Renal actions of neuropeptide Y in the primate

1989 ◽  
Vol 256 (4) ◽  
pp. F524-F531 ◽  
Author(s):  
S. F. Echtenkamp ◽  
P. F. Dandridge
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Neuropeptide Y ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Arterial Plasma ◽  
Dose Dependent

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.

Genetic co-segregation of renal haemodynamics and blood pressure in the spontaneously hypertensive rat

1988 ◽  
Vol 74 (1) ◽  
pp. 63-69 ◽  
Author(s):  
S. B. Harrap ◽  
A. E. Doyle
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Spontaneously Hypertensive Rat ◽  
Plasma Renin ◽  
Spontaneously Hypertensive

1. To determine the relevance of renal circulatory abnormalities found in the immature spontaneously hypertensive rat (SHR) to the genetic hypertensive process, glomerular filtration rate and renal blood flow were measured in conscious F2 rats, derived from crossbreeding SHR and normotensive Wistar–Kyoto rats (WKY), at 4, 11 and 16 weeks of age by determining the renal clearances of 51Cr-ethylenediaminetetra-acetate and 125I-hippuran respectively. Plasma renin activity was measured at 11 and 16 weeks of age. 2. Mean arterial pressure, glomerular filtration rate and renal blood flow increased between 4 and 11 weeks of age. Between 11 and 16 weeks the mean glomerular filtration rate and renal blood flow did not alter, although the mean arterial pressure rose significantly. At 11 weeks of age, during the developmental phase of hypertension, a significant negative correlation between mean arterial pressure and both glomerular filtration rate and renal blood flow was noted. However, by 16 weeks when the manifestations of genetic hypertension were more fully expressed, no correlation between mean arterial pressure and renal blood flow or glomerular filtration rate was observed. Plasma renin activity was negatively correlated with both glomerular filtration rate and renal blood flow, but the relationship was stronger at 11 than at 16 weeks of age. 3. These results suggest that the reduction in renal blood flow and glomerular filtration rate, found in immature SHR, is genetically linked to the hypertension and may be of primary pathogenetic importance. It is proposed that the increased renal vascular resistance in these young animals stimulates the rise of systemic arterial pressure which returns renal blood flow and glomerular filtration rate to normal.

Protective effect of renal denervation on normotensive endotoxemia-induced acute renal failure in mice

2002 ◽  
Vol 283 (3) ◽  
pp. F583-F587 ◽  
Author(s):  
Wei Wang ◽  
Sandor A. Falk ◽  
Suparoek Jittikanont ◽  
Patricia E. Gengaro ◽  
Charles L. Edelstein ◽  
...  
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Filtration Rate ◽  
Renal Denervation ◽  
Plasma Renin

Acute renal failure (ARF) contributes substantially to the high morbidity and mortality observed during endotoxemia. We hypothesized that selective blockade of the renal nerves would be protective against ARF during the early (16 h) stage of endotoxemia [5 mg lipopolysaccharide (LPS)/kg ip in mice]. At 16 h after LPS, there was no change in mean arterial pressure, but plasma epinephrine (4,604 ± 719 vs. 490 ± 152 pg/ml, P < 0.001), norepinephrine (2,176 ± 306 vs. 1,224 ± 218 pg/ml, P < 0.05), and plasma renin activity (40 ± 5 vs. 27 ± 2 ng · ml−1 · h−1, P < 0.05) were higher in the LPS-treated vs. control mice. The high plasma renin activity level decreased to the control level with renal denervation in endotoxemic mice. After intravenous injection of phentolamine (200 μg/kg), the decrement in mean arterial pressure was significantly greater in LPS-treated vs. control mice (19.4 ± 3.5 vs. 8.1 ± 1.5 mmHg, P < 0.01). Sixteen hours after LPS administration, there were significant decreases in glomerular filtration rate (52 ± 18 vs. 212 ± 23 μl/min, P < 0.01) and renal blood flow (0.58 ± 0.08 vs. 0.85 ± 0.06 ml/min, P < 0.01) in sham-operated mice. The decrement in glomerular filtration rate during endotoxemia was significantly attenuated in mice with denervated kidneys (32 vs. 79%). Moreover, there was no change in renal blood flow during endotoxemia in mice with renal denervation. The present results therefore demonstrate a protective role of renal denervation during normotensive endotoxemia-related ARF in mice, an effect that may be, at least in part, due to a diminished activation of the renin-angiotensin system.

Effect of KCl infusion on renin secretory rates and aldosterone excretion in dogs

1975 ◽  
Vol 229 (2) ◽  
pp. 370-375 ◽  
Author(s):  
W Flamenbaum ◽  
JG Kleinman ◽  
JS McNeil ◽  
RJ Hamburger ◽  
TA Kotchen
Keyword(s):  
Blood Flow ◽  
Plasma Renin Activity ◽  
Renal Blood Flow ◽  
Flow Distribution ◽  
Plasma Renin ◽  
Systemic Blood Pressure ◽  
Renin Activity ◽  
Secretory Rate ◽  
Arterial Plasma ◽  
Renal Blood Flow Distribution

The effects of unilateral intrarenal arterial KCl infusion in dogs (12 mueq/kg per min) on bilateral renal function, renin secretory rates, and aldosterone excretion were studied. During KCl infusion, infused-side renal arterial plasma [K+] increased by 2.2 +/- 0.6 meq/liter. Systemic plasma [K+] simultaneously rose by 0.6 +/- 0.1 meq/liter. Plasma renin activity decreased 29 +/- 9%, and the decrease correlated with the increases in plasma [K+]. Renin secretory rate decreased bilaterally, the decrease being greater in each experiment on the infused side. Aldosterone excretion increased during KCl infusion by 72 +/- 17%, despite a decrease in plasma renin activity. With KCl infusion there was a bilateral increase in K+ excretion, and a positive correlation was observed between the net alterations in K+ and Na+ excretion. No significant alterations in systemic blood pressure, glomerular filtration rate, total renal blood flow, or intracortical renal blood flow distribution were observed. These studies suggest that K+ inhibits the release of renin by an intrarenal mechanism, which may be related to a K+-induced alteration in Na+ absorption.

Effects of Endothelin on Systemic and Renal Haemodynamics and Neuroendocrine Hormones in Conscious Dogs

1989 ◽  
Vol 77 (5) ◽  
pp. 567-572 ◽  
Author(s):  
Hidetomo Nakamoto ◽  
Hiromichi Suzuki ◽  
Marohito Murakami ◽  
Yo Kageyama ◽  
Akira Ohishi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Plasma Renin Activity ◽  
Renal Blood Flow ◽  
Arginine Vasopressin ◽  
Adrenocorticotropic Hormone ◽  
Bolus Injection ◽  
Plasma Renin ◽  
Peak Level ◽  
Dependent Manner ◽  
Dose Dependent

1. The effects of endothelin on systemic and renal haemodynamics and plasma concentrations of neuroendocrine hormones including plasma renin activity, aldosterone, adrenocorticotropic hormone, Cortisol, catecholamines and arginine vasopressin were investigated in 18 conscious dogs. 2. Bolus injection of 4 pmol of endothelin/kg did not cause any significant changes in haemodynamics. Mean arterial pressure was elevated by both doses of 40 pmol/kg [91 ± 2 to 99 ± 2 mmHg (12.1 ± 0.3 to 13.2 ± 0.3 kPa), P < 0.05] or 200 pmol/kg [93 ± 2 to 107 ± 3 mmHg (12.4 ± 0.3 to 14.3± 0.4 kPa), P < 0.01], the latter dose increasing cardiac output (14%, P < 0.05) and heart rate (9%, P < 0.05), and the former reducing these parameters (14% and 8%, P < 0.05, respectively). 3. In contrast with the various changes in systemic haemodynamics, renal blood flow transiently increased immediately after bolus injection in a dose-dependent manner (28%, P < 0.05, 50%, P < 0.01 and 110%, P < 0.01 with 4, 40 and 200 pmol of endothelin/kg, respectively). This transient elevation of renal blood flow was followed by a gradual decrease (16%, P < 0.05; 31%, P < 0.01 and 36%, P < 0.01) at 10 min. 4. All neurohormones were elevated in a dose-dependent manner. 5. Among these hormones, arginine vasopressin and plasma renin activity reached a peak level at 5 min (from 2.21 ± 0.45 to 6.37 ± 0.60 pmol/l, P < 0.01, and from 0.65 ± 0.08 to 1.09 ± 0.10 pmol of angiotensin 1 h−1 ml−1P < 0.01, respectively) after bolus injection of 200 pmol of endothelin/kg, whereas adrenocorticotropic hormone and Cortisol reached a peak level at 15 min (from 6.0 ± 0.7 to 18.2 ± 1.5 pmol/l, P < 0.01, and from 4.4 ± 0.9 to 16.5 ± 2.7 × 10−2 μmol/l, P < 0.01, respectively). 6. These results suggest that endothelin is a potent vasoconstrictive peptide in vivo with a marked effect on the renal vascular system, and that it induces elevation of vasoactive hormones directly and/or through central effects.

Influence of the renin–angiotensin system in the renal haemodynamic responses to modest renal nerve stimulation in the rat

1982 ◽  
Vol 93 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Stephen Ball ◽  
E. J. Johns
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Plasma Renin Activity ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Nerve Stimulation ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Renal Nerves ◽  
Filtration Fraction

The renal nerves of the left kidney of sodium-replete anaesthetized rats were stimulated for 30-min periods at 2–3 Hz (15 V, 0·2 ms). Renal blood flow was reduced by 22% and glomerular filtration rate by 14% which resulted in a rise in filtration fraction of 12%. Circulating plasma renin activity was increased by 30% during such nerve stimulation. In rats treated for 3–4 weeks with deoxycorticosterone acetate (DOCA) and saline (150 mm-NaCl) basal values of arterial blood pressure, renal blood flow, glomerular filtration rate and filtration fraction were not significantly different from those observed in sodium-replete rats. However, plasma renin activity was lower, being approximately one-third of that observed in sodium-replete animals. Stimulation of the renal nerves in rats treated with DOCA and saline resulted in a fall in renal blood flow of 32% and a much larger fall in glomerular filtration rate of 33% which resulted in no change in filtration fraction. Plasma renin activity was not changed by renal nerve stimulation in the animals treated with DOCA and saline. It is suggested that these renal responses provide evidence in the rat for a role of locally generated angiotensin II in regulating glomerular filtration rate during electrical activation of the renal nerves by causing preferential vasoconstriction of the efferent arteriole.

Electrical stimulation of paraventricular nucleus increases plasma renin activity

1988 ◽  
Vol 254 (2) ◽  
pp. R325-R330 ◽  
Author(s):  
J. P. Porter
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Electrical Stimulation ◽  
Plasma Renin Activity ◽  
Renal Blood Flow ◽  
Paraventricular Nucleus ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Renin Activity ◽  
Stimulation Of

Studies employing direct electrical stimulation of the renal nerves have shown that, depending on the frequency used, selective effects on renal function can be evoked. With low frequencies, an increase in renin secretion can be elicited without affecting glomerular filtration rate, sodium excretion, or renal blood flow. In the present investigation the possibility was addressed that the central nervous system (CNS) is also organized to evoke selective changes in renal function. The paraventricular nucleus (PVN) of the hypothalamus was electrically stimulated in conscious rats with 150 microA and frequencies of 2.5, 5, 10, and 15 Hz. Blood samples for determination of plasma renin activity (PRA) were collected before and at the end of each 5-min stimulation period. The lower frequencies had no effect on PRA, but stimulation with 10 and 15 Hz produced a significant increase. This effect on PRA was not accompanied by changes in arterial pressure or renal blood flow. In a separate group of animals, stimulation of the PVN with 15 Hz produced a marked decrease in urine volume, but sodium excretion did not change. These data raise the possibility that the CNS is organized to evoke selective increases in sympathetic outflow to the kidney and to produce separate changes in renal functions.

Renal blood flow, early distal sodium, and plasma renin concentrations during osmotic diuresis

2000 ◽  
Vol 279 (4) ◽  
pp. R1268-R1276 ◽  
Author(s):  
Paul P. Leyssac ◽  
Niels-Henrik Holstein-Rathlou ◽  
Ole Skøtt
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Urine Flow ◽  
Sodium Reabsorption ◽  
Osmotic Diuresis ◽  
Nacl Concentration ◽  
Proximal Tubular ◽  
Distal Tubules

Inconsistencies in previous reports regarding changes in early distal NaCl concentration (EDNaCl) and renin secretion during osmotic diuresis motivated our reinvestigation. After intravenous infusion of 10% mannitol, EDNaCl fell from 42.6 to 34.2 mM. Proximal tubular pressure increased by 12.6 mmHg. Urine flow increased 10-fold, and sodium excretion increased by 177%. Plasma renin concentration (PRC) increased by 58%. Renal blood flow and glomerular filtration rate decreased, however end-proximal flow remained unchanged. After a similar volume of hypotonic glucose (152 mM), EDNaClincreased by 3.6 mM, ( P < 0.01) without changes in renal hemodynamics, urine flow, sodium excretion rate, or PRC. Infusion of 300 μmol NaCl in a smaller volume caused EDNaCl to increase by 6.4 mM without significant changes in PRC. Urine flow and sodium excretion increased significantly. There was a significant inverse relationship between superficial nephron EDNaCl and PRC. We conclude that EDNa decreases during osmotic diuresis, suggesting that the increase in PRC was mediated by the macula densa. The results suggest that the natriuresis during osmotic diuresis is a result of impaired sodium reabsorption in distal tubules and collecting ducts.

L-arginine analogues inhibit aldosterone secretion in rats

1995 ◽  
Vol 268 (5) ◽  
pp. R1137-R1142 ◽  
Author(s):  
J. C. Simmons ◽  
R. H. Freeman
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Bilateral Nephrectomy ◽  
Aldosterone Secretion ◽  
Series Of Experiments

L-Arginine analogues, e.g., NG-nitro-L-arginine methyl ester (L-NAME), increase arterial pressure and suppress renin release in the rat. On the basis of these observations, it was hypothesized that L-arginine analogues also would attenuate aldosterone secretion. This hypothesis was tested in anesthetized rats treated with L-NAME or NG-nitro-L-arginine (L-NNA, 185 mumol/kg ip). The aldosterone secretion rate, plasma renin activity, and adrenal blood flow were attenuated in rats treated with L-NAME and L-NNA compared with control animals. Similar experiments were performed in anephric rats to examine the effects of L-NAME on aldosterone secretion independent of the circulating reninangiotensin system. The administration of L-NAME reduced adrenal blood flow but failed to reduce aldosterone secretion in these anephric rats. Bilateral nephrectomy reduced plasma renin activity essentially to undetectable levels in these animals. In a third series of experiments, two groups of anephric rats were infused with angiotensin II (3 micrograms/kg body wt iv) to provide a stimulus for aldosterone secretion. Aldosterone secretion and adrenal blood flow were markedly reduced in angiotensin II-infused rats pretreated with L-NAME compared with the control anephric animals infused with angiotensin II. Overall these results suggest that L-arginine analogues attenuate aldosterone secretion by inhibiting the adrenal steroidogenic effects of endogenous or exogenous angiotensin II and/or by reducing plasma levels of renin/angiotensin.

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