Stimulation of renin secretion by vasoactive intestinal peptide

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

doi:10.1152/ajprenal.1982.243.3.f306

Cited by 9 publications

(8 citation statements)

References 162 publications

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“…In anesthetized dogs, VIP infusions which resulted in a two-to threefold increase in circulating levels of the peptide were shown to increase PRA without any change in blood pressure, sodium excretion, or plasma potassium concen tration [12]. In addition, propranolol pretreatment failed to block the renin-stimulating effect of VIP [unpublished ob servation], Taken together these data suggested that VIP could increase PRA without activating the sympathetic ner vous system, the intrarenal baroreceptor, or the macula densa.…”

Section: Discussionmentioning

confidence: 96%

“…There is evidence that it is a neuroeffector involved in the release of several hormones includ ing prolactin [5], thyroxine [1], and insulin and glucagon [16], We have reported that infusions of exogenous VIP re sulted in an increase in renin secretion in anesthetized dogs [11,12]. Since other mechanisms known to regulate renin se cretion such as the intrarenal baroreceptor and macula densa did not appear to mediate the effect of VIP on renin re lease, we postulated that the peptide acted directly on the re nin-secreting juxtaglomerular cells.…”

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confidence: 96%

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

Porter¹,

Said²,

Ganong³

1983

Neuroendocrinology

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The effect of vasoactive intestinal peptide (VIP) and isoproterenol on renin release in vitro was investigated using an isolated superfused rat glomerular preparation. VIP at a dose of 10^–9–10^–7M significantly stimulated renin release in a dose-related manner while 10^–10M was ineffective. These data are consistent with the hypothesis that VIP is a renin-stimulating factor and can have this effect by acting directly on the renal juxtaglomerular cells.

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Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 96%

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

Porter¹,

Said²,

Ganong³

1983

Neuroendocrinology

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“…It could be that activation of indirect vasoconstrictor mechanisms during infusion of VIP had a predominant influence in the renal and mesenteric vascular beds. But, in the presence of L-NAME, the highest dose of VIP had an enhanced hypotensive effect, (Porter et al, 1982) it should occur in the presence of L-NAME, unless VIP-induced stimulation of renin release involved NO. An indirect action of VIP to stimulate renin release through P2-adrenoceptors is consistent with the finding that ICI 118551 abolished the renal vasoconstrictor response to VIP.…”

Section: Discussionmentioning

confidence: 90%

“…In dogs (Porter et al, 1982), and rabbits (Dimaline et al, 1983), VIP stimulates renin release, possibly through direct and indirect mechanisms. However, there are no data available relating to the involvement of the renin-angiotensin system in the regional haemodynamic responses to VIP and so, our fourth objective was to determine the effects of the AT,-receptor antagonist, losartan potassium (DuP 753; Wong et al, 1990;Batin et al, 1991) on regional haemodynamic responses to PACAP27 or VIP in conscious rats.…”

Section: Introductionmentioning

confidence: 99%

Regional haemodynamic responses to pituitary adenylate cyclase‐activating polypeptide and vasoactive intestinal polypeptide in conscious rats

Gardiner

Rakhit

Kemp

et al. 1994

British J Pharmacology

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1 Regional haemodynamic responses to the homologous peptides, pituitary adenylate cyclase-activating peptide (1-27) (PACAP27) and vasoactive intestinal polypeptide (VIP) were assessed by giving 20 min infusions (1.5-15nmol kg-' h-') in conscious, chronically-instrumented, Long Evans rats. 2 PACAP27 caused dose-dependent depressor and tachycardic effects associated with renal, mesenteric and hindquarters vasodilatations, although only in the latter vascular bed was there a sustained increase in flow. 3 VIP caused dose-dependent depressor and tachycardic effects that were not significantly different from those caused by equimolar doses of PACAP27. However, the hindquarters vasodilator effects of VIP (at 7.5 and 15 nmol kg-' h-') were greater than those of PACAP27 (at the same doses), and accompanied by reductions in renal and mesenteric flows and conductances. 4 In the presence of the nitric oxide (NO) synthase inhibitor, N0-nitro-L-arginine methyl ester (L-NAME; 11 gymol kg-' h-'), there was significant inhibition of the hindquarters vasodilator effects of PACAP27 and VIP (at 7.5 and 15 nmol kg-' h-'). Under these circumstances the renal and mesenteric vasoconstrictor effects of VIP were abolished.5 The P2-adrenoceptor antagonist, ICI 118551 (670 nmol kg-' bolus, 335 nmol kg-l h-' infusion), reduced the matched hindquarters vasodilator responses to PACAP27 (15nmolkg-'h-') and VIP (7.5 nmol kg-l h-), and also abolished the renal vasoconstrictor effects of VIP.6 The AT,-receptor antagonist, losartan potassium (20 pmol kg-'), had no significant effect on the haemodynamic response to PACAP27 (15 nmol kg-' h-'), but augmented the hypotensive action of VIP (7.5 nmol kg-h-'). This influence of losartan was associated with conversion of the renal and mesenteric vasoconstrictor effect of VIP to vasodilatation. 7 Our findings show that similar changes in mean systemic arterial blood pressure in response to PACAP27 and VIP conceal substantial differences in their regional haemodynamic actions. Although the hindquarters vasodilator effects of both peptides involve NO-and P2-adrenoceptor-mediated mechanisms, it appears that activation of the renin-angiotensin system contributes significantly to the haemodynamic effects of VIP, but not to those of PACAP27.

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“…'- 2 The possibility that certain peptides do indeed serve such a role in the regulation of cardiovascular function seems even more likely in view of the interactions between peptides and "classical" hormonal transmitters. Examples of such interactions in the case of VIP are: VIP stimulates the synthesis or release of prolact i n 65-67 g r o w t h hormone, 65 "* 9 and LHRH, 65 M as well as of renin 70 and steroids. 71 At the same time, VIP release is stimulated by neostigmine 72 and by serotonin.…”

Section: Physiological Rolementioning

confidence: 99%

Vasoactive peptides. State-of-the-art review.

Said¹

1983

Hypertension

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SUMMARY At least 16 naturally occurring peptides either constrict or dilate blood vessels. Many of these peptides are present in nerve cells and nerve terminals supplying systemic and pulmonary blood vessels and the heart. Such neuropeptides are released locally as neurotransmitters, and can influence vascular tone, local and regional blood flow, arterial blood pressure, and cardiac function. There is evidence for the participation of at least some vasoactive peptides in the regulation of these functions and in the mediation or modulation of systemic shock and arterial hypertension. The investigation of vasoactive peptides in relation to cardiovascular function and dysfunction is at a promising threshold. There is a growing conviction that these peptides participate in the regulation of many organ functions. Neuroscientists, endocrinologists, and gastroenterologists have led other groups in recognizing the likely physiological and clinical significance of these peptides, most of which are found in the brain and gut.1 " 1 Since many biologically active peptides are capable of influencing vascular smooth muscle, and thus blood flow and blood pressure, peptides with these vasoactive properties are reviewed here. Emphasis is placed on the cardiovascular effects of the more recently identified peptides, with special reference to their possible roles in the regulation of blood pressure in normal and abnormal states. Bradykinin and angiotensins, which are extensively reviewed elsewhere, are only briefly mentioned here. Biological Activity of PeptidesWhich Peptides are Vasoactive?Peptides with vasoactive properties are given in the accompanying list (see box), which is not meant to be complete. For some of these peptides (e.g., angiotensin II, bradykinin), vasoactivity is a dominant feature of their biological actions; for others (e.g., prolactin, parathyroid hormone), the pressor or vasodepressor activity has generally been overshadowed by other actions of the peptide.As will become apparent in the following para : graphs, the ability to induce either vasodilation or vasoconstriction is shared by a variety of apparently unrelated peptides. It is possible in some instances, however, t o ' recognize certain structural features among these peptides that correlate with their vasodilator or vasoconstrictor activity. Such features will be noted. AngiotensinsAngiotensin II (table 1) is one of the most potent systemic vasopressors known. Its formation from angiotensin I through the action of angiotensin-converting enzyme, the localization and properties of this enzyme, and the physiology, pathophysiology, and pharmacology of the renin-angiotensin systems in the body are topics of recent comprehensive reviews.5 "" Bombesin A 14-residue peptide (table 1) isolated from the skin of the frog Bombina bombina, bombesin has spasmogenic activity on a variety of vascular and non-vascular smooth muscle structures.12 It induces vasoconstriction and systemic hypertension in most animal species, hypotension in monkeys, but neither in humans...

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Stimulation of renin secretion by vasoactive intestinal peptide

Cited by 9 publications

References 162 publications

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

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

Regional haemodynamic responses to pituitary adenylate cyclase‐activating polypeptide and vasoactive intestinal polypeptide in conscious rats

Vasoactive peptides. State-of-the-art review.

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