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Literatura académica sobre el tema "Resine angiotensine"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 1 de febrero de 2022

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Artículos de revistas sobre el tema "Resine angiotensine"

Meng, Q. C., J. Durand, Y. F. Chen y S. Oparil. "Effects of dietary salt on angiotensin peptides in kidney." Journal of the American Society of Nephrology 6, n.º 4 (octubre de 1995): 1209–15. http://dx.doi.org/10.1681/asn.v641209.

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This study used a novel simple method for the extraction, separation, identification, and quantitation of angiotensin-like immunoactivity from tissue to examine the effects of altering dietary NaCl intake on intrarenal angiotensin I, II, and III levels in salt-sensitive, spontaneously hypertensive rats, salt-resistant Wistar-Kyoto rats, and Sprague-Dawley rats. Seven-week-old male spontaneously hypertensive rats, Wistar-Kyoto rats, and Sprague-Dawley rats were assigned randomly to a diet containing either 8% (high) or 1% (basal) salt and were maintained on these diets for 3 wk. Rats were then decapitated without prior anesthesia, and kidneys were rapidly (< 30 s) removed, snap frozen in liquid nitrogen, and stored at -80 degrees C. Frozen tissue was extracted in 2 M acetic acid and then subjected to solid-phase extraction with the cation exchange resin AG 50W X4. Angiotensin peptides were separated by reversed-phase high-performance liquid chromatography on a phenyl silica gel column with an eluent consisting of 20% acetonitrile in 0.1 M ammonium phosphate buffer, pH 4.9, and quantitated by radioimmunoassay. The elution of standard peptides under isocratic conditions revealed clear resolution of angiotensin I, II, and III and the (1-7) and (3-8) peptides. Recoveries of both labeled and unlabeled angiotensin peptide standards from the extraction step were > 90%. Renal angiotensin II stores were significantly higher in spontaneously hypertensive rats than in Wistar-Kyoto or Sprague-Dawley rats, independent of diet. Renal angiotensin II and III were further suppressed during dietary salt supplementation in both salt-resistant strains but not in the spontaneously hypertensive rat. These findings are consistent with an enhanced (compared with Wistar-Kyoto and Sprague-Dawley rats) role for angiotensin II in the kidney of the salt-sensitive, spontaneously hypertensive rat, particularly under conditions of dietary salt supplementation.

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Zangrillo, Alberto, Sergio Colombo, Anna Mara Scandroglio, Evgeny Fominskiy, Marina Pieri, Maria Grazia Calabrò, Paolo Federico Beccaria et al. "Angiotensin II infusion and markers of organ function in invasively ventilated COVID-19 patients". Critical Care and Resuscitation 23, n.º 2 (7 de junio de 2021): 215–24. http://dx.doi.org/10.51893/2021.2.oa9.

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OBJECTIVE: The use of angiotensin II in invasively ventilated patients with coronavirus disease 2019 (COVID-19) is controversial. Its effect on organ function is unknown. DESIGN: Prospective observational study. SETTING: Intensive care unit (ICU) of a tertiary academic hospital in Milan, Italy. PARTICIPANTS: Adult patients receiving mechanical ventilation due to COVID-19. INTERVENTIONS: Use angiotensin II either as rescue vasopressor agent or as low dose vasopressor support. MAIN OUTCOME MEASURES: Patients treated before angiotensin II was available or treated in an adjacent COVID-19 ICU served as controls. For data analysis, we applied Bayesian modelling as appropriate. We assessed the effects of angiotensin II on organ function. RESULTS: We compared 46 patients receiving angiotensin II therapy with 53 controls. Compared with controls, angiotensin II increased the mean arterial pressure (median difference, 9.05 mmHg; 95% CI, 1.87–16.22; P = 0.013) and the Pao2/Fio2 ratio (median difference, 23.17; 95% CI, 3.46–42.88; P = 0.021), and decreased the odds ratio (OR) of liver dysfunction (OR, 0.32; 95% CI, 0.09–0.94). However, angiotensin II had no effect on lactate, urinary output, serum creatinine, C-reactive protein, platelet count, or thromboembolic complications. In patients with abnormal baseline serum creatinine, Bayesian modelling showed that angiotensin II carried a 95.7% probability of reducing the use of renal replacement therapy (RRT). CONCLUSIONS: In ventilated patients with COVID-19, angiotensin II therapy increased blood pressure and Pao2/Fio2 ratios, decreased the OR of liver dysfunction, and appeared to decrease the risk of RRT use in patients with abnormal baseline serum creatinine. However, all of these findings are hypothesis-generating only. TRIAL REGISTRATION: ClinicalTrials.gov NCT04318366.

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Selvam, R., K. C. Rohini, C. Arunan y K. P. Subashchandran. "Synthesis of Biologically Important Angiotensin-II and Angiotensin-IV Peptides by Using 4-(2',4'-Dimethoxypenyl-Fmoc-Aminomethyl)phenoxy Resin". Asian Journal of Chemistry 25, n.º 15 (2013): 8673–76. http://dx.doi.org/10.14233/ajchem.2013.14998.

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Raff, H. y B. Jankowski. "Inhibition of aldosterone release by hypoxia in vitro: interaction with carbon monoxide". Journal of Applied Physiology 76, n.º 2 (1 de febrero de 1994): 689–93. http://dx.doi.org/10.1152/jappl.1994.76.2.689.

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We have demonstrated that the aldosteronogenic pathway of the zona glomerulosa is unusually sensitive to modest changes in PO2 (Michaelis constant for O2 approximately 95 Torr). The current study evaluated the interaction of CO (the classic ligand for P-450 enzymes) and the decreases in O2 on aldosteronogenesis in vitro. Bovine adrenocortical zona glomerulosa cells were incubated for 2 h and stimulated with either adenosine 3′,5′-cyclic monophosphate (cAMP) or angiotensin II. Ten and 20% CO led to significant decreases in cAMP- and angiotensin II-stimulated aldosteronogenesis. The combination of 20% CO and moderate decreases in PO2 (from approximately 140 to approximately 100 Torr) led to an interactive decrease in aldosterone production. The conversion of corticosterone to aldosterone catalyzed by aldosterone synthase, which is the site of O2 sensitivity, was not significantly inhibited by CO. We conclude that the aldosterone pathway is not exceptionally sensitive to CO compared with other steroidogenic pathways. This observation suggests that the unique O2-sensitive properties of the aldosterone pathway located primarily within aldosterone synthase may not reside in its CO binding site (i.e., heme).

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Edwards, Aurélie y Thomas L. Pallone. "Mechanisms underlying angiotensin II-induced calcium oscillations". American Journal of Physiology-Renal Physiology 295, n.º 2 (agosto de 2008): F568—F584. http://dx.doi.org/10.1152/ajprenal.00107.2008.

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To gain insight into the mechanisms that underlie angiotensin II (ANG II)-induced cytoplasmic Ca2+ concentration ([Ca]cyt) oscillations in medullary pericytes, we expanded a prior model of ion fluxes. ANG II stimulation was simulated by doubling maximal inositol trisphosphate (IP3) production and imposing a 90% blockade of K+ channels. We investigated two configurations, one in which ryanodine receptors (RyR) and IP3 receptors (IP3R) occupy a common store and a second in which they reside on separate stores. Our results suggest that Ca2+ release from stores and import from the extracellular space are key determinants of oscillations because both raise [Ca] in subplasmalemmal spaces near RyR. When the Ca2+-induced Ca2+ release (CICR) threshold of RyR is exceeded, the ensuing Ca2+ release is limited by Ca2+ reuptake into stores and export across the plasmalemma. If sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) pumps do not remain saturated and sarcoplasmic reticulum Ca2+ stores are replenished, that phase is followed by a resumption of leak from internal stores that leads either to [Ca]cyt elevation below the CICR threshold (no oscillations) or to elevation above it (oscillations). Our model predicts that oscillations are more prone to occur when IP3R and RyR stores are separate because, in that case, Ca2+ released by RyR during CICR can enhance filling of adjacent IP3 stores to favor a high subsequent leak that generates further CICR events. Moreover, the existence or absence of oscillations depends on the set points of several parameters, so that biological variation might well explain the presence or absence of oscillations in individual pericytes.

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Leckenby, Simon y Timothy Chimunda. "Terlipressin rescue therapy in renin-aldosterone-angiotensin system dysregulation induced shock". Australian Critical Care 33 (2020): S35. http://dx.doi.org/10.1016/j.aucc.2020.04.110.

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Gur, Yael, Haim Breitbart, Yehudit Lax, Sara Rubinstein y Nadav Zamir. "Angiotensin II induces acrosomal exocytosis in bovine spermatozoa". American Journal of Physiology-Endocrinology and Metabolism 275, n.º 1 (1 de julio de 1998): E87—E93. http://dx.doi.org/10.1152/ajpendo.1998.275.1.e87.

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Ejaculated mammalian spermatozoa must reside in the female genital tract for some time before gaining the ability to fertilize the egg. During this time, spermatozoa undergo some physiological changes that collectively are called capacitation. Capacitation of mammalian spermatozoa is a prerequisite for acrosome reaction, which is an exocytotic event occurring before fertilization. The specific biophysical and biochemical changes that accompany sperm capacitation and the agonists inducing acrosome reaction are not fully understood. Using SDS-gel electrophoresis and immunoblotting, we demonstrate the existence of a class of angiotensin receptors (AT1) in bovine spermatozoa. In capacitated sperm, we show that angiotensin II (ANG II) AT1 receptors are localized in the head and tail, whereas in noncapacitated cells the receptors are localized in the tail only. We find that ANG II markedly stimulates acrosomal exocytosis of capacitated bovine spermatozoa in vitro in a concentration range of 0.1–10 nM. No effect of ANG II was found in noncapacitated cells. The ability of ANG II to stimulate the acrosome reaction depends on the presence of calcium ions in the incubation medium. The ANG II-induced acrosome reaction was markedly inhibited by a selective AT1 receptor antagonist, losartan (DUP 753). PD-123319, a selective antagonist of the ANG II AT2 receptor, had no effect on the ANG II-induced acrosome reaction. Thus ANG II via activation of AT1 receptors may play a regulatory role in the induction of the acrosome reaction.

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Lee, Shin-Hann, Sarah M. Gomes, Judy Ghalayini, Konstantin G. Iliadi y Gabrielle L. Boulianne. "Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor Blockers Rescue Memory Defects in Drosophila-Expressing Alzheimer’s Disease-Related Transgenes Independently of the Canonical Renin Angiotensin System". eneuro 7, n.º 6 (15 de octubre de 2020): ENEURO.0235–20.2020. http://dx.doi.org/10.1523/eneuro.0235-20.2020.

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Sun, Bei, Jonathan S. Williams, Luminita Pojoga, Bindu Chamarthi, Jessica Lasky-Su, Benjamin A. Raby, Paul N. Hopkins et al. "Renin gene polymorphism: its relationship to hypertension, renin levels and vascular responses". Journal of the Renin-Angiotensin-Aldosterone System 12, n.º 4 (13 de abril de 2011): 564–71. http://dx.doi.org/10.1177/1470320311405873.

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The renin gene has been previously reported to be associated with essential hypertension in a variety of ethnic groups. However, no studies have systematically evaluated the relationship between single nucleotide polymorphisms (SNPs) representing coverage of the entire renin gene and hypertension risk. To evaluate the association between renin gene variation and hypertension we investigated data on HyperPATH cohort with 570 hypertensive and 222 normotensive Caucasian subjects. Six tagging SNPs and resultant haplotypes were tested for associations with hypertension risk, followed by mean arterial pressure (MAP), plasma renin activity (PRA) and the change in MAP in response to angiotensin II (AngII) infusion (AngII ΔMAP). The A allele of SNP rs6693954 and the haplotype containing rs6696954A were significantly associated with higher risk for hypertension (OR = 1.98, p = 0.0001; OR = 1.63 p = 0.0005, respectively). The same haplotype block was also associated with altered PRA levels and blunted AngII ΔMAP (global p-value = 0.02, 0.047, respectively). Our results confirm that polymorphisms in the renin gene are associated with increased risk for hypertension in an independent cohort, and that the underlying mechanism may reside in the interaction of renin activity and vascular responsiveness to angiotensin II.

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Royea, Jessika, Maria Lacalle-Aurioles, Lianne J. Trigiani, Alice Fermigier y Edith Hamel. "AT2R’s (Angiotensin II Type 2 Receptor’s) Role in Cognitive and Cerebrovascular Deficits in a Mouse Model of Alzheimer Disease". Hypertension 75, n.º 6 (junio de 2020): 1464–74. http://dx.doi.org/10.1161/hypertensionaha.119.14431.

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Antihypertensive medications targeting the renin-angiotensin system have lowered the incidence and progression of Alzheimer disease. Understanding how these medications function could lead to novel therapeutic strategies. AT4Rs (angiotensin IV receptors) have been associated with angiotensin receptor blockers’ cognitive, cerebrovascular, and neuroinflammatory rescue in Alzheimer disease models. Yet, whether AT4Rs act alone or with AT2Rs remains unknown. Here, we investigated whether AT2Rs contribute to losartan’s benefits and whether chronic AT2R activation could mimic angiotensin receptor blocker benefits in transgenic mice overexpressing familial Alzheimer disease mutations of the human APP (amyloid precursor protein). Losartan-treated mice (10 mg/kg per day, drinking water, 7 months) received intracerebroventricular (1 month) administration of vehicle or AT2R antagonist PD123319 (1.6 nmol/day). PD123319 countered losartan’s benefits on spatial learning and memory, neurovascular coupling, and hampered those on oxidative stress and nitric oxide bioavailability. PD123319 did not oppose losartan’s benefits on short-term memory and vasodilatory function and had no benefit on neuroinflammation or Aβ (amyloid β) pathology. Mice receiving either vehicle or selective AT2R agonist compound 21 (intracerebroventricular: 1 nmol/day, 1 month or drinking water: 10 mg/kg per day, 7 months), showed no improvement in memory, vasodilatory function, or nitric oxide bioavailability. Compound 21 treatment normalized neurovascular coupling, reduced astrogliosis independent of persisting microgliosis, and exacerbated oxidative stress in APP mice. Compound 21 reduced dense core Aβ plaques, but not diffuse plaques or Aβ species. Our findings suggest that targeting AT2Rs is not an ideal strategy for restoring Aβ-related cognitive and cerebrovascular deficits.

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Tesis sobre el tema "Resine angiotensine"

Saussine, Christian. "Actions de l'hormone parathyroidienne et de sa proteine apparentee sur la secretion de renine". Strasbourg 1, 1994. http://www.theses.fr/1994STR15089.

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Claflin, Kristin Elizabeth. "The brain renin-angiotensin system in metabolic and cardiovascular regulation". Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/2196.

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Leptin acts within the brain to increase resting metabolic rate (RMR) and blood pressure (BP). The renin-angiotensin system (RAS) elicits similar effects in the brain, as reviewed in chapter 1, and it has previously been shown that central angiotensin II type 1 (AT1) receptors are required for leptin-mediated inductions in sympathetic nerve activity to the brown adipose tissue. Thus, we hypothesize that the brain RAS mediates the metabolic effects of leptin. To investigate the interaction between the RAS and leptin, we generated the AT1ALepR-KO mouse which lacks the AT1A receptor in leptin-sensitive cells. In chapter 2, we demonstrated that stimulation of RMR by DOCA-salt and high fat diet requires AT1A receptors in leptin receptor-expressing cells and that these cells expressing both AT1A and the leptin receptor appear to be agouti related-peptide (AgRP) neurons. In chapter 3, we investigated the role of AT1A specifically in AgRP neurons by utilizing AT1AAgRP-KO mice. Similar to AT1ALepR-KO mice, AT1AAgRP-KO mice exhibited deficits in BAT SNA responses to leptin and induction of RMR by alpha melanocyte stimulating hormone. In chapter 4, we utilized a novel transgenic mouse model to demonstrate that microglia do not express the AT1A receptor under chow or high fat diet fed conditions. Taken together, we conclude that a subset of AgRP neurons, which express both the leptin receptor and the AT1A receptor, are critical for the control of sympathetic nerve activity and ultimately RMR.

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Jaquith, James B. "Synthesis of Angiotensin-converting Enzyme, ACE, inhibitors using dynamic kinetic resolution, Synthesis of the highly methylated tryptophan residue of hemiasterlin using glycidic ester ring opening reactions ; Synthesis of benz(o)indenes". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0019/NQ46525.pdf.

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Lu, Chi-Jui y 呂啟瑞. "Expression of nitric oxide synthase and angiotensin type I receptor gene of Nivienter coxingi resided in different altitude". Thesis, 2003. http://ndltd.ncl.edu.tw/handle/31759775140855839798.

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碩士
國立中山大學
生物科學系研究所
91
Environmental factors such as ambient temperature and oxygen availability are variation in different altitude. Individuals within a species, living in variable environments often display phenotypic plasticity by changing morphology, behavior, reproduction, and physiology to meet the individual’s ability to survive demanding conditions. This study was aimed to investigate the expression of angiotensin receptor and nitric oxide synthase genes of individuals resided at differential altitude, in an attempt to find the role of these molecules in cardiovascular adaptation to altitude. Spiny rats (Niviventer coxingi) are widely elevational distributed in Taiwan. They were studied under more natural conditions to provide an ecological context data on physiological plasticity between the different altitudes. I examined the body weight, blood pressure, heart rate and the expression of angiotensin type 1 or type 2 (ATI or ATII) receptor and nitric oxide synthase (NOS) genes in tissues (cortex, hypothalamus, medulla, lung, heart, aorta, adrenal gland and kidney) of spiny rats resided at differential altitude and during the domesticated period. The results of the study showed that spiny rats resided at higher altitudes were lighter than that at lower altitudes (750 m: 178.6±35.8 g and 1600 m: 122.3±29.3 g). Spiny rats resided at 1600 m did not change their body weight during the domesticated period, but rats resided at 750 m gradually reduced their body weight. Blood pressure and heart rate were similar between rats resided at different altitudes, and did not change during the domesticated period. ATI receptor, endothelelial NOS (eNOS), inducible NOS (iNOS) and neuronal NOS (nNOS) mRNA expression in these tissues were similar between rats resided at different altitudes. ATII receptor mRNA expressed in these tissues under our detection limit. Rats resided at 750 m declined the level of nNOS in heart, when they were domesticated at 100 m. ATI receptor in kidney reduced at first, but subsequently increase to same level like native. Moreover, rats resided at 1600 m declined the level of iNOS in heart, when they were domesticated at 100 m. Together, these results indicate that heart rate, blood pressure, ATI receptor, eNOS, iNOS and nNOS mRNA expressions in these tissues were similar between rats resided at different altitudes. If there was no other compensatory mechanism, individuals resided at higher altitude were limited in low available oxygen. A reduced body weight could help in adaptation to high-altitude.

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Capítulos de libros sobre el tema "Resine angiotensine"

Therrien, Kimberley A., Maud Deraët, Anick Dubois, Lenka Rihakova, Eric A. Kitas, Walter Meister, Robert Speth y Emanuel Escher. "Tools for the Identification of Receptor Dimmers: Synthesis and Biological Evaluation of On-Resin Dimerized, Photosensitive Analogues of Angiotensin II". En Peptides: The Wave of the Future, 888–89. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0464-0_414.

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Clayton, Daniel, Iresha Hanchapola, Patrick Perlmutter, A. Ian Smith y Marie-Isabel Aguilar. "The active site specificity of angiotensin II converting enzyme 2 investigated through single and multiple residue changes and β-amino acid substrate analogs." En Advances in Experimental Medicine and Biology, 559–60. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-73657-0_245.

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Boffa, Giovanni. "Cardiomyopathy". En The ESC Handbook on Cardiovascular Pharmacotherapy, editado por Claudio Ceconi, Francesca Mantovani y Erland Erdmann, 285–88. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198759935.003.0018.

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Hypertrophic cardiomyopathy (HCM) is characterized by the presence of increased left ventricular (LV) wall thickness that is not explained by loading conditions. The LV diastolic function is impaired in the majority of patients, and resting or provocable LV outflow tract obstruction is often present. The management of HCM is directed towards minimizing symptoms, improving LV diastolic function, and reducing LV outflow tract obstrucion. Beta-blockers reduce myocardial oxygen demand and improve LV filling via their negative chronotropic and inotropic effects. Moreover, they decrease LV outflow tract obstruction. The calcium channel blockers verapamil and diltiazem can be used when beta-blockers are contraindicated or ineffective. Diuretics improve dyspnoea in patients with increased pulmonary capillary pressure, and their use is mandatory if signs of fluid retention are present. The role of non-pharmacological treatment (surgery, electrical and mechanical device implantation) is important in specific groups of patients. Dilated cardiomyopathy is defined by the presence of LV dilatation and systolic dysfunction in the absence of abnormal loading conditions or coronary artery disease. Treatment of symptomatic patients should follow the therapeutic algorithm proposed by European Society of Cardiology guidelines on heart failure. First-line treatment includes diuretics, angiotensin-converting enzyme (ACE) inhibition (or angiotensin receptor blockade), beta-blockade, and aldosterone antagonism. The complex neprilysin inhibitor sacubitril/valsartan is recommended to replace ACE inhibitors in patients who remain symptomatic despite optimal treatment. The If channel inhibitor ivabradine should be considered for patients in sinus rhythm and with a resting heart rate of >70 bpm. ICD implantation with cardiac resynchronization function, LV assist devices, and heart transplantation are indicated in selected patients.

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Hypertrophic cardiomyopathy (HCM) is characterized by the presence of increased left ventricular (LV) wall thickness that is not explained by loading conditions. The LV diastolic function is impaired in the majority of patients, and resting or provocable LV outflow tract obstruction is often present. The management of HCM is directed towards minimizing symptoms, improving LV diastolic function, and reducing LV outflow tract obstruction. Beta-blockers reduce myocardial oxygen demand and improve LV filling via their negative chronotropic and inotropic effects. Moreover, they decrease LV outflow tract obstruction. The calcium channel blockers verapamil and diltiazem can be used when beta-blockers are contraindicated or ineffective. Diuretics improve dyspnoea in patients with increased pulmonary capillary pressure, and their use is mandatory if signs of fluid retention are present. The role of non-pharmacological treatment (surgery, electrical and mechanical device implantation) is important in specific groups of patients. Dilated cardiomyopathy is defined by the presence of LV dilatation and systolic dysfunction in the absence of abnormal loading conditions or coronary artery disease. Treatment of symptomatic patients should follow the therapeutic algorithm proposed by European Society of Cardiology guidelines on heart failure. First-line treatment includes diuretics, angiotensin-converting enzyme (ACE) inhibition (or angiotensin receptor blockade), beta-blockade, and aldosterone antagonism. The complex neprilysin inhibitor sacubitril/valsartan is recommended to replace ACE inhibitors in patients who remain symptomatic despite optimal treatment. The If channel inhibitor ivabradine should be considered for patients in sinus rhythm and with a resting heart rate of >70 bpm. ICD implantation with cardiac resynchronization function, LV assist devices, and heart transplantation are indicated in selected patients.

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Mari, F. y X. Xie. "Multidimensional NMR investigation of the Neurotoxic Peptide Mastoparan in the Absence and Presence of Calmodulin". En Biological NMR Spectroscopy. Oxford University Press, 1997. http://dx.doi.org/10.1093/oso/9780195094688.003.0019.

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Calmodulin (CaM) is the major Ca2+ receptor in eukaryotic cells (Means and Rasmussen, 1988). This paper begins an investigation into the structural requirements for neurotoxic peptide binding to CaM. In resting cells, CaM is deficient in Ca2+ (the protein has the potential for binding four Ca2+ ions with high affinity, pKd > 6 (Means and Rasmussen, 1988)). Following nerve cell excitation, intracellular levels of Ca2+ increase dramatically, from about 0.1 μM to about 10 μM, allowing CaM to become fully-loaded with Ca2+ . Ca2+ - loaded CaM has the ability to activate a number of neural enzymes, including cyclic nucleotide phosphodiesterase, adenylate cyclase, Ca2+ - CaM kinase and calcineurin (Kennedy, 1989). A tight-binding neurotoxic peptide would be expected to competitively inhibit activation of these enzymes. The high level of intercellular coordination required by higher organisms is attained, in part, by the complex interplay of the nervous and endocrine systems. Two important second messengers are involved in information transfer processes associated with the normal operation of these two systems: cyclic AMP (cAMP) and Ca2+ . Cyclic AMP is involved in trans-membrane information flow following the interaction of cell surface receptors with certain hormones (e.g., glucagon, epinephrine and ACTH), while Ca2+ is the principal information carrier in the nerve cell following stimulation of the system by membrane depolarization. CaM plays a pivotal role in second messenger function in both the nervous and endocrine systems. In the nervous system, calmodulin is the principal target for Ca2+. In the endocrine system, CaM (complexed with Ca2+) is responsible for activating the enzymes responsible for both cAMP synthesis (i.e., adenylate cyclase) and degradation (i.e., cyclic nucleotide phosphodiesterase). Additional linkage between the nervous and endocrine systems is evident from the fact that both systems are responsive to some of the same peptide messengers. For example, insulin, glucagon, angiotensin, and somatostatin have been found in the brain, and may function as neurotransmitters (Malencik and Anderson, 1982) perhaps through CaM mediation.

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Fields, Gregg B. y Janelle L. Lauer-Fields. "Principles and Practice of Solid-Phase Peptide Synthesis". En Synthetic Peptides. Oxford University Press, 2002. http://dx.doi.org/10.1093/oso/9780195132618.003.0006.

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Peptides play key structural and functional roles in biochemistry, pharmacology, and neurobiology, and are important probes for research in enzymology, immunology, and molecular biology. The amino acid building blocks can be among the 20 genetically encoded L-residues, or else unusual ones, and the sequences can be linear, cyclic, or branched. It follows that rapid, efficient, and reliable methodology for the chemical synthesis of these molecules is of utmost interest. A number of synthetic peptides are significant commercial or pharmaceutical products, ranging from the sweet dipeptide L-Asp-L-Phe-OMe (aspartame) to clinically used hormones such as oxytocin, adrenocorticotropic hormone, calcitonin, and gonadotropin releasing hormone (GnRH) super-agonists. Synthesis can lead to potent and selective new drugs by judicious substitutions that change functional groups and/or conformations of the parent peptide. These include introduction of N- or C-alkyl substituents, unnatural or D-amino acids, side-chain modifications including sulfate or phosphate groups or carbohydrate moieties, and constraints such as disulfide bridges between half-cystines or side-chain lactams between Lys and Asp or Glu. Commercially important products that evolved from such studies include protease inhibitors, such as captopril and other angiotensin converting enzyme (ACE) inhibitors, peptidomimetic HIV protease inhibitors, and the somatostatin analog lanreotide. Most of the biologically or medicinally important peptides which are the targets for useful structure-function studies by chemical synthesis comprise under 50 amino acid residues, but occasionally a synthetic approach can lead to important conclusions about small proteins (full or domains) in the 100-200 residue size range. Methods for synthesizing peptides are divided conveniently into two categories: solution (classical) and solid-phase pep tide synthesis (SPPS). The classical methods have evolved since the beginning of the twentieth century, and they are described amply in several reviews and books (Wünsch, 1974; Finn and Hofmann, 1976; Bodanszky and Bodanszky, 1984; Goodman et al, 2001). The solid-phase alternative was conceived and elaborated by R. B. Merrifield beginning in 1959, and has also been covered comprehensively (Erickson and Merrifield, 1976; Birr, 1978; Barany and Merrifield, 1979; Stewart and Young, 1984; Merrifield, 1986; Barany et al., 1987, 1988; Kent, 1988; Atherton and Sheppard, 1989; Fields and Noble, 1990; Barany and Albericio, 1991; Fields et al., 1992; Gutte, 1995; Fields, 1997; Lloyd-Williams et al., 1997; Chan and White, 2000; Kates and Albericio, 2000).

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Actas de conferencias sobre el tema "Resine angiotensine"

Lazo, K., J. Yang y S. M. Pastores. "Angiotensin-II to the Rescue: Assessing Angiotensin-II in Cancer Patients with Refractory Septic Shock". En American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2747.

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Wösten-van Asperen, Roelie M., R. Lutter, Patricia A. Specht, Gert N. Moll, Job B. van Woensel, Chris M. van der Loos, Harry van Goor, Jelena Kamilic, Sandrine Florquin y Albert P. Bos. "Imbalance Between Ace And Ace2 Activity Modulates Acute Respiratory Distress Syndrome; Rescue By Angiotensin-(1-7)". En American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4001.

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Ordioni, U., G. Labrosse, F. Campana, R. Lan, J. H. Catherine y A. F. Albertini. "Granulomatose oro-faciale révélatrice d’une maladie de Crohn : présentation d’un cas". En 66ème Congrès de la SFCO. Les Ulis, France: EDP Sciences, 2020. http://dx.doi.org/10.1051/sfco/20206603017.

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La granulomatoses oro-faciale (GOF) est une entité rare regroupant toutes les pathologies caractérisées par une inflammation granulomateuse non caséeuse de la région oro-faciale. Le diagnostic est histologique. L’étiologie n’est pas connue. L’oedème labial d’abord intermittent, pouvant s’installer de manière permanente, est un symptôme classique de la GOF. D’autres signes cliniques, extra-oraux, peuvent être associées lorsque la GOF s’inscrit dans le cadre d’une pathologie systémique : maladie de Crohn, Sarcoïdose, maladie de Wegener. Nous présentons le cas d’un patient pour qui l’exploration de sa GOF a conduit au diagnostic de maladie de Crohn (MC). Un patient de 29 ans consultait pour une tuméfaction labiale évoluant depuis an après échec de traitement locaux (dermocorticoïdes). On notait des diarrhées chroniques étiquetées maladie coeliaque et un épisode d’hyperplasie gingivale à l’âge de 14 ans (gingivectomie réalisée par un parodontiste mais sans analyse anatomopathologique). L’examen clinique montrait un oedème labial supérieur et inférieur associé à un érythème, une hyperplasie gingivale, une ulcération vestibulaire et une langue géographique associée à une langue plicaturée. On ne notait pas de paralysie faciale. Des biopsies étaient réalisées. La biopsie labiale montrait une muqueuse normokératosique, avec des remaniements spongiotiques, sans micro-abcès. Le chorion sous-jacent était oedémateux avec des vaisseaux dilatés. On observait plus en profondeur un vaisseau altéré avec un granulome lympho-épithéioïde sans cellule géante et sans nécrose. La biopsie gingivale montrait une muqueuse oedémateuse sans granulome. L’examen biologique (NFS, VS, CRP, bilan martial, dosage enzyme conversion angiotensine, sérologie VIH, VHC, VHB) et la radiologie thoracique était sans particularité. Compte tenu de la présente d’une pathologie intestinale et à la vue de ces nouvelles données, un avis gastro-entérologique était demandé. L’examen proctologique montrait des marisques anales. L’entero-IRM confirmait le diagnostic de MC. La macrochéilie a été traité par injection de triamcinolone retard 40ml. Un traitement par anti- TNF était instauré. La MC est une maladie inflammatoire chronique de l’intestin pouvant atteindre le tube digestif de la bouche à l’anus. Les manifestations oro-faciales (macrochéilie, ulcérations buccales, hyperplasie gingivale, pseudo-polypes, erythèmes muqueux, fissures gingivales ou pyostomatite végétante) de la maladie de Crohn peuvent précéder l’atteinte intestinale. Des atteintes extra-intestinales peuvent exister : érythème noueux, uvéite, arthralgie, arthrite entéropathique. Le diagnostic de GOF doit faire rechercher des signes extra-oraux afin de déterminer si elle est isolée ou associée à une MC, à une sarcoidose ou un Wegener. En cas de GOF isolé, la question du suivi de dépistage d’une MC reste non élucidée.

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