Neuropeptide Y lowers plasma renin activity in the anaesthetised cat

Corder, Roger; Vallotton, Michel B.; Lowry, P. J.; Ramage, Andrew G.

doi:10.1016/0143-4179(89)90067-x

Cited by 13 publications

(8 citation statements)

References 14 publications

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“…Thus, inhibition of renin release and/or lowering of plasma renin activity by NPY have been observed under a variety of experimental conditions. These include the isolated perfused rat kidney [52], systemic infusion in conscious [8] and anaesthetized rats [18], conscious rabbits [6], anaesthetized cats [28] and conscious humans [2,95]. On the other hand, studies in conscious dogs [91] and in the primate Macaca fascicularis [33] have not reported alterations of plasma renin activity or renin secretion on intrarenal or systemic NPY administration.…”

Section: Regulation Of Water and Electrolyte Excretion By Npymentioning

confidence: 99%

Renal effects of neuropeptide Y

Bischoff¹,

Michel²

1998

Pfl�gers Archiv European Journal of Physiology

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Neuropeptide Y (NPY) is a co-transmitter of the sympathetic nervous system including the renal nerves. The kidney expresses NPY receptors, which can also be activated by peptide YY (PYY), a circulating hormone released from gastrointestinal cells. Five subtypes of NPY receptors have been cloned, among which Y1, Y2 and Y5 appear to be involved in the regulation of renal function. NPY produces potent renal vasoconstriction in vitro in isolated interlobar arteries and in the isolated perfused kidney and in vivo upon intrarenal or systemic administration via a Y1 receptor. Nevertheless glomerular filtration rate is altered only little if at all by NPY, indicating a greater effect on the vas efferens than the vas afferens. NPY can inhibit renin release via Y1-like receptors. NPY can stimulate Na+/K+ adenosine triphosphatase (Na+/K+-ATPase) in proximal tubules via Y2 receptors and can antagonize the effects of vasopressin on isolated collecting ducts. It can also act prejunctionally to inhibit noradrenaline release via Y2 receptors. Despite the profound reductions of renal blood flow, systemic NPY infusion can cause diuresis and natriuresis; this is largely independent of pressure natriuresis mechanisms and is possibly mediated by an extrarenal Y5 receptor. Studies with the converting enzyme inhibitor ramiprilat and the bradykinin receptor antagonist icatibant indicate that bradykinin mediates, at least partly, diuretic NPY effects. NPY antagonists enhance basal renal blood flow but do not alter basal diuresis or natriuresis indicating that renovascular, but not tubular, NPY receptors may be tonically activated by endogenous NPY.

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Section: Regulation Of Water and Electrolyte Excretion By Npymentioning

confidence: 99%

Renal effects of neuropeptide Y

Bischoff¹,

Michel²

1998

Pfl�gers Archiv European Journal of Physiology

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“…Therefore, a possible role for NPY in the release of renin has been suggested. It has been shown that the infusion of NPY inhibited renin secretion in isolated perfused rat kidney and in animal models, which was paralleled by renal vasoconstriction (77,168,292). Furthermore, NPY was found to decrease the PRA in adrenalectomized rats (693), in postmyocardial infarction rats (982), in response to isoproterenol or epinephrine (10,38,221), and in two-kidney one-clip renal hypertensive rats (920).…”

Section: Neuropeptide Ymentioning

confidence: 99%

Physiology of Kidney Renin

Castrop

Höcherl

Kurtz

et al. 2010

Physiological Reviews

232

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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“…However, in a more recent study, Y 1 -immunoreactive staining was detected by immunohistochemistry in the juxtaglomerular apparatus of the mouse but not in rats [51]. Indeed, several studies in the past have suggested that NPY may negatively regulate renin secretion via a pressure-independent, pertussis-sensitive mechanism, involving the Y 1 -receptor [23,34,38,[52][53][54]. Such an inhibitory effect was reported in the rat, cat, and humans, but not in dogs or primates [40,44].…”

Section: Effects Of Npy On Renin Secretionmentioning

confidence: 87%

Role of neuropeptide Y in the regulation of kidney function

Winaver

Abassi

Experientia Supplementum

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Neuropeptide Y lowers plasma renin activity in the anaesthetised cat

Cited by 13 publications

References 14 publications

Renal effects of neuropeptide Y

Renal effects of neuropeptide Y

Physiology of Kidney Renin

Role of neuropeptide Y in the regulation of kidney function

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