Role of the renal nerves in the control of renin synthesis during different sodium intakes in the rat

Golin, Raffaello; Pieruzzi, Federico; Munforti, Carlotta; Busca, Giuseppe; Blasio, Anna Di; Zanchetti, Alberto

doi:10.1097/00004872-200107000-00012

Cited by 10 publications

(10 citation statements)

References 21 publications

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“…Thus, we conclude that salt-induced regulation of renin release and mRNA content is not primarily dependent on changes in ␤-adrenergic input. Most previous studies are in agreement with this conclusion, because neither renal denervation nor ␤-blockers prevented the rise of renin mRNA or plasma renin caused by a low-salt diet 11,12,15 nor its inhibition by high-salt intake, 12,15 though, in some studies, mostly in humans and dogs, propranolol has been found to reduce the stimulation of renin release during salt restriction to some extent. 10 Although the current data show that the absence of ␤-adrenergic input does not prevent salt regulation of renin release, pre-existing expression levels of renin appear to be an important determinant of the change in PRC and the magnitude of the response to the dietary stimulus.…”

Section: Discussionmentioning

confidence: 77%

“…The present results are also more dramatic than those predicted on the basis of results obtained in denervated kidneys. Although most studies have reported a decrease of renal mRNA levels in denervated compared with innervated kidneys, 11,12 the findings in such studies have not been entirely uniform. 13 Furthermore, plasma renin was reported to be reduced by bilateral renal denervation in 1 study, though there was no significant change in another.…”

Section: Discussionmentioning

confidence: 96%

“…13 Furthermore, plasma renin was reported to be reduced by bilateral renal denervation in 1 study, though there was no significant change in another. 12,14 Renal denervation differs from selective ablation of ␤-receptors in that responses to circulating epinephrine may be retained. Furthermore, renal denervation may also remove an inhibitory effect of ␣-adrenergic receptors on PRC.…”

Section: Discussionmentioning

confidence: 99%

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Regulation of Renin Secretion and Expression in Mice Deficient in β1- and β2-Adrenergic Receptors

et al. 2007

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Abstract-The present experiments were performed in ␤1/␤2-adrenergic receptor-deficient mice (␤1/␤2ADR Ϫ/Ϫ ) to assess the role of ␤-adrenergic receptors in basal and regulated renin expression and release. On a control diet, plasma renin concentration (in ng angiotensin I per mL per hour), determined in tail vein blood, was significantly lower in ␤1/␤2ADR Ϫ/Ϫ than in wild-type (WT) mice (222Ϯ65 versus 1456Ϯ335; PϽ0.01). Renin content and mRNA were 77% and 65Ϯ5% of WT. Plasma aldosterone (in picograms per mL) was also significantly reduced (420Ϯ36 in ␤1/␤2ADR Ϫ/Ϫ versus 692Ϯ59 in WT). A low-salt diet (0.03%) for 1 week increased plasma renin concentration significantly in both ␤1/␤2ADR Ϫ/Ϫ and WT mice (to 733Ϯ54 and 2789Ϯ555), whereas a high-salt diet (8%) suppressed it in both genotypes (to 85Ϯ24 in ␤1/␤2ADR Ϫ/Ϫ and to 676Ϯ213 in WT). The absolute magnitude of salt-induced changes of plasma renin concentration was markedly greater in WT mice. Acute stimulation of renin release by furosemide, quinaprilat, captopril, or candesartan caused significant increases of plasma renin concentration in both ␤1/␤2ADRϪ/Ϫ and WT mice, but again the absolute changes were greater in WT mice. We conclude that maintenance of normal levels of renin synthesis and release requires tonic ␤-adrenergic receptor activation. In the chronic absence of ␤-adrenergic receptor input, the size of the releasable renin pool decreases with a concomitant reduction in the magnitude of the plasma renin concentration changes caused by variations of salt intake or acute stimulation with furosemide, angiotensin-converting enzyme, or angiotensin type 1 receptor inhibition, but regulatory responsiveness is nonetheless maintained. Key Words: plasma renin Ⅲ salt intake Ⅲ aldosterone Ⅲ furosemide Ⅲ angiotensin-converting enzyme inhibition Ⅲ candesartan Ⅲ sympathetic nervous system T he juxtaglomerular cells in the media of renal afferent arterioles are the major sites of synthesis of the aspartic protease renin, the rate-limiting enzyme in the formation of angiotensin II. Renin is stored in dense core vesicles and released in response to specific tubular and vascular signals transduced by the epithelial cells of the macula densa or by pressure-sensitive cells in the arteriolar wall. In addition, juxtaglomerula (JG) cells are in contact with sympathetic nerve varicosities and express postjunctional ␤1-adrenergic receptors. Activation of ␤-adrenergic receptors directly increases renin secretion, even in the absence of changes in renal vascular tone or macula densa signals. 1 Although the directional effects of the main determinants of renin release are known, the contributions of the baroreceptor, the macula densa, and the renal sympathetic nerves to complex disturbances such as changes in body salt content have been difficult to untangle. For example, the change in renin release that results from varying dietary NaCl intake could be mediated by a change of luminal NaCl concentration at the macula densa, a change of baroreceptor activity, or a change of sympat...

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

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Regulation of Renin Secretion and Expression in Mice Deficient in β1- and β2-Adrenergic Receptors

et al. 2007

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“…Thus the pharmacological inhibition of ␤ 1 -receptors results in reduced renin secretion (130,423). Similarly, renal denervation to excise sympathetic input was shown to lower renin expression (271,354), but it should be noted that renal denervation also removes the input of the sympathetic system mediated by ␣-receptors, including hemodynamic and tubular effects (335). Most notably, double-knockout mice deficient in ␤ 1 -and ␤ 2 -receptors have substantially reduced basal PRC, ϳ85% lower than that observed in wild-type controls (434).…”

Section: Neural Control Of Renin Secretionmentioning

confidence: 99%

“…However, most studies suggest that modulation of the activity of the renin system is not crucially dependent on intact ␤-adrenergic input. That is, most reports indicate that neither renal denervation nor pharmacological ␤-blockade considerably influence the stimulation of the renin system by a salt-deficient diet or its suppression by a high-salt diet (271,353,354). In some studies in humans, dogs, and rats, however, the ␤-receptor antagonist propranolol was shown to reduce the magnitude of the renin system stimulation during a salt-deprived diet (423,879).…”

Section: Neural Control Of Renin Secretionmentioning

confidence: 99%

Physiology of Kidney Renin

Castrop

Höcherl

Kurtz

et al. 2010

Physiological Reviews

234

277

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The protease renin is the key enzyme of the renin-angiotensin-aldosterone cascade, which is relevant under both physiological and pathophysiological settings. The kidney is the only organ capable of releasing enzymatically active renin. Although the characteristic juxtaglomerular position is the best known site of renin generation, renin-producing cells in the kidney can vary in number and localization. (Pro)renin gene transcription in these cells is controlled by a number of transcription factors, among which CREB is the best characterized. Pro-renin is stored in vesicles, activated to renin, and then released upon demand. The release of renin is under the control of the cAMP (stimulatory) and Ca2+(inhibitory) signaling pathways. Meanwhile, a great number of intrarenally generated or systemically acting factors have been identified that control the renin secretion directly at the level of renin-producing cells, by activating either of the signaling pathways mentioned above. The broad spectrum of biological actions of (pro)renin is mediated by receptors for (pro)renin, angiotensin II and angiotensin-( 1 – 7 ).

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Salt feedback on the renin-angiotensin-aldosterone system

Schweda

2014

Pflugers Arch - Eur J Physiol

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The renin-angiotensin-aldosterone system (RAAS) is a central element in the control of the salt and water balance of the body and arterial blood pressure. The activity of the RAAS is controlled by the protease renin, which is released from renal juxtaglomerular epithelioid cells (JGE cells) into the circulation. Renin release is regulated by a complex interplay of several locally acting hormones or mechanisms and longer feedback loops one of which involves salt intake. Acute NaCl loads or longer lasting high salt intakes suppress plasma renin activity, whereas reductions in NaCl intake stimulate it. Because the activation of the RAAS conserves the salt content of the body, a classical feedback loop between salt intake/body salt content and renin is established. Despite of its important role for body fluid homeostasis, the precise signaling pathways connecting salt intake with the synthesis and release of renin are only incompletely understood. Four putative controllers of the salt-dependent regulation of the RAAS have been suggested: (1) the macula densa mechanism which adjusts renin release in response to changes in the renal tubular salt concentration; (2) salt-dependent changes in the arterial blood pressure; (3) circulating salt-dependent hormones, particularly the atrial natriuretic peptide (ANP); and (4) renal sympathetic nervous activity, which is regulated by extracellular volume and arterial blood pressure. In this review, the role of these known controllers of the RAAS will be discussed with special emphasis on their relative contributions to the salt-dependent regulation of the RAAS at different time frames.

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Role of the renal nerves in the control of renin synthesis during different sodium intakes in the rat

Abstract: The activation of renin gene expression during sodium depletion in rats is dependent on the presence of the renal nerves, while the suppression of renin gene expression during a sodium load seems to be due to the macula densa mechanism alone.

Cited by 10 publications

References 21 publications

Regulation of Renin Secretion and Expression in Mice Deficient in β1- and β2-Adrenergic Receptors

Regulation of Renin Secretion and Expression in Mice Deficient in β1- and β2-Adrenergic Receptors

Physiology of Kidney Renin

Salt feedback on the renin-angiotensin-aldosterone system

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