Vasoactive Intestinal Peptide Stimulates Renin Secretion in vitro:Evidence for a Direct Action of the Peptide on the Renal Juxtaglomerular Cells

Porter, James P.; Said, Sami I.; Ganong, William F.

doi:10.1159/000123488

Cited by 30 publications

(11 citation statements)

References 10 publications

(14 reference statements)

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“…We have also been able to demonstrate VIP stimulation of adenylate cyclase in isolated glomeruli (and associated vascular elements). This finding provides further support for a role for VIP in the regulation of glomerular and juxta-glomerular apparatus function (Porter et al 1983(Porter et al , 1985 (Cerione, Staniszewski, Caron, Lefkowitz, Codina & Birnbaumer, 1985) will also affect the fold stimulation compared to basal values, by reducing basal values. This may explain the observed variation between cellular elements and in the thick ascending-limb preparation.…”

Section: Discussionsupporting

confidence: 59%

“…Infusions of VIP are known to influence both renal haemodynamics and the release of renin (Porter & Ganong, 1982;PHY 387 N. M. GRIFFITHS AND N. L. SIMMONS Porter, Said & Ganong, 1983;Dimaline et al 1983;Porter, Thrasher, Said & Ganong, 1985). In addition there seems to be evidence for a role for VIP regulation of tubular transport unconnected with haemodynamic effects Rosa, Silva, Stoff & Epstein, 1985).…”

Section: Introductionmentioning

confidence: 99%

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Vasoactive intestinal polypeptide regulation of rabbit renal adenylate cyclase activity in vitro.

Griffiths

Simmons

1987

The Journal of Physiology

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SUMMARY1. The effect of vasoactive intestinal polypeptide (VIP) upon adenylate cyclase activity was determined in purified cortical basolateral membranes and in glomeruli and tubular elements obtained from rabbit kidney.2. In purified basolateral membranes prepared from cortex, 1 /LM-VIP consistently stimulated adenylate cyclase activity above basal levels (1 55 ± 009-fold (mean + S.E. ofmean), n = 10 animals). Half-maximal stimulation was observed at 17 + 11 nM-VIP (S.D., n = 9).3. Related peptides, e.g. secretin, glucagon, gastric inhibitory peptide, human pancreatic growth hormone releasing factor, and peptide having N-terminal histidine and C-terminal isoleucine amide (PHI), were without effect or gave lower stimulations of adenylate cyclase activity when tested at 1 ,/bM. 4. Significant VIP degradation was observed under the assay conditions used but this did not substantially alter the response or selectivity to VIP. 5. In separate preparations of isolated glomeruli and proximal tubules addition of 1 /LM-VIP resulted in a 3-3+ 1 1-fold (S.D., n = 3) and 2-2+1 0-fold (S.D., n = 3) stimulation (respectively) of adenylate cyclase activity.6. In isolated medullary tubule suspensions, isolated by collagenase-hyaluronidase digestion of outer (red) medulla, and in thick ascending-limb-enriched preparations prepared by Percoll density gradient fractionation, 1 ,tM-VIP significantly increased adenylate cyclase activity by 2-4+0-6-fold (S.D., n = 3) and 2-1 +0-7-fold (S.D., n = 3) respectively. 7. A possible role for VIP in the regulation of renal function in the rabbit is discussed in relation to the occurrence of VIP stimulation of adenylate cyclase activity in several renal cellular elements.

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Section: Discussionsupporting

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Vasoactive intestinal polypeptide regulation of rabbit renal adenylate cyclase activity in vitro.

Griffiths

Simmons

1987

The Journal of Physiology

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“…Catecholamines act through β1-adrenoreceptors (123), and dopamine acts through D1 receptors (124). Renin-stimulatory neuropeptides include adrenomedullin (125), pituitary adenylyl cyclase-activating peptide (PACAP) (126), vasoactive intestinal peptide (VIP) (127), and calcitonin gene-related peptide (CGRP) (128). A second group of stimulatory mediators consists of prostanoids like prostaglandin E 2 (PGE 2 ), which act through EP2 and EP4 receptors, and prostacyclin, which acts through prostaglandin I 2 (PGI 2 ) prostacyclin receptors (129).…”

Section: Hormones and Mediatorsmentioning

confidence: 99%

Renin Release: Sites, Mechanisms, and Control

Kurtz

2011

Annu. Rev. Physiol.

102

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In the adult organism, systemically circulating renin almost exclusively originates from the juxtaglomerular cells in the afferent arterioles of the kidneys. These cells share similarities with pericytes and myofibro-blasts. They store renin in a vesicular network and granules and release it in a regulated fashion. The release mode of renin is not understood; in particular, the involvement of SNARE proteins is unknown. Renin release is acutely increased via the cAMP signaling pathway, which is triggered mainly by catecholamines and other G(s)-coupled agonists, and is inhibited by calcium-related pathways that are commonly activated by vasoconstrictors. Renin release from juxtaglomerular cells is directly modulated in an inverse fashion by the blood pressure inside the afferent arterioles and by the chloride content in the tubule fluid at the macula densa segment of the distal tubule. Renin release is stimulated by nitric oxide and by prostanoids released by neighboring endothelial and macula densa cells. Steady-state renin concentrations in the plasma are determined essentially by the number of renin-producing cells in the afferent arterioles, which changes in parallel with challenges to the renin-angiotensin-aldosterone system.

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“…Renal afferent innervation is composed of both chemoreceptor and mechanoreceptor fibers [1696] . Afferent nerve endings contain the neuropeptides, CGRP, substance P, and vasoactive intestinal peptide [1764][1765][1766] . Renal mechanoreceptors respond to changes in arterial, renal venous and pelvic hydrostatic pressure.…”

Section: Afferent Renal Nervesmentioning

confidence: 99%