Neuronal nitric oxide synthase and renin stimulation by sodium deprivation are dependent on the renal nerves

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

doi:10.1097/00004872-200210000-00024

Cited by 6 publications

(5 citation statements)

References 17 publications

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“…However, it is well known that renal sympathetic tone regulates renin release from the juxtaglomerular apparatus. This finding is consistent with those of previous studies, which demonstrated that plasma renin activity is not affected in high-salt–fed SHR following renal denervation (43, 44). Thus, the contribution of the sympathetic nervous system on renin release may be reduced on a high-salt diet.…”

Section: Discussionsupporting

confidence: 94%

N-type Calcium Channel Inhibition With Cilnidipine Elicits Glomerular Podocyte Protection Independent of Sympathetic Nerve Inhibition

et al. 2012

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We recently demonstrated that cilnidipine, an L/N-type calcium channel blocker, elicits protective effects against glomerular podocyte injury, in particular, in obese hypertensive rats that express the N-type calcium channel (N-CC). Since the N-CC is known to be expressed in sympathetic nerve endings, we evaluated the reno-protective effects of cilnidipine in innervated and denervated spontaneously hypertensive rats (SHR). Male SHR were uninephrectomized and fed 4% high-salt diet (HS-UNX-SHR). Animals were divided into groups, as follows, and observed from 9 to 27 weeks of age: 1) vehicle (n = 14), 2) vehicle plus renal-denervation (n = 15), 3) cilnidipine (50 mg/kg per day, p.o.; n = 10), and 4) cilnidipine plus renal-denervation (n = 15). Renal denervation attenuated elevations in blood pressure, but failed to suppress urinary protein excretion and podocyte injury in HS-UNX-SHR. Cilnidipine in both innervated and denervated HS-UNX-SHR similarly induced significant antihypertensive effects, as well as suppressing the urinary protein excretion and podocyte injury, compared to vehicle-treated HS-UNX-SHR. These data indicate that renal nerves have a limited contribution to the cilnidipine-induced reno-protective effects in HS-UNX-SHR.

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Section: Discussionsupporting

confidence: 94%

N-type Calcium Channel Inhibition With Cilnidipine Elicits Glomerular Podocyte Protection Independent of Sympathetic Nerve Inhibition

et al. 2012

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“…During a low-sodium diet, the nNOS mRNA expression is upregulated in the renal cortex. 16,17 NO from the MD could then diffuse into the JG cells and increase renin exocytosis through cGMP-mediated inhibition of PDE3, as suggested by Reid in 1994. 18 In the present study, this hypothesis is supported by the increased sensitivity to PDE3 inhibition in the nNOS −/− , which suggests that the PDE3 isoform in the JG cells is less inhibited due to the absence of nNOS-derived NO.…”

Section: Discussionsupporting

confidence: 70%

“…16,17 During higher sodium loads, the differences in milrinone response between the genotypes would be expected to be lower, given the reduced nNOS expression.…”

Section: Discussionmentioning

confidence: 99%

Neuronal Nitric Oxide Synthase Supports Renin Release During Sodium Restriction Through Inhibition of Phosphodiesterase 3

et al. 2010

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“…A general stimulatory role of renal sympathetic nerve activity has been shown by pharmacological blockade of ß1-receptors, renal denervation, and genetic deletion of both ß1-and ß2-receptors (ß1/ß2 double knockout mice), which all significantly reduced the renin synthesis and/or plasma renin levels under control conditions [18,26,37,50,58,82]. In some but not all studies, renal denervation or ß-receptor blockade affected the saltdependent regulation of the renin system such that the absolute levels of renal renin mRNA expression and plasma renin activity were lower under low or high salt load compared with those in the animals or humans with intact renal efferent inputs [47,49,53,82,96,119]. Notably, the salt-dependent regulation of the renin system was not abrogated in any of these studies, and the relative stimulation of the renin system, which was calculated as the stimulation relative to baseline values under normal salt intake, was maintained in the absence of renal ß-adrenergic innervation [82].…”

Section: Renal Sympathetic Nerve Activitymentioning

confidence: 99%

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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Neuronal nitric oxide synthase and renin stimulation by sodium deprivation are dependent on the renal nerves

Cited by 6 publications

References 17 publications

N-type Calcium Channel Inhibition With Cilnidipine Elicits Glomerular Podocyte Protection Independent of Sympathetic Nerve Inhibition

N-type Calcium Channel Inhibition With Cilnidipine Elicits Glomerular Podocyte Protection Independent of Sympathetic Nerve Inhibition

Neuronal Nitric Oxide Synthase Supports Renin Release During Sodium Restriction Through Inhibition of Phosphodiesterase 3

Salt feedback on the renin-angiotensin-aldosterone system

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