The renin angiotensin system: importance in physiology and pathology

Ferrario, Carlos M.; Schiavone, Marc

doi:10.3949/ccjm.56.4.439

Cited by 59 publications

(90 citation statements)

References 24 publications

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“…Ang II modulates the activity of the sympathetic nervous system by facilitating adrenergic nerve transmission and inhibiting the arterial baroreceptor reflex. 1 ' 2 One action of Ang II blockade is improvement of the baroreceptor reflex. 1 In conscious rabbits with Ang II-dependent hypertension, the Ang II receptor antagonist [Sar 1 , Ala^Ang II not only reversed the high blood pressure but increased the maximum gain of the baroreceptor reflex control of renal sympathetic nerve activity (RSNA).…”

Section: Role Of Nitric Oxide and Angiotensin II In The Regulation Ofmentioning

confidence: 99%

“…1 ' 2 One action of Ang II blockade is improvement of the baroreceptor reflex. 1 In conscious rabbits with Ang II-dependent hypertension, the Ang II receptor antagonist [Sar 1 , Ala^Ang II not only reversed the high blood pressure but increased the maximum gain of the baroreceptor reflex control of renal sympathetic nerve activity (RSNA). 3 These data support the hypothesis that the antihypertensive effects of angiotensin converting enzyme (ACE) inhibitors are in part due to a centrally mediated decrease in sympathetic outflow.…”

Section: Role Of Nitric Oxide and Angiotensin II In The Regulation Ofmentioning

confidence: 99%

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Role of nitric oxide and angiotensin II in the regulation of sympathetic nerve activity in spontaneously hypertensive rats.

et al. 1993

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This study evaluated the actions of nitric oxide on the blood pressure and renal sympathetic nerve activity responses produced by angiotensin II (Ang II) blockade in conscious spontaneously hypertensive rats. Two days after implantation of electrodes, we measured mean arterial pressure, heart rate, and renal sympathetic nerve activity. Baroreceptor reflex function was assessed with a logistic function curve; the maximum slope of the curve estimated the baroreceptor reflex gain. Data were obtained in rats given acute intravenous administration of either vehicle, the Ang II type 1 receptor antagonist losartan, the type 2 antagonist CGP 42112A, or the converting enzyme inhibitor lislnopriL In comparison with vehicle (-l.l±02 %/rara Hg), both losartan (-1J$±O.3 %/mrn Hg) and lisinopril (-2.4±0.2 %/rara Hg) significantly increased the maximum gain of the baroreceptor reflex control of nerve activity (/><0.05). In contrast, the type 2 receptor antagonist did not alter baroreceptor reflex function. Similar studies were performed in rats that received an intravenous injection of A rG -monomethyl L-arginine (10 ing/kg). The nitric oxide synthase inhibitor increased baseline blood pressure and decreased renal sympathetic nerve activity. Subsequent administration of losartan or lisinopril returned blood pressure to initial hypertensive level, whereas sympathetic nerve activity was increased to a level above the initial control value. The maximum gain of the baroreceptor reflex control of renal nerve activity was increased after the nitric oxide inhibition. The present study demonstrates that blunted baroreceptor reflex function in conscious spontaneously hypertensive rats is mediated by an Ang II type 1 receptor. Moreover, nitric oxide may play a dual role in the antihypertensive effect of Ang II blockade. 1 In conscious rabbits with Ang II-dependent hypertension, the Ang II receptor antagonist [Sar 1 , Ala^Ang II not only reversed the high blood pressure but increased the maximum gain of the baroreceptor reflex control of renal sympathetic nerve activity (RSNA).3 These data support the hypothesis that the antihypertensive effects of angiotensin converting enzyme (ACE) inhibitors are in part due to a centrally mediated decrease in sympathetic outflow.Because there are no in vivo studies on the Ang II receptor subtype that is functionally involved in the baroreceptor reflex, we compared the effects of angiotensin type 1 (AT^ and type 2 (AT 2 ) receptor antagonists on the baroreceptor reflex control of RSNA and heart rate (HR) in conscious spontaneously hypertensive rats (SHRs). We contrasted the effects of these two Ang II receptor antagonists with results obtained in rats treated with the ACE inhibitor lisinopril to assess the role of the renin-angiotensin system in the actions of lisinopril. Recent data have demonstrated that the antihypertensive effects of both an ATj receptor antagonist and an ACE inhibitor are in part mediated by release of endothelium-derived nitric oxide (NO).4 -3 Moreover, Lewis et al 67 found that ...

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Section: Role Of Nitric Oxide and Angiotensin II In The Regulation Ofmentioning

confidence: 99%

Section: Role Of Nitric Oxide and Angiotensin II In The Regulation Ofmentioning

confidence: 99%

Role of nitric oxide and angiotensin II in the regulation of sympathetic nerve activity in spontaneously hypertensive rats.

et al. 1993

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“…Ang II receptor antagonists have proved to lower blood pressure effectively, and they are better tolerated than other classes of drugs. The renin-angiotensin system (RAS) plays a key role in regulating cardiovascular homeostasis and electrolyte/ fluid balance in normotensive and hypertensive subjects [1]. Activation of renin-angiotensin cascade begins with renin secretion from the juxtaglomerular apparatus of the kidney and culminates in the formation of the octapeptide angiotensin II (AII), which then interacts with specific receptors present in different tissues [2].…”

Section: Introductionmentioning

confidence: 99%

Synthesis and biological evaluation of some new benzimidazoles derivatives 4'-{5-amino-2-[2-substituted-phenylamino)-phenyl-methyl]-benzimidazol-1 ylmethyl}-biphenyl-2-carboxylic acid: Nonpeptide angiotensin II receptor antagonists.

Sharma

Kohli

Sharma³

2010

Int j Drug delivery

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A new series of non peptide angiotensin (A-II) receptor antagonist has been prepared. This N-(biphenyl methyl) imidazoles e.g. Some new 4'-{5-amino-2-[2-substituted-phenylamino)-phenyl-methyl]-benzimidazol-1-ylmethyl}-biphenyl-2-carboxylic acid derivatives were synthesized by 2-( α -hydroxy benzyl) benzimidazole was converted to 2-(α-bromo benzyl) benzimidazole by reacting with HBr and Anhydrous ZnCl 2 Schiff bases react with biphenyl carboxylic acid with different substituents amino group cyclocondensation with appropriate reagents. Differ from the previously reported and related compounds in that they produce a potent hypertensive effect. The compounds synthesized were identified by 1 H NMR, 13 C NMR, FAB Mass and FT-IR spectroscopic techniques. All compounds studied in this work were screened for their antihypertensive activity by tail cuff method and direct method measurement of blood pressure.

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“…The functions of the systemic renin-angiotensin system (RAS), and the generation of angiotensin II, have been widely studied over three decades, and its role in mammalian electrolyte homeostasis and haemodynamics, particularly through the regulation of aldosterone secretion and cardiovascular function, is reasonably well understood (Peach 1977, Ferrario 1990, Jeunemaitre et al 1992, Vinson et al 1995a.…”

Section: Introductionmentioning

confidence: 99%

The role of the tissue renin-angiotensin system in the response of the rat adrenal to exogenous angiotensin II

Vinson

Teja²,

Ho³

et al. 1998

Journal of Endocrinology

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The tissue renin-angiotensin systems (RAS) may have specific roles that complement those of the systemic RAS. In the adrenal, the tissue RAS has been implicated in the regulation of glomerulosa tissue growth and function, and in mediating the response of the tissue to stimulation by ACTH and potassium ions.To examine the role of the rat adrenal tissue RAS in its response to angiotensin II stimulation, adrenals were incubated either as bisected glands or as separated capsular glands (largely glomerulosa) under control conditions, or in the presence of the angiotensin-converting enzyme inhibitor captopril, or of angiotensin II, or both.Captopril inhibited the two different tissue preparations in different ways. In the capsular gland it inhibited basal aldosterone output, but facilitated its response to angiotensin II. In the bisected gland, captopril inhibited the response of aldosterone to angiotensin II.Other data suggest that one way in which captopril functions is by preventing the conversion of fasciculatagenerated 18-hydroxydeoxycorticosterone (18-OH-DOC) to aldosterone in the glomerulosa. Immunolocalisation of 18-OH-DOC in perfused rat adrenal confirms that one function of angiotensin II is to mobilise tissue-sequestered 18-OH-DOC.The results illustrate the importance of tissue RAS in the synthesis of aldosterone and the response to angiotensin II.

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The renin angiotensin system: importance in physiology and pathology

Cited by 59 publications

References 24 publications

Role of nitric oxide and angiotensin II in the regulation of sympathetic nerve activity in spontaneously hypertensive rats.

Role of nitric oxide and angiotensin II in the regulation of sympathetic nerve activity in spontaneously hypertensive rats.

Synthesis and biological evaluation of some new benzimidazoles derivatives 4'-{5-amino-2-[2-substituted-phenylamino)-phenyl-methyl]-benzimidazol-1 ylmethyl}-biphenyl-2-carboxylic acid: Nonpeptide angiotensin II receptor antagonists.

The role of the tissue renin-angiotensin system in the response of the rat adrenal to exogenous angiotensin II

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