Relevant bibliographies by topics / Angiotensine II – Antagonistes / Journal articles
To see the other types of publications on this topic, follow the link: Angiotensine II – Antagonistes.

Journal articles on the topic 'Angiotensine II – Antagonistes'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Angiotensine II – Antagonistes.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Corvol, Pierre, and Pierre-Francois Plouin. "Antagonistes des r??cepteurs de l???angiotensine II." Drugs 62, Special Issue 1 (2002): 53–64. http://dx.doi.org/10.2165/00003495-200262991-00006.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Turek, Marika, and Piotr Bałczewski. "Pharmaceutical co-crystals of angiotensin II receptor blockers." Chemistry. Environment. Biotechnology 22 (2019): 13–19. http://dx.doi.org/10.16926/cebj.2019.22.02.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Maillard, Marc P., Catherine Centeno, Åsa Frostell-Karlsson, Hans R. Brunner, and Michel Burnier. "Does protein binding modulate the effect of angiotensin II receptor antagonists?" Journal of the Renin-Angiotensin-Aldosterone System 2, no. 1_suppl (March 2001): S54—S58. http://dx.doi.org/10.1177/14703203010020010901.

Full text
Abstract:
Introduction Angiotensin II AT 1-receptor antagonists are highly bound to plasma proteins (≥ 99%). With some antagonists, such as DuP-532, the protein binding was such that no efficacy of the drug could be demonstrated clinically. Whether protein binding interferes with the efficacy of other antagonists is not known. We have therefore investigated in vitro how plasma proteins may affect the antagonistic effect of different AT1-receptor antagonists. Methods A radio-receptor binding assay was used to analyse the interaction between proteins and the ability of various angiotensin II (Ang II) antagonists to block AT1-receptors. In addition, the Biacore technology, a new technique which enables the real-time monitoring of binding events between two molecules, was used to evaluate the dissociation rate constants of five AT1-receptor antagonists from human serum albumin. Results The in vitro AT 1-antagonistic effects of different Ang II receptor antagonists were differentially affected by the presence of human plasma, with rightward shifts of the IC50 ranging from one to several orders of magnitude. The importance of the shift correlates with the dissociation rate constants of these drugs from albumin. Our experiments also show that the way that AT1-receptor antagonists bind to proteins differs from one compound to another. These results suggest that the interaction with plasma proteins appears to modulate the efficacy of some Ang II antagonists. Conclusion Although the high binding level of Ang II receptor antagonist to plasma proteins appears to be a feature common to this class of compounds, the kinetics and characteristics of this binding is of great importance. With some antagonists, protein binding interferes markedly with their efficacy to block AT1-receptors.
APA, Harvard, Vancouver, ISO, and other styles
4

García-Sáinz, J. A., M. Martínez-Alfaro, M. T. Romero-Avila, and C. González-Espinosa. "Characterization of the AT1 angiotensin II receptor expressed in guinea pig liver." Journal of Endocrinology 154, no. 1 (July 1997): 133–38. http://dx.doi.org/10.1677/joe.0.1540133.

Full text
Abstract:
Abstract In guinea pig hepatocytes angiotensin II induced phosphorylase a activation. This effect was mimicked by other angiotensins with the potency order: angiotensin II (EC50 ≈1 nm)>angiotensin III (EC50 ≈30 nm)>angiotensin I (EC50 ≈300 nm). The effect of 10 nm angiotensin II was blocked by the angiotensin II receptor AT1-selective antagonists irbesartan and losartan (Ki values of ≈1 nm and ≈10 nm for irbesartan and losartan respectively) but not by the AT2-selective antagonist PD123177. Similar data were obtained when the production of [3H]IP3 from [3H]myo-inositol-labeled cells was studied. Angiotensin II induced a dose-dependent increase in [3H]IP3 production; the maximal effect (≈3-fold) was observed at a concentration of 10 μm. This effect of angiotensin II was completely blocked by the AT1-selective antagonists irbesartan and losartan, but only in a very limited fashion by PD123177. [125I][Sar1-Ile8]angiotensin II bound with high affinity (≈3·8 nm) to a moderately abundant number of sites (≈660 fmol/mg protein) in guinea pig liver membranes. Binding competition experiments indicate the following orders of potency for agonists: angiotensin II (≈1·5 nm)>angiotensin III (≈7 nm)>angiotensin I (≈176 nm), and for antagonists: irbesartan (≈0·5 nm)>losartan (≈36 nm)>> PD123177 (>> 10 000 nm). The functional and binding data strongly indicate that the effects of angiotensin II were mediated through AT1 receptors. Expression of the mRNA for these receptors was confirmed by RT-PCR and hybridization of the reaction product with a radiolabeled rat AT1 receptor cDNA probe. Journal of Endocrinology (1997) 154, 133–138
APA, Harvard, Vancouver, ISO, and other styles
5

Nicholls, Kathy. "Angiotensin II antagonists." Nephrology 11 (April 2006): S92—S97. http://dx.doi.org/10.1111/j.1440-1797.2006.00617.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Brunner, Hans R., Jürg Nussberger, Michel Burnier, and Bernard Waeber. "Angiotensin II Antagonists." Clinical and Experimental Hypertension 15, no. 6 (January 1993): 1221–38. http://dx.doi.org/10.3109/10641969309037107.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Smith, RD, G. Cunningham, and SD Kivlighn. "Angiotensin II antagonists." Emerging Drugs 3, no. 1 (June 1998): 81–94. http://dx.doi.org/10.1517/14728214.3.1.81.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Mooney, Richard D., Yi Zhang, and Robert W. Rhoades. "Effects of angiotensin II on visual neurons in the superficial laminae of the hamster's superior colliculus." Visual Neuroscience 11, no. 6 (November 1994): 1163–73. http://dx.doi.org/10.1017/s0952523800006969.

Full text
Abstract:
AbstractSuperficial layer superior colliculus (SC) neurons were recorded extracellularly with multibarreled recording/ejecting micropipettes. Angiotensin II was delivered via micropressure ejection during visual stimulation (n = 215 cells), or during electrical stimulation of either the optic chiasm (OX; n = 150 cells) or visual cortex (CTX; n = 42 cells). Application of angiotensin II decreased visual responses of SC cells to 43.8% ± 30.7% (mean ± S.D.) and reduced responses to electrical stimulation of the OX and CTX to 58.6% ± 34.1% and 43.8% ± 30.7% of control values, respectively. Angiotensin II enhanced responses by at least 30% in only 6 cells (1.5%). Of the 35 neurons tested with both OX and CTX stimulation, the correlation of evoked response suppression by angiotensin II was highly significant (r = 0.69; P < 0.001). This suggests that the suppressive effects of angiotensin II were common to both pathways. To test whether the inhibitory effects of angiotensin II were presynaptic or postsynaptic, Mg2+ ions were ejected iontophoretically to abolish synaptic responses, and the neurons were activated by iontophoresis of glutamate and then tested with angiotensin II. Angiotensin II reduced the glutamate-evoked responses to an average 29.1% ± 21.1% of control values (n = 9 cells). This suggests that the site of action of angiotensin II is most likely postsynaptic. To identify which receptors were involved in these effects, angiotensin II was ejected concurrently with the AT1 antagonist Losartan (DUP753) or with either of two AT2 antagonists, CGP42112A or PD123177. Losartan antagonized the action of angiotensin II in 65.6% of the cells tested (n = 99) and CGP42112A and PD123177 had antagonistic effects in 58% (n = 65) and 60% (n = 5), respectively. Both classes of antagonists were tested in 29 cells; and there was no significant correlation between their effectiveness. These results suggest that both AT1, and AT2 receptors may independently mediate the suppressive effects of angiotensin II, and that collicular neurons may have either or both receptor subtypes.
APA, Harvard, Vancouver, ISO, and other styles
9

Baltatu, Ovidiu, Marco A. P. Fontes, Maria J. Campagnole-Santos, Sordaine Caligiorni, Detlev Ganten, Robson A. S. Santos, and Michael Bader. "Alterations of the renin-angiotensin system at the RVLM of transgenic rats with low brain angiotensinogen." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 2 (February 1, 2001): R428—R433. http://dx.doi.org/10.1152/ajpregu.2001.280.2.r428.

Full text
Abstract:
The transgenic rats TGR(ASrAOGEN) (TGR) with low levels of brain angiotensinogen were analyzed for cardiovascular reactivity to microinjections of ANG II and angiotensin receptor (AT1) antagonists [CV-11974, AT1 specific; A-779, ANG-(1–7) selective; sarthran, nonspecific] into the rostral ventrolateral medulla (RVLM) of conscious rats. Microinjection of ANG II resulted in a significantly higher increase in the mean arterial pressure (MAP) of TGR than control [Sprague-Dawley (SD)] rats, suggesting an upregulation of ANG II receptors in TGR. CV-11974 produced an increase in MAP of SD but not in TGR rats. A-779 produced a depressor response in SD but not in TGR rats. Conversely, sarthran produced a similar decrease of MAP in both rat groups. The pressor effect of the AT1 antagonist may indicate an inhibitory role of AT1 receptors in the RVLM. On the other hand, ANG-(1–7) appears to have a tonic excitatory role in this region. The altered response to specific angiotensin antagonists in TGR further supports the functionally relevant decrease in angiotensins in the brains of TGR and corroborates the importance of the central renin-angiotensin system in cardiovascular homeostasis.
APA, Harvard, Vancouver, ISO, and other styles
10

Tatarciuc, Diana, Decebal Vasincu, Gabriela Stoleriu, Roxana Irina Iancu, and Marcel Costuleanu. "Biochemical Effects of Intraliposomal Angiotensins on Isolated Vascular Smooth Muscle Cells." Revista de Chimie 69, no. 5 (June 15, 2018): 1187–90. http://dx.doi.org/10.37358/rc.18.5.6285.

Full text
Abstract:
The intracellular renin-angiotensin effectors (peptides, enzymes, receptors) and their effects are intriguing for a lot of systems. That�s why we aimed the effects of intracellularly-administered angiotensins (angiotensin II, angiotensin III, angiotensin IV, angiotensin fragment 1-7), angiotensinogen, CGP-42112A, apelin, and angiotensin receptors blockers (losartan, PD123319), by the means of liposomes, on apoptosis of cultured isolated rat aortic vascular smooth muscle cells. We evidenced that CGP-42112A (a potent AT2 angiotensin II receptor agonist), administered intracellularly, induced the apoptosis of the cultured isolated vascular smooth muscle cells in a much higher proportion than other agonists and antagonists of angiotensin system: CGP-42112A ] angiotensin II] angiotensin III@ angiotensinogen. Moreover, losartan (an AT1 angiotensin II receptor antagonist), administered intracellularly, induced an important degree of apoptosis of cultured isolated vascular smooth muscle cells. Losartan, administered as concomitant treatment for other angiotensin peptides and CGP-42112A, did not significantly modified the apoptotic effects of these peptides. On the other hand, PD123319 (an AT2 angiotensin II receptor antagonist) was able to significantly reduce the losartan effects when administered as co-treatment for 24 h. The same effects were obtained when LY294002, a PI3K/Akt signaling inhibitor, was administered as a co-treatment. We can conclude an involvement of an AT2 angiotensin II receptor and PI3K/Akt signaling in these apoptotic effects induced by some angiotensin peptides and losartan on cultured isolated rat aortic vascular smooth muscle cells.
APA, Harvard, Vancouver, ISO, and other styles
11

Nicholls, Charlotte, and Mojgan Sani. "Angiotensin II receptor antagonists." Nursing Older People 16, no. 5 (July 2004): 31–32. http://dx.doi.org/10.7748/nop2004.07.16.5.31.c2322.

Full text
APA, Harvard, Vancouver, ISO, and other styles
12

Burrell, Louise M., and Colin I. Johnston. "Angiotensin II Receptor Antagonists." Drugs & Aging 10, no. 6 (June 1997): 421–34. http://dx.doi.org/10.2165/00002512-199710060-00003.

Full text
APA, Harvard, Vancouver, ISO, and other styles
13

&NA;. "Angiotensin II receptor antagonists." Reactions Weekly &NA;, no. 927 (November 2002): 6. http://dx.doi.org/10.2165/00128415-200209270-00016.

Full text
APA, Harvard, Vancouver, ISO, and other styles
14

Burnier, M., and HR Brunner. "Angiotensin II receptor antagonists." Lancet 355, no. 9204 (February 2000): 637–45. http://dx.doi.org/10.1016/s0140-6736(99)10365-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
15

Messerli, FH. "Angiotensin II Receptor Antagonists." Journal of Human Hypertension 15, no. 7 (July 2001): 507. http://dx.doi.org/10.1038/sj.jhh.1001202.

Full text
APA, Harvard, Vancouver, ISO, and other styles
16

&NA;. "ANGIOTENSIN II RECEPTOR ANTAGONISTS." Southern Medical Journal 91, no. 8 (August 1998): 794. http://dx.doi.org/10.1097/00007611-199808000-00033.

Full text
APA, Harvard, Vancouver, ISO, and other styles
17

Tocci, Giuliano, Francesca Giovannelli, and Caterina Facciolo. "Angiotensin II Receptor Antagonists." High Blood Pressure & Cardiovascular Prevention 14, no. 1 (2007): 39–47. http://dx.doi.org/10.2165/00151642-200714010-00006.

Full text
APA, Harvard, Vancouver, ISO, and other styles
18

Huang, Yi-You. "IONTOPHORETIC TRANSDERMAL DELIVERY OF ANGIOTENSIN II AND ITS ANTAGONISTS." Biomedical Engineering: Applications, Basis and Communications 13, no. 05 (October 25, 2001): 242–47. http://dx.doi.org/10.4015/s1016237201000303.

Full text
Abstract:
Angiotensin II and its antagonists were used as permeant probes to investigate the mechanism of transdermal iontophoretic delivery of peptide/protein drugs and compare the effect of hydrophobic difference between the peptides drugs on the skin permeability. Transport of angiotensin II and its antagonists through excised rabbit pinna skin were enhanced with iontophoresis by monophase periodically pulsed current, amplituide=1mA, frequency=1000Hz and on/off ratio equals 50%. The delivery rate was proportional both to the current intensity and pulse duration of the stimulation. Results showed that the permeation rate of [Sar, Ile] Angiotensin II > [Sar,Ala]Angiotensin II > Angiotensin II. Iontophoretic mobility and hydrophobicity were the key factors dominating the transdermal iontophoretic delivery rate of angiotensin II and its antagonists.
APA, Harvard, Vancouver, ISO, and other styles
19

de Klaver, P. A. G. "Angiotensine II-antagonisten en mycardinfarct." Medisch-Farmaceutische Mededelingen 47, no. 8 (August 2009): 120. http://dx.doi.org/10.1007/bf03080011.

Full text
APA, Harvard, Vancouver, ISO, and other styles
20

Foote, Edward F., and Charles E. Halstenson. "New Therapeutic Agents in the Management of Hypertension: Angiotensin II-Receptor Antagonists and Renin Inhibitors." Annals of Pharmacotherapy 27, no. 12 (December 1993): 1495–503. http://dx.doi.org/10.1177/106002809302701216.

Full text
Abstract:
OBJECTIVE: To review the chemistry, pharmacokinetics, and clinical trials of two new classes of antihypertensive drugs, angiotensin II-receptor antagonists and renin inhibitors. DATA SOURCES: Primary literature on angiotensin II-receptor antagonists and renin inhibitors was identified through a comprehensive medical literature search from 1961 through 1993. This search included journal articles, abstracts, and reports of both animal and human research published in the English language. Indexing terms included renin-angiotensin aldosterone system, renin inhibitors, angiotensin II antagonists, DuP 753, losartan, MK954, A-64662, and Ro 42–5892. STUDY SELECTIONS: Emphasis was placed on clinical and pharmacokinetic studies in humans for drugs that are currently in Phase I—III research protocols in the US. DATA EXTRACTION: All available data from human studies were reviewed. DATA SYNTHESIS: Angiotensin II-receptor antagonists and renin inhibitors may be effective antihypertensives with few adverse effects noted in the small studies completed. Their potential advantage over angiotensin-converting enzyme (ACE) inhibitors includes a possible smaller adverse effect profile. In the past, the clinical utility of angiotensin II-receptor antagonists and renin inhibitors has been limited because of poor oral bioavailability, although newer agents are more readily bioavailable. CONCLUSIONS: Angiotensin II-receptor antagonists and renin inhibitors may be the next new classes of antihypertensives marketed. However, definitive conclusions about their roles in the management of hypertension are not possible until larger clinical trials assessing their efficacy and safety and comparing them with ACE inhibitors are completed.
APA, Harvard, Vancouver, ISO, and other styles
21

Halbach, Oliver Von Bohlen Und, Thomas Walther, Michael Bader, and Doris Albrecht. "Interaction Between Mas and the Angiotensin AT1 Receptor in the Amygdala." Journal of Neurophysiology 83, no. 4 (April 1, 2000): 2012–21. http://dx.doi.org/10.1152/jn.2000.83.4.2012.

Full text
Abstract:
The Mas-protooncogene is a maternally imprinted gene encoding an orphan G protein–coupled receptor expressed mainly in limbic structures of the rodent CNS. Because Mas and the product of the Mas-related gene enhance the effects of angiotensins on cells expressing angiotensin receptors of the AT1 subtype, we first compared the distribution of cells expressing AT1 receptors in different limbic and thalamic brain structures in Mas-knockout mice and in wildtype mice by an immunohistochemical approach. No significant differences could be found between the two strains. The Mas-protooncogene seems to be implicated in the signal transduction of angiotensin receptors and is expressed in the amygdala. Therefore we then analyzed whether field potentials are altered by angiotensin II in brain slices of the basolateral amygdala. An opposite action of angiotensin II was obtained in mice lacking the Mas-protooncogene in comparison to wildtype mice. The use of different angiotensin receptor antagonists provides the first in vitro evidence for a functional interaction between the Mas-protooncogene and the AT1 receptor.
APA, Harvard, Vancouver, ISO, and other styles
22

Jutte, Sara B., and Jon E. Sprague. "Pharmacologic Regulation of the Renin—Angiotensin System: Physiologic and Pathologic Effects." Journal of Pharmacy Technology 16, no. 4 (July 2000): 138–46. http://dx.doi.org/10.1177/875512250001600408.

Full text
Abstract:
Objective: To review the physiologic and pathologic roles of the renin-angiotensin system in maintaining blood pressure, glomerular filtration rate, and myocardial tissue growth. The pharmacologic regulations of the pathologic effects of the renin-angiotensin system are emphasized, with a comparison between angiotensin-converting enzyme (ACE) inhibitors and angiotensin1 receptor (AT1) antagonists. Data Sources: English-language basic science, clinical studies, and review articles were identified using MEDLINE, IOWA, and a manual search from January 1966 through September 1999. References were also obtained from the reference section of relevant published articles. Study Selection and Data Extraction: All articles identified were evaluated for possible inclusion in this review. Evaluative and comparative data from basic science and controlled clinical studies were reviewed. Data Synthesis: The renin-angiotensin system has a plethora of physiologic and pathologic roles in the regulation of blood pressure, renal function, and cell growth. The cellular mechanisms involved in eliciting the responses to the renin-angiotensin system are discussed in detail, with an emphasis on the pharmacologic regulation of the cellular responses. The role of angiotensin II in maintaining blood pressure, glomerular filtration rate, and in regulating myocardial cell growth secondary to myocardial infarction or as a complication of congestive heart failure are all reviewed. The ACE inhibitors and AT1 antagonists have comparable pharmacologic effects that can influence their therapeutic application. The ACE inhibitors and AT, antagonists are compared regarding clinically and experimentally observed differences that may affect their therapeutic application. Conclusions: The physiologic and pathologic roles of the renin-angiotensin system make the ACE inhibitors and AT1 antagonists ideal candidates in treating many conditions. Presently, few studies have been conducted that directly compare ACE inhibitors and AT, antagonists. An understanding of the basic underlying pharmacologic principles is essential when attempting to apply the scientific and clinical information of the ACE inhibitors and AT1 antagonists with the intention of extrapolating to therapeutic utility.
APA, Harvard, Vancouver, ISO, and other styles
23

Kumar, Surendra, Dharm Raj Maurya, and Mahesh Chandra. "ACE Inhibition versus Angiotensin-II Antagonism in Heart Failure." Asian Cardiovascular and Thoracic Annals 8, no. 2 (June 2000): 195–203. http://dx.doi.org/10.1177/021849230000800229.

Full text
Abstract:
Heart failure is becoming increasingly frequent. Once diagnosed, 5-year survival is less than 50% and a substantial percentage of patients (25% to 50%) die suddenly. Angiotensin-converting enzyme inhibitors are the only agents shown to reduce mortality in heart failure. All angiotensin-converting enzyme inhibitors appear to have similar clinical benefits in heart failure. Therapy should be started with a low dose and titrated up to the target dosage in major trials. Although angiotensin-I receptor antagonists provide more complete inhibition of angiotensin-II effects, they have not been found to be superior to long-acting angiotensin-converting enzyme inhibitors in reducing morbidity and mortality in heart failure. Therefore, in current clinical practice, angiotensin-II antagonists should be used as an alternative to angiotensin-converting enzyme inhibitors when the latter are not tolerated. The combined use of angiotensin-converting enzyme inhibitors and angiotensin-II antagonists is not currently recommended in the treatment of heart failure.
APA, Harvard, Vancouver, ISO, and other styles
24

Timmermans, Pieter B. M. W. M., David J. Carini, Andrew T. Chiu, John V. Duncia, William A. Price, Gregory J. Wells, Pancras C. Wong, Ruth R. Wexler, and Alexander L. Johnson. "Nonpeptide Angiotensin II Receptor Antagonists." American Journal of Hypertension 3, no. 8_Pt_1 (August 1990): 599–604. http://dx.doi.org/10.1093/ajh/3.8.599.

Full text
APA, Harvard, Vancouver, ISO, and other styles
25

Lee, Robert J. "Nonpeptide Angiotensin II Receptor Antagonists." American Journal of Hypertension 4, no. 4_Pt_2 (April 1991): 271S—272S. http://dx.doi.org/10.1093/ajh/4.4.271s.

Full text
APA, Harvard, Vancouver, ISO, and other styles
26

Steinberg, Mitchell I., Sally A. Wiest, and Alan D. Palkowitz. "Nonpeptide Angiotensin II Receptor Antagonists." Cardiovascular Drug Reviews 11, no. 3 (September 1993): 312–58. http://dx.doi.org/10.1111/j.1527-3466.1993.tb00194.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
27

Kurup, Alka, Rajni Garg, D. J. Carini, and Corwin Hansch. "Comparative QSAR: Angiotensin II Antagonists." Chemical Reviews 101, no. 9 (September 2001): 2727–50. http://dx.doi.org/10.1021/cr000025g.

Full text
APA, Harvard, Vancouver, ISO, and other styles
28

Wada, Takeo, Yoshiyuki Inada, Yumiko Shibouta, and Kohei Nishikawa. "Nonpeptide angiotensin II-receptor antagonists." Japanese Journal of Pharmacology 64 (1994): 45. http://dx.doi.org/10.1016/s0021-5198(19)49910-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
29

INADA, Yoshiyuki, Takeo WADA, Yumiko SHIBOUTA, and Kohei NISHIKAWA. "Nonpeptide angiotensin II-receptor antagonists." Folia Pharmacologica Japonica 104, no. 3 (1994): 217–28. http://dx.doi.org/10.1254/fpj.104.217.

Full text
APA, Harvard, Vancouver, ISO, and other styles
30

Ouaret, S., P. Carlier, S. Choulika, C. Tchinou, and C. Kreft-Jais. "FOETOTOXICITY OF ANGIOTENSIN II ANTAGONISTS." Journal of Hypertension 22, Suppl. 2 (June 2004): S318. http://dx.doi.org/10.1097/00004872-200406002-01103.

Full text
APA, Harvard, Vancouver, ISO, and other styles
31

Atwal, Karnail S., Syed Z. Ahmed, J. Eileen Bird, Carol L. Delaney, Kenneth E. J. Dickinson, Francis N. Ferrara, Anders Hedberg, Arthur V. Miller, and Suzanne Moreland. "Dihydropyrimidine angiotensin II receptor antagonists." Journal of Medicinal Chemistry 35, no. 25 (December 1992): 4751–63. http://dx.doi.org/10.1021/jm00103a014.

Full text
APA, Harvard, Vancouver, ISO, and other styles
32

Timmermans, Pieter B. M. W. M., Pancras C. Wong, Andrew T. Chiu, and William F. Herblin. "Nonpeptide angiotensin II receptor antagonists." Trends in Pharmacological Sciences 12 (January 1991): 55–62. http://dx.doi.org/10.1016/0165-6147(91)90498-h.

Full text
APA, Harvard, Vancouver, ISO, and other styles
33

Bovy, Philippe R., David B. Reitz, Joseph T. Collins, Timothy S. Chamberlain, Gillian M. Olins, Valerie M. Corpus, Ellen G. McMahon, et al. "Nonpeptide angiotensin II antagonists: N-phenyl-1H-pyrrole derivatives are angiotensin II receptor antagonists." Journal of Medicinal Chemistry 36, no. 1 (January 1993): 101–10. http://dx.doi.org/10.1021/jm00053a013.

Full text
APA, Harvard, Vancouver, ISO, and other styles
34

Bivalacqua, Trinity J., Hunter C. Champion, Albert L. Hyman, Dennis B. McNamara, and Philip J. Kadowitz. "Analysis of responses to angiotensin II in the mouse." Journal of the Renin-Angiotensin-Aldosterone System 2, no. 1_suppl (March 2001): S48—S53. http://dx.doi.org/10.1177/14703203010020010801.

Full text
Abstract:
Responses to angiotensin II (Ang II) were investigated in anaesthetised CD1 mice. Injections of Ang II caused dose-related increases in systemic arterial pressure that were antagonised by candesartan. Responses to Ang II were not altered by PD 123319. At the lowest dose studied (20 µg/kg i.v.), the inhibitory effects of candesartan were competitive, whereas at the highest dose (100 µg/kg i.v.), the dose-response curve for Ang II was shifted to the right in a non-parallel manner. The inhibitory effects of candesartan were selective and were similar in animals pretreated with enalaprilat to reduce endogenous Ang II production. Pressor responses to Ang II were not altered by propranolol, phentolamine or atropine, but were enhanced by hexamethonium. Increases in total peripheral resistance were inhibited by the AT1-receptor antagonist (ARB) but were not altered by AT2-receptor, alpha- or beta-receptor antagonists. These results suggest that pressor responses to Ang II are mediated by AT 1-receptors, are buffered by the baroreceptors, are not modulated by effects on AT2receptors, and that activation of the sympathetic nervous system plays little role in mediating rapid haemodynamic responses to the peptide in anaesthetised mice.
APA, Harvard, Vancouver, ISO, and other styles
35

Маслов, Л. Н., Н. В. Нарыжная, С. Ю. Цибульников, Н. С. Воронков, and Ю. В. Бушов. "Angiotensin ii and its role in regulation of heart tolerance to ischemia/reperfusion inhibitors and angiotensin ii at1-receptor antagonists." ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», no. 3() (June 27, 2019): 118–26. http://dx.doi.org/10.25557/0031-2991.2019.03.118-126.

Full text
Abstract:
Цель обзора - анализ данных о роли ангиотензина II в регуляции толерантности сердца к действию ишемии/реперфузии, а также анализ данных о кардиопротекторных свойствах ингибиторов ангиотензинпревращающего фермента (АПФ) и антагонистов АТ1-рецептора ангиотензина II. Установлено, что ангиотензин II оказывает инфаркт-лимитирующий эффект, который, по одним данным, связан с активацией АТ1-рецептора, по другим - является следствием стимуляции АТ2-рецептора. Кроме того, ангиотензин способствовал улучшению сократимости сердца в реперфузионном периоде, эффект был связан с активацией AT1-рецептора. Установлено, что ангиотензин II и АТ1-рецептор участвуют в инфаркт-лимитирующем эффекте ишемического прекондиционирования. Экспериментальные данные о способности антагонистов AT1-рецептора влиять на размер инфаркта носят противоречивый характер: есть сообщения о способности этих антагонистов оказывать инфаркт-лимитирующий эффект, есть данные об отсутствии у них подобного эффекта. Экспериментальные данные свидетельствуют, что ингибиторы АПФ оказывают инфаркт-лимитирующий эффект, который связан с увеличением уровня брадикинина и усилением продукции NO. Нет убедительных данных о том, ингибиторы АПФ и антагонисты АТ1-рецептора оказывают инфаркт-лимитирующий эффект у пациентов с острым инфарктом миокарда. Однако ингибиторы АПФ и антагонисты АТ1-рецептора препятствуют постинфарктному ремоделированию сердца. The review analyzes reports on the role of angiotensin II in regulation of heart tolerance to ischemia/reperfusion and cardioprotective properties of angiotensin converting enzyme (ACE) inhibitors and angiotensin II AT1-receptor antagonists. Angiotensin II is known to have an infarct-limiting effect, which according to some reports is associated with activation of the AT1 receptor and according to other reports results from stimulation of the AT2 receptor. In addition, angiotensin improves heart contractility during reperfusion, which is associated with activation of the AT1 receptor. Angiotensin II and AT1 receptor are also involved in the infarct-reducing effect of ischemic preconditioning. Experimental data on the ability of AT1 receptor antagonists to influence the infarct size are inconsistent; one study showed that these antagonists can exert an infarct-limiting effect whereas there is some evidence against such effect. Experimental studies have suggested that ACE inhibitors can restrict the infarct size, which is associated with increased bradykinin level and NO production. There is no convincing evidence that ACE inhibitors and AT1 receptor antagonists can restrict the infarct size in patients with acute myocardial infarction. However, ACE inhibitors and AT1 receptor antagonists prevent post-infarction heart remodeling.
APA, Harvard, Vancouver, ISO, and other styles
36

Widdop, R. E., S. M. Gardiner, P. A. Kemp, and T. Bennett. "Differential blockade of central effects of angiotensin II by AT2-receptor antagonists." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 1 (July 1, 1993): H226—H231. http://dx.doi.org/10.1152/ajpheart.1993.265.1.h226.

Full text
Abstract:
In conscious, chronically instrumented, male Long-Evans rats, we showed previously that central administration (intracerebroventricular) of the AT1-receptor antagonist EXP-3174 (1 microgram) caused a rapid-onset marked, but transient, blockade of the regional hemodynamic responses to intracerebroventricular angiotensin II (ANG II). In contrast, the AT2-receptor antagonist PD-123319 (80 micrograms) caused a slow-onset, but marked and persistent, antagonism of the effects of intracerebroventricular ANG II. In the present study we attempted to mimic the actions of PD-123319 by giving a supramaximal dose of EXP-3174 (10 micrograms), and we also assessed the effects of PD-123177 (80 micrograms), an AT2-receptor antagonist that differs from PD-123319 only by a dimethyl group. The higher dose of EXP-3174 did not exert prolonged antagonistic effects against responses to intracerebroventricular ANG II, and PD-123177 was without inhibitory effects in this model. The results indicate important functional differences between putative AT2-receptor antagonists, when assessed in vivo, that are not apparent from binding studies.
APA, Harvard, Vancouver, ISO, and other styles
37

Patel, J. M., F. R. Yarid, E. R. Block, and M. K. Raizada. "Angiotensin receptors in pulmonary arterial and aortic endothelial cells." American Journal of Physiology-Cell Physiology 256, no. 5 (May 1, 1989): C987—C993. http://dx.doi.org/10.1152/ajpcell.1989.256.5.c987.

Full text
Abstract:
Angiotensin II (ANG II) is formed from angiotensin I by the action of angiotensin-converting enzyme located on the luminal surface of vascular endothelial cells. We determined whether binding sites specific for ANG II exist on pulmonary artery and aortic endothelial cells. The binding of 125I-ANG II to pulmonary artery and aortic endothelial cells was time dependent, saturable, and reversible. Scatchard analysis indicated a single class of high-affinity binding sites with equilibrium dissociation constants (Kd) of 0.85 and 0.81 nM and total binding capacities of 70 and 73 fmol/mg protein in pulmonary artery and aortic endothelial cells, respectively. Angiotensin analogues [Sar1,Ile8]ANG II and [Sar1,Ala8]ANG II, as well as angiotensin I and angiotensin III, competitively displaced 125I-ANG II in both pulmonary artery and aortic endothelial cells. The degree of inhibition of 125I-ANG II binding by these angiotensin analogues and antagonists was comparable except that [Sar1,Ala8]ANG II was 65% less potent than the other antagonists in both cell types. The binding of 125I-ANG II in pulmonary artery and aortic endothelial cells was not affected by vasopressin, substance P, or insulin, suggesting the presence of specific angiotensin receptors on these cells. These receptors appear to recognize the general configuration of angiotensin peptide rather than being specific to ANG II with no major differences between endothelial cells from pulmonary arterial or aortic vessels.
APA, Harvard, Vancouver, ISO, and other styles
38

Kromer, E. P. "Angiotensin-II-Rezeptor-Antagonisten bei Herzinsuffizienz." Der Internist 41, no. 9 (August 31, 2000): 917–24. http://dx.doi.org/10.1007/s001080050646.

Full text
APA, Harvard, Vancouver, ISO, and other styles
39

NAKA, Takehiko, Keiji KUBO, and Yoshiyasu FURUKAWA. "Non-peptide Angiotensin II Receptor Antagonists." Journal of Synthetic Organic Chemistry, Japan 53, no. 9 (1995): 802–10. http://dx.doi.org/10.5059/yukigoseikyokaishi.53.802.

Full text
APA, Harvard, Vancouver, ISO, and other styles
40

Carlson, Robert. "Angiotensin II antagonists offer additional benefits." Inpharma Weekly &NA;, no. 1115 (November 1997): 3–4. http://dx.doi.org/10.2165/00128413-199711150-00003.

Full text
APA, Harvard, Vancouver, ISO, and other styles
41

WEIR, M. "Therapeutic coverage with angiotensin II antagonists." American Journal of Hypertension 11, no. 4 (April 1998): 249A. http://dx.doi.org/10.1016/s0895-7061(97)91630-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
42

Vanderheyden, Patrick M. L., Frederik L. P. Fierens, and Georges Vauquelin. "Angiotensin II type 1 receptor antagonists." Biochemical Pharmacology 60, no. 11 (December 2000): 1557–63. http://dx.doi.org/10.1016/s0006-2952(00)00388-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
43

Pitt, Bertram, and Marvin A. Konstam. "Overview of angiotensin II-receptor antagonists." American Journal of Cardiology 82, no. 9 (November 1998): 47S—49S. http://dx.doi.org/10.1016/s0002-9149(98)00807-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
44

Pitt, Bertram, and Marvin A. Konstam. "Overview of angiotensin II-receptor antagonists." American Journal of Cardiology 82, no. 10 (November 1998): S47—S49. http://dx.doi.org/10.1016/s0002-9149(98)90434-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
45

Kirch, W., B. Horn, and J. Schweizer. "Comparison of angiotensin II receptor antagonists." European Journal of Clinical Investigation 31, no. 8 (August 2001): 698–706. http://dx.doi.org/10.1046/j.1365-2362.2001.00871.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
46

Mimran, Albert, Jean Ribstein, and Guilhem Ducailar. "Angiotensin II Receptor Antagonists and Hypertension." Clinical and Experimental Hypertension 21, no. 5-6 (January 1999): 847–58. http://dx.doi.org/10.3109/10641969909061014.

Full text
APA, Harvard, Vancouver, ISO, and other styles
47

NAKA, Takehiko, Keiji KUBO, Kohei NISHIKAWA, Yoshiyuki INADA, and Yoshiyasu FURUKAWA. "Angiotensin II Receptor Antagonists : Candesartan Cilexetil." YAKUGAKU ZASSHI 120, no. 12 (2000): 1261–75. http://dx.doi.org/10.1248/yakushi1947.120.12_1261.

Full text
APA, Harvard, Vancouver, ISO, and other styles
48

Burnier, M., and HR Brunner. "Angiotensin II receptor antagonists - antihypertensive agents." Expert Opinion on Investigational Drugs 6, no. 5 (May 1997): 489–500. http://dx.doi.org/10.1517/13543784.6.5.489.

Full text
APA, Harvard, Vancouver, ISO, and other styles
49

Macdonald, J. M. S. "Anaesthesia and angiotensin II receptor antagonists." Anaesthesia 55, no. 10 (October 2000): 1038. http://dx.doi.org/10.1046/j.1365-2044.2000.01727-26.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
50

Dina, Raquel, and Mahtab Jafari. "Angiotensin II-receptor antagonists: An overview." American Journal of Health-System Pharmacy 57, no. 13 (July 1, 2000): 1231–41. http://dx.doi.org/10.1093/ajhp/57.13.1231.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Angiotensine II – Antagonistes' for other source types:
Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography