleus in vitro." In MOL2NET 2017, International Conference on Multidisciplinary Sciences, 3rd edition. MDPI, 2017. http://dx.doi.org/10.3390/mol2net-03-05082.
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Bogaard, Harm J., Ramesh Natarajan, Shiro Mizuno, Donatas Kraskauskas, and Norbert F. Voelkel. "Carvedilol Reverses Maladaptive Right Ventricular Remodeling In Two Unrelated Animal Models Of Pulmonary Hypertension And Involves More Than ²1-adrenergic Receptor Blockade Alone." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4888.
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Johnson, G. J., P. C. Dunlop, M. J. Rabiet, L. A. Leis, and AH L. From. "THE DIHYDROPYRIDINE CALCIUM CHANNEL AGONIST, BAY K 8644, AND THE ANTAGONIST, NIFEDIPINE, INHIBIT U46619-INDUCED HUMAN PLATELET ACTIVATION BY COMPETITIVE BINDING TO THE THROMBOXANE A22/PGH2 RECEPTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643756.
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The dihydropyridine (DP) Ca2+ channel antagonist, nifedipine (NF), inhibits platelet aggregation .in vitro and ex vivo by an undefined mechanism. Inhibition of Ca2+ influx via Ca2+ channels is a postulated mechanism, but voltage-dependent Ca2+ channels have not been demonstrated in platelets. We previously observed that NF blocked thromboxane A2 (TXA2)-induced platelet aggregation and secretion. In order to further evaluate the mechanism of DP inhibition of platelet activation, we studied the effects of NF and BAY K 8644, (BAY), a DP with opposite (agonist) effects on muscle cells, on human platelet aggregation and secretion induced by the TXA2 mimic, U46619. We also observed the effects of DP on biochemical consequences of platelet activation: cytoplasmic ionized Ca2+ ([Ca2+]i) by fura-2 fluorescence; phosphorylation of 40,000 Dalton protein (40KP) substrate of protein kinase C by SDS-PAGE and [32p] counting; TXA2 formation by RIA of TXB2. 1μM BAY and 10μM NF inhibited the 2nd wave of platelet aggregation and secretion induced by ADP or epinephrine and blocked aggregation and secretion induced by U46619. A Schild plot gave a slope of -1 indicating competitive inhibition of U46619 by BAY (K1[=0.7μM).BAY and NF also blocked U46619-induced phosphorylation of 40KP, rise in [Ca2+]i and TXB2 formation. The (+)-(R) enantiomer of BAY (BAY+) was responsible for BAY inhibition. BAY, BAY(+), and the R enantiomer of another DP, 202-791, all functioned as competitive antagonists of [3H]-U4661 9 binding (K1[ for BAY=2.8 μM-comparable to known receptor antagonists, 13-azaprostanoic acid and BM 13.177; K1 for BAY(+)=0.69μM). Neither BAY nor NF inhibited[3H]-yohimbine binding to α adrenergic receptors.NF, BAY, BAY(+) and BAY(-) in nM concentrations slightly stimulated platelet aggregation,secretion and biochemical events induced by U46619 similar to their effects on muscle. Therefore, DP's do not inhibit platelet activation by blocking voltage-dependent Ca2+ channels. The mechanism of DP inhibition of TXA2-induced platelet activation is stereoselective, competitive binding to the TXA2/PGH2 receptor. DP's may exert similar effects on TXA2-induced vascular smooth muscle contraction.
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Nawroth, Peter P., Jerry Brett, Susan Steinberg, Charles T. Esmon, and David M. Stern. "ENDOTHELIUM AND PROTEIN S: SYNTHESIS, RELEASE AND REGULATION OF ANTICOAGULANT ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642962.
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The protein C-protein S pathway is closely linked to the vessel wall. In terms of protein C, endothelium has been shown to provide the receptor thrombomodulin, which promotes thrombin-mediated formation of activated protein C. Optimal anticoagulant function of activated protein C requires protein S and a cellular surface. Recent studies have indicated that endothelium can facilitate assembly of the activated protein C-protein S complex and that bovine endothelium expresses specific binding site(s) for protein S which promote its anticoagulant function. Expression of protein S binding sites is subject to down-regulation by Tumor Necrosis Factor (TNF) . Exposure of cultured bovine endothelium to TNF results in decreased 125I-protein s binding and attenuated rates of Factor Va inactivation after 2 hrs followed by negligible 125I-protein S binding and Factor Va inactivation by 10 hrs. These changes persist for over 48 hrs, in contrast to the more transient rise in endothelial cell tissue factor induced by TNF which returns to baseline by 24 hrs.In addition to providing binding sites for protein S, endothelium constitutively synthesizes and releases this vitamin K-dependent anticoagulant cofactor. Release of protein S is blocked by addition of warfarin, indicating that y-carboxylation facilitates the release of intracellular protein S. Morphologic studies, at the level of electron microscope, have shown protein S antigen to be present in cisternae of rough endoplasmic reticulum, the trans face of the golgi and a population of intracellular vesicles which appear to be distributed at the cellular periphery. By immunofluorescence, the distribution of protein S is distinct from that of von Willebrand Factor. The intracellular vesicles containing protein S constitute a storage pool potentially available for rapid release. Treatment of endothelium with norepinephrine results in release of protein S over the next 20 min. Release is half-maximal at a norepinephrine concentration of about 0.1 uM and is not observed with the biologically inactive entantiomer (+) norepinephrine. Norepinephrine-induced release of intracellular protein S can be blocked by prazosine (10-7 7 M), but not by propranolol (10-6 M) or yohimbine (10-5 M). These data are consistent with release of protein S being a receptor-mediated process dependent on an endothelial cell alpha 1 adrenergic receptor. Blockade of norepinephrine-induced release of protein S by pertussis toxin treatment of endothelium further defines the intracellular pathway of protein S and implicates regulatory G proteins in the stimulus-response coupling. Electron microscopic studies have shown that following exposure of endothelium to norepinephrine the intracellular vesicles containing protein S undergo exocytosis at the plasma membrane. These data define a new relationship between the autonomic nervous system and the coagulation mechanism.Protein S is clearly an endothelial cell-associated anticoagulant protein. A specific binding site on the endothelial cell surface can regulate its anticoagulant function on the vessel wall. Endothelial cell synthesis and release of protein S defines a new level of participation of endothelium in the protein C-protein S pathway.