Repeated renal and splenic sympathetic nerve stimulation in anaesthetized pigs: maintained overflow of neuropeptide Y in controls but not after reserpine

Modin, Agnes; Pernow, John; Lundberg, Jan M.

doi:10.1016/0165-1838(94)90132-5

Cited by 17 publications

(11 citation statements)

References 32 publications

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“…An approximate 50% inhibition of the vasoconstrictor response evoked by PYY in spleen (a vascular response mediated by both NPY Y 1 and Y 2 receptors; Malmström 2001a) was used as indication of an established NPY Y 2 receptor blockade in the present study. The overflow of noradrenaline and NPY-LI is fully reproducible and not susceptible to any spontaneous decline as has been demonstrated in earlier studies (Pernow and Lundberg 1989;Modin et al 1994). The doses of PYY and yohimbine were chosen according to a study by Pernow and Lundberg (1989).…”

Section: Methodsmentioning

confidence: 94%

Effects of the neuropeptide Y Y2 receptor antagonist BIIE0246 on sympathetic transmitter release in the pig in vivo

Malmström

Lundberg

Weitzberg

2002

Naunyn-Schmied Arch Pharmacol

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This study investigated the effects of BIIE0246, a novel neuropeptide Y (NPY) Y(2) receptor antagonist, on renal sympathetic nerve-evoked release of noradrenaline and NPY-like immunoreactivity (-LI) in the pig in vivo. Stimulation (5 Hz, 60 s) of renal sympathetic nerves evoked vasoconstriction and overflow of noradrenaline and NPY-LI. Infusion of peptide YY (PYY; 1 microg/kg per min) strongly inhibited the stimulation-evoked overflow of noradrenaline and NPY-LI. BIIE0246 (100 nmol/kg) abolished the inhibitory effect of PYY. BIIE0246 did not however affect the stimulation-evoked overflow of noradrenaline and NPY-LI, or basal cardiovascular parameters, per se. The alpha(2)-adrenoceptor antagonist yohimbine (0.2 mg/kg) significantly elevated both basal plasma levels and the nerve stimulation-evoked overflow of noradrenaline and NPY-LI. Subsequent administration of BIIE0246 did not further alter these effects. However, BIIE0246 caused splenic vasodilatation per se when given after yohimbine. It is concluded that the renal sympathetic nerves in the pig possess NPY Y(2) receptors, which upon activation inhibit transmitter (noradrenaline and NPY) release. Furthermore, when circulating levels of NPY were enhanced after blockade of alpha(2)-adrenoceptors, an involvement of endogenous NPY, acting on the NPY Y(2) receptor, in regulation of basal splenic vascular tone was unveiled.

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Section: Methodsmentioning

confidence: 94%

Effects of the neuropeptide Y Y2 receptor antagonist BIIE0246 on sympathetic transmitter release in the pig in vivo

Malmström

Lundberg

Weitzberg

2002

Naunyn-Schmied Arch Pharmacol

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“…In reserpine-treated pigs the initial NPY release upon renal nerve stimulation is enhanced but with repeated stimulation trains NPY release gradually decreases, indicating a possible feedback role of noradrenaline in the filling of neuronal NPY stores [78]. NPY release in the porcine kidney can be inhibited by infusion of PYY and enhanced by the α 2 -adrenoceptor antagonist, yohimbine, or by angiotensin II; infusion of the converting enzyme inhibitor, captopril, or of endothelin does not alter renal NPY release [79,90].…”

Section: Presence and Release Of Npy In The Kidneymentioning

confidence: 96%

“…Release of NPY together with noradrenaline has been detected following renal nerve stimulation in pigs in vivo [78] and with the isolated perfused rat kidney [83]. In reserpine-treated pigs the initial NPY release upon renal nerve stimulation is enhanced but with repeated stimulation trains NPY release gradually decreases, indicating a possible feedback role of noradrenaline in the filling of neuronal NPY stores [78].…”

Section: Presence and Release Of Npy In The Kidneymentioning

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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“…endothelin, reduce diuresis and natriuresis [11,16]. Neuropeptide Y (NPY), is a cotransmitter in the sympathetic nervous system which is also found in, and released from, renal nerves [9,13].…”

Section: Introductionmentioning

confidence: 99%

Renovascular and tubular effects of neuropeptide Y are discriminated by PP56 ( D - myo -inositol 1,2,6-triphosphate) in anaesthetized rats

Bischoff¹,

Stickan-Verfürth²,

Michel³

1997

Pfl�gers Archiv European Journal of Physiology

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Systemic infusion of neuropeptide Y (NPY; 1 microg kg-1 min-1) for 120 min rapidly reduced renal blood flow and increased mean arterial pressure and renovascular resistance and, at later time points (> 30 min), enhanced diuresis, natriuresis and calciuresis in anaesthetized rats. Infusion of the reported NPY antagonist PP56 (D-myo-inositol 1,2,6-triphosphate, 333 mg kg-1 min-1) slightly but significantly enhanced renal blood flow and reduced renovascular resistance over the course of the infusion period. Infusion of PP56 together with NPY (starting 30 min prior to the NPY infusion) significantly inhibited NPY-induced alterations of mean arterial pressure, renal blood flow and renovascular resistance. Coinfusion of PP56 also attenuated the renovascular effects of bolus injections of NPY (0.1-10 microg/kg) but at the highest NPY dose the antagonistic effect of PP56 could partially be overcome. In contrast to the antagonism of the vascular NPY effects, infusion of PP56 did not significantly affect NPY-induced enhancements of diuresis, natriuresis and calciuresis. Thus, PP56 is a surmountable antagonist of vascular but not tubular NPY effects. We conclude that tubular NPY effects occur largely independently of alterations of renal haemodynamics.

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Repeated renal and splenic sympathetic nerve stimulation in anaesthetized pigs: maintained overflow of neuropeptide Y in controls but not after reserpine

Cited by 17 publications

References 32 publications

Effects of the neuropeptide Y Y2 receptor antagonist BIIE0246 on sympathetic transmitter release in the pig in vivo

Effects of the neuropeptide Y Y2 receptor antagonist BIIE0246 on sympathetic transmitter release in the pig in vivo

Renal effects of neuropeptide Y

Renovascular and tubular effects of neuropeptide Y are discriminated by PP56 ( D - myo -inositol 1,2,6-triphosphate) in anaesthetized rats

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