Decreased perfusion pressure modulates renin and ANG II type 1 receptor gene expression in the rat kidney

Tufro-McReddie, Alda; Chevalier, Robert L.; Gómez, R. Ariel

doi:10.1152/ajpregu.1993.264.4.r696

Cited by 29 publications

(20 citation statements)

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“…The increase in renin release is due to the recruitment of microvascular cells secreting and synthesizing renin (11). These results in vitro corroborate many reports in whole animals demonstrating that in response to physiological stress, increased circulating renin is achieved by increasing the number of cells expressing renin (3,14,17,26,48,49).…”

supporting

confidence: 87%

Identity of the renin cell is mediated by cAMP and chromatin remodeling: an in vitro model for studying cell recruitment and plasticity

Pentz¹,

López²,

Cordaillat³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

105

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Pentz ES, Sequeira Lopez ML, Cordaillat M, Gomez RA. Identity of the renin cell is mediated by cAMP and chromatin remodeling: an in vitro model for studying cell recruitment and plasticity. Am J Physiol Heart Circ Physiol 294: H699-H707, 2008. First published November 30, 2007 doi:10.1152/ajpheart.01152.2007.-The renin-angiotensin system (RAS) regulates blood pressure and fluid-electrolyte homeostasis. A key step in the RAS cascade is the regulation of renin synthesis and release by the kidney. We and others have shown that a major mechanism to control renin availability is the regulation of the number of cells capable of making renin. The kidney possesses a pool of cells, mainly in its vasculature but also in the glomeruli, capable of switching from smooth muscle to endocrine renin-producing cells when homeostasis is threatened. The molecular mechanisms governing the ability of these cells to turn the renin phenotype on and off have been very difficult to study in vivo. We, therefore, developed an in vitro model in which cells of the renin lineage are labeled with cyan fluorescent protein and cells actively making renin mRNA are labeled with yellow fluorescent protein. The model allowed us to determine that it is possible to culture cells of the renin lineage for numerous passages and that the memory to express the renin gene is maintained in culture and can be reenacted by cAMP and chromatin remodeling (histone H4 acetylation) at the cAMPresponsive element in the renin gene.

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supporting

confidence: 87%

Identity of the renin cell is mediated by cAMP and chromatin remodeling: an in vitro model for studying cell recruitment and plasticity

Pentz¹,

López²,

Cordaillat³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

105

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“…As a case in point, there are major differences in the regulation of AT receptors in vessels and tubules in the kidney. In contrast to the renal vasculature (8,21,25,47), increased ANG II levels are associated with upregulation of AT 1 mRNA and ANG II receptor density in proximal tubular cells and isolated basolateral membranes, and also in the adrenal gland (2,18,(21)(22)(23).…”

Section: Discussionmentioning

confidence: 99%

Regulation of angiotensin II receptor AT1 subtypes in renal afferent arterioles during chronic changes in sodium diet.

et al. 1997

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Studies determined the effects of chronic changes in sodium diet on the expression, regulation, and function of different angiotensin II (ANG II) receptor subtypes in renal resistance vessels. Rats were fed low-or high-sodium diets for 3 wk before study. Receptor function was assessed in vivo by measuring transient renal blood flow responses to bolus injections of ANG II (2 ng) into the renal artery. ANG II produced less pronounced renal vasoconstriction in rats fed a low-compared with high-sodium diet (16% vs. 56% decrease in renal blood flow, P Ͻ 0.001). After acute blockade of ANG II formation by iv enalaprilat injection in sodiumrestricted animals, ANG II produced a 40% decrease in renal blood flow, a level between untreated dietary groups and less than high salt diet. Intrarenal administration of angiotensin II receptor type 1 (AT 1 ) receptor antagonists losartan or EXP-3174 simultaneously with ANG II caused dosedependent inhibition of ANG II responses. Based on maximum vasoconstriction normalized to 100% ANG II effect in each group, AT 1 receptor antagonists produced the same degree of blockade in all groups, with an apparent maximum of 80-90%. In contrast, similar doses of the angiotensin II receptor type 2 (AT 2 ) receptor ligand CGP-42112 had only a weak inhibitory effect. In vitro equilibrium-saturation 125 I-ANG II binding studies on freshly isolated afferent arterioles indicated that ANG II receptor density was lower in the low-vs. high-sodium animals (157 vs. 298 fmol/mg, P Ͻ 0.04); affinity was similar (0.65 nM). Losartan and EXP-3174 displaced up to 80-90% of the ANG II binding; fractional displacement was similar in both diet groups. In contrast, the AT 2 receptor analogues PD-123319 and CGP-42112 at concentrations Ͻ 10 Ϫ 6 M had no effect on ANG II binding. RT-PCR assays revealed the expression of both angiotensin II receptor type 1A (AT 1A ) and angiotensin II receptor type 1B (AT 1B ) subtypes in freshly isolated afferent arterioles, while there was very little AT 2 receptor expression. Total AT 1 receptor mRNA expression was suppressed by low sodium intake to 66% of control levels, whereas it was increased to 132% of control by high-sodium diet, as indicated by ribonuclease protection assay. Receptor regulation was associated with parallel changes in AT 1A and AT 1B expression; the AT 1A /AT 1B ratio was stable at 3.7. We conclude that AT 1 receptors are the predominant ANG II receptor type in renal resistance vessels of 7-wk-old rats. Chronic changes in sodium intake caused parallel regulation of expression and amount of receptor protein of the two AT 1 receptor genes that modulate receptor function and altered reactivity of renal vessels to ANG II. ( J. Clin. Invest.

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“…A more evident mediator of the inhibitory effect of NOS blockade on renin mRNA levels could be the increase of systemic blood pressure, because renin gene expression has been found to be inversely related to the renal perfusion pressure (37)(38)(39)(40). Systolic blood pressure decreased after Physiology: Schricker et al…”

Section: Discussionmentioning

confidence: 99%

Tonic stimulation of renin gene expression by nitric oxide is counteracted by tonic inhibition through angiotensin II.

Schricker

Hegyi

Hamann

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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This study was designed to examine the possible involvement of prostaglandins and nitric oxide (NO) in the renin stimulatory effect ofangiotensin 11 (AngII) antagonists. To this end, plasma renin activities (PRAs) and renal renin mRNA levels were assayed in rats that were treated with the Angconverting enzyme inhibitor ramipril or with the AnglI AT1-receptor antagonist losartan. Ramipril and losartan increased PRA values from 7.5 + 1.6 to 86 ± 6 and 78 ± 22 ng of AngI per h per ml and renin mRNA levels from 112 ± 9% to 391 + 20%o and 317 ± 10%o, respectively. Inhibition of prostaglandin formation with indomethacin did not influence basal or ramiprilaffected PRA. Basal renin mRNA levels also were unchanged by indomethacin, while increases in renin mRNA levels after ramipril treatment were slightly reduced by indomethacin. Inhibition of NO synthase by nitro-L-arginine methyl ester (L-NAME) reduced PRA values to 3.2 ± 0.9, 34 ± 13, and 12.1 ± 2.7 ng of AngI per h per ml in control, ramipril-treated, and losartan-treated animals, respectively. Renin mRNA levels were reduced to 77 + 14% under basal conditions and ramipril-and losartan-induced increases in renin mRNA levels were completely blunted after addition of L-NAME. The AngIH antagonists, furthermore, induced an upstream recruitment of reninexpressing cells in the renal afferent arterioles, which was also blunted by L-NAME. These findings suggest that renin mRNA levels are tonically increased by NO and that the action of NO is counteracted by AngII.One of the most prominent in vivo effects of angiotensin (Ang)-converting enzyme (ACE) inhibitors is a marked stimulation of renin secretion and renin gene expression in the kidneys (1-5). Since ANGII is known as a negative feedback regulator of renin secretion and of renin gene expression (6, 7), it is thought that the renin stimulatory effects of ACE inhibitors are related to the inhibition of AnglI formation and consequently to the lowering of circulating and tissue AnglI levels (8).There is evidence that several in vivo effects of ACE inhibitors are not, as originally thought, due to the inhibition of AnglI formation but to the inhibition of kinin degradation (9-12). Inhibition of kinin degradation results in elevated tissue levels of autacoids such as prostaglandins and nitric oxide (NO), the formation of which is stimulated by kinins (11)(12)(13)(14). Although NO is reported to inhibit the renin system (15-17), contradictory findings suggest that NO stimulates the renin system (18-25) and also that prostaglandins stimulate the renin system (for review, see ref. 26). With such a stimulatory effect of NO and prostaglandins on the renin system, it is possible that the renin stimulatory effect of ACE inhibitors could be related to an enhanced formation of prostaglandins and NO.To investigate the mode of action of ACE inhibitors on the renin system, we studied renin release and renin mRNA levels in the kidneys of conscious rats that were treated with the ACE inhibitor ramipril (27) or with the Angll AT1-rec...

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Decreased perfusion pressure modulates renin and ANG II type 1 receptor gene expression in the rat kidney

Cited by 29 publications

References 0 publications

Identity of the renin cell is mediated by cAMP and chromatin remodeling: an in vitro model for studying cell recruitment and plasticity

Identity of the renin cell is mediated by cAMP and chromatin remodeling: an in vitro model for studying cell recruitment and plasticity

Regulation of angiotensin II receptor AT1 subtypes in renal afferent arterioles during chronic changes in sodium diet.

Tonic stimulation of renin gene expression by nitric oxide is counteracted by tonic inhibition through angiotensin II.

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