Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atrial natriuretic peptides (ANP) are released into the circulation in response to enhanced atrial stretching. These peptides not only have diuretic and natriuretic properties, but also exert a relaxing effect on the vasculature. Moreover, they antagonize the contractions induced by norepinephrine and angiotensin II. Neuropeptide Y (NPY) is also a vasoactive peptide. It is widely distributed throughout the central and peripheral nervous systems. NPY is coreleased with norepinephrine by perivascular nerve endings. At high concentrations, this peptide has a direct vasoconstrictor effect. In addition, it enhances the vascular effect of various agonists, including norepinephrine and angiotensin II. Both ANP and NPY have an inhibitory effect on renin secretion. This effect may have important implications for the role of these peptides in cardiovascular regulation.
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PMID:Role of atrial natriuretic peptides and neuropeptide Y in blood pressure regulation. 215 74

Neuropeptide Y is known to enhance blood pressure responsiveness to various constrictors, including angiotensin II, and to suppress renin secretion. This study was undertaken to assess the effect of neuropeptide Y on the development of two-kidney, one clip renal hypertension. Normotensive rats either had a silver clip placed on the left renal artery or were sham-operated upon. An osmotic minipump, which was connected via a catheter to a jugular vein, was implanted subcutaneously in all rats. These pumps delivered either neuropeptide Y (0.001 microgram/min) or saline intravenously. Eight days later, an intra-arterial catheter was inserted and the rats were studied while not anesthetized on the following day. Neuropeptide Y did not affect body weight. In clipped rats, neuropeptide Y prevented the development of hypertension and suppressed renin secretion. Neuropeptide Y significantly decreased blood pressure also in sham-operated rats, although it had no effect on plasma renin activity. These data indicate that prolonged neuropeptide Y infusion may lower blood pressure by different mechanisms, one of which is probably a suppression of renin release.
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PMID:Prevention of renal hypertension in the rat by neuropeptide Y. 215 52

Neuropeptide Y (NPY) is a potent vasoconstrictor peptide contained in sympathetic nerve terminals and is co-released with norepinephrine. Previous studies in the rat have suggested that NPY influences renal sodium reabsorption and renin release. However, little is known about the physiological effects of NPY on the kidney in the human. In the present study NPY was infused intravenously and directly into the renal artery of the primate Macaca fascicularis, an experimental model of the human. Intravenous NPY infusion at doses of 20-1,000 ng.kg-1.min-1 produced dose-dependent rises in renal vascular resistance with minimal changes in arterial pressure. Urine flow and sodium excretion were changed significantly only at doses of NPY that significantly reduced renal blood flow and filtration rate. Arterial plasma renin activity and renin secretion rate were not significantly altered at any dose of NPY. Intrarenal infusion of NPY at doses of 20-400 ng.kg-1.min-1 produced potent dose-dependent renal vasoconstriction with minimal changes in arterial pressure. Under these conditions sodium excretion was significantly reduced concurrent with decreases in renal blood flow and glomerular filtration rate. However, no significant changes in arterial plasma renin activity or renin secretion rate were found at any dose of NPY. These data indicate that in the nonhuman primate NPY is a potent renal vasoconstrictor agent that has variable effects on renal excretory and secretory function, which may be secondary to its vasoconstrictor actions.
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PMID:Renal actions of neuropeptide Y in the primate. 270 32

Neuropeptide Y (NPY) is a peptide with vasoconstrictor properties known to be present in the central nervous system as well as in sympathetic nerve endings and the adrenal medulla. The purposes of this study were to investigate in normotensive conscious rats the effects of nonpressor doses of NPY on cardiac output and regional blood flow distribution (using radiolabeled microspheres) as well as on plasma renin activity, plasma catecholamine and vasopressin levels. NPY (0.1 microgram/min) infused i.v. for 30 min modified neither blood pressure nor heart rate. Cardiac index was at comparable levels in NPY- as in vehicle-treated rats (17.7 +/- 1.6, n = 8, vs. 21.3 +/- 0.9 ml/min/100 g, n = 8, mean +/- S.E.M.). There was no significant difference in regional blood flow distribution between the two groups of rats, except for the large intestine (0.42 +/- 0.06 vs. 0.71 +/- 0.1 ml/min/g in NPY- and vehicle-treated rats, respectively, P less than .05). Basal plasma renin activity and catecholamine levels were not modified by NPY whereas plasma vasopressin levels were lower (P less than .05) in rats given NPY (0.76 +/- 0.3 pg/ml, n = 8) than in those having received the vehicle (2.2 +/- 0.4 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of a nonpressor dose of neuropeptide Y on cardiac output, regional blood flow distribution and plasma renin, vasopressin and catecholamine levels. 307 38

In the periphery, neuropeptide Y is present in the circulation, in the adrenal medulla as well as at the level of nerve endings and of the juxtaglomerular apparatus. The aim of the present study was to assess the effect of this neuropeptide on renin secretion. Normotensive rats were biadrenalectomized or sham-operated and made hypertensive with methylprednisolone acetate (20 mg/kg s.c. once weekly). Deoxycorticosterone pivalate (10 mg/kg s.c. once weekly) was also given to prevent mineralocorticoid deficiency. Two weeks after that initial surgery 12 adrenalectomized rats and 8 sham-operated rats were infused for 30 min with neuropeptide Y (0.1 microgram/min) whereas 8 adrenalectomized rats and 9 sham-operated rats received in similar conditions the vehicle of neuropeptide Y (10 microliters/min). At that time, the rats were conscious and there was no significant difference in blood pressure and heart rate between the 4 groups of rats. At the end of the experiment, adrenalectomized rats exhibited a markedly stimulated renin-angiotensin system. Neuropeptide Y made it possible to normalize plasma renin activity in these rats, thus suggesting that neuropeptide Y plays an important role in regulating renin secretion.
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PMID:[Normalization of renin secretion by neuropeptide Y in adrenalectomized rats with glucocorticoid-induced hypertension]. 309 5

Neuropeptide Y, a potent vasoconstrictor peptide with 36 amino acid residues, is co-stored and released with catecholamines in sympathetic nerve endings. In this study responses in circulating neuropeptide Y induced by baroreceptor activation during change from the supine to the head-up position was measured in normal subjects and untreated essential hypertensives. Furthermore, the relationships with plasma catecholamines, endothelin-1, renin and serotonin were studied. No significant differences of plasma neuropeptide Y were found between normotensive and hypertensive subjects, before or after postural changes, and there was no correlation with a range of the vasoactive substances studied. Our results suggest that plasma neuropeptide Y does not increase with noradrenaline on sympathetic activation during postural stress both in normals and in hypertensive subjects. In man, measurement of plasma neuropeptide Y during head-up tilt does not provide a useful estimation of sympathetic nervous activity.
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PMID:Levels of plasma neuropeptide Y and other vasoactive substances during head-up tilt in normal and essential hypertensive subjects. 762 Feb 95

Neuropeptide Y is a vasoactive peptide and is widely distributed throughout the central and peripheral nervous systems. Neuropeptide Y is co-released with noradrenaline by perivascular nerve endings. At high concentrations, it has a direct vasoconstrictor effect. In addition, it enhances the vascular effect of various agonists, including noradrenaline and angiotensin II. Moreover, neuropeptide Y has an inhibitory effect on renin secretion. This peptide may have an important role in cardiovascular regulation.
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PMID:Neuropeptide Y and cardiovascular regulation. 792 57

Neuropeptide Y (NPY) is stored in sympathetic nerves and NPY levels increase several times during exercise. NPY administration during prolonged exercise causes reduced splanchnic glucose production. To elucidate the effects of NPY on adrenaline (Adr)-stimulated splanchnic glycogenolysis these substances were infused to seven healthy subjects in the post-absorptive state. Blood samples were drawn from an arterial and a central hepatic vein catheter for determination of splanchnic blood flow, exchanges of metabolites and arterial levels of NPY, catecholamines, insulin, glucagon and renin in the basal state and during 20 min Adr infusion (0.1-0.3 nmol kg-1 min-1). After basal values were reached a 60 min NPY infusion was initiated. At 40 min of NPY infusion the Adr infusion was repeated. Adr alone increased splanchnic blood flow (41%, P < 0.01), arterial glucose concentration (29%, P < 0.001) and splanchnic glucose production (102%, P < 0.01). During the NPY infusion both splanchnic blood flow and arterial glucose fell (P < 0.05). Although the combined NPY and Adr infusion caused the same proportional increases in splanchnic blood flow, arterial glucose and splanchnic glucose production as with Adr alone the absolute values were lower (all P < 0.05). Arterial insulin as well as Adr and noradrenaline increased with the combined NPY-and Adr infusion as with Adr alone. Arterial plasma renin activity was 12% lower with the combined NPY and Adr-infusion compared to Adr infusion alone. These results indicate further an inhibitory effect of NPY on splanchnic glycogenolysis and suggest that NPY inhibits Adr-stimulated renin release.
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PMID:Inhibitory effects of neuropeptide Y on splanchnic glycogenolysis and renin release in humans. 820 50

Neuropeptide Y (NPY) is a vasoconstrictor peptide possibly involved in the regulation of renal sodium handling and renin release. This investigation was undertaken to assess in conscious normotensive rats the acute effects of a non-pressor dose of NPY on renal plasma flow, glomerular filtration rate, sodium excretion and plasma renin activity. Experiments were also performed during concomitant beta-adrenoceptor stimulation with isoproterenol. NPY per se had no effect on the studied parameters. Renal plasma flow was increased by isoproterenol and was significantly higher when the beta-adrenoceptor stimulant was infused alone (13.4 +/- 2.1 ml/min, p < 0.05, mean +/- SEM) that when administered together with NPY (7.2 +/- 2.0 ml/min). This was also true for glomerular filtration rate (3.3 +/- 0.3 vs. 1.8 +/- 0.3 ml/min, p < 0.01) and plasma renin activity (6.3 +/- 1.7 vs. 2.1 +/- 0.4 ng Ang I/ml/h, p < 0.05). Our data however do not allow to deduce whether the inhibitory effect of NPY on isoproterenol-induced renin release is mediated by changes in intrarenal hemodynamics or a direct effect on juxtaglomerular cells.
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PMID:Effects of neuropeptide Y on intrarenal hemodynamics, plasma renin activity and urinary sodium excretion in rats. 883 9

Neuropeptide Y (NPY) has been recently characterized as a circulating vasoconstrictor peptide which is co-stored with noradrenaline in sympathetic neurons. To investigate the role of NPY concentration in hypertension we measured the circulating NPY, endothelin-1,2 (ET-1,2), atrial natriuretic peptide (ANP), aldosterone, plasma renin activity (PRA) and noradrenaline (NA) in patients with stable mild to moderate primary hypertension. Circulating levels of NPY, ET-1,2, ANP, aldosterone and PRA were measured with radioimmunoassay, NA by double-isotope radioenzymatic assay. There were significant increase in concentrations NPY, ET-1,2, ANP and NA in patients with moderate primary hypertension, and significant positive correlations between the plasma levels of NPY, ET-1,2 and NA.
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PMID:[Concentration of neuropeptide Y in serum of patients with primary hypertension]. 884 9


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