Angiotensin II in antinatriuresis of low-level renal nerve stimulation

1976 ◽  
Vol 231 (4) ◽  
pp. 1105-1110 ◽  
Author(s):  
EJ Zambraski ◽  
GF DiBona
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Nerve Stimulation ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Sodium Reabsorption ◽  
Renal Nerve ◽  
Low Level ◽  
Renal Nerve Stimulation ◽  
Renal Tubular

Low-level direct renal nerve stimulation increases both renal tubular sodium reabsorption and renal renin secretion rate without changing arterial pressure, glomerular filtration rate, renal blood flow, or intrarenal blood flow distribution. The possibility was considered that intrarenal angiotensin II formation might mediate the antinatriuretic effect by directly enhancing renal tubular sodium reabsorption. Low-level direct renal nerve stimulation was performed in anesthetized saline-loaded dogs before and after intrarenal blockade to angiotensin II with [1-sarcosine, 8-alanine]angiotensin II. The antinatriuretic response to low-level direct renal nerve stimulation was not altered by intrarenal blockade to angiotensin II. Renal renin secretion rate was increased by low-level direct renal nerve stimulation in the absence of changes in systemic or renal hemodynamics. The antinatriuretic effect of low-level direct renal nerve stimulation does not depend on the intrarenal action of angiotensin II.

scholarly journals Effect of angiotensin II on renal nerve stimulation-induced norepinephrine release in dogs

1987 ◽  
Vol 43 ◽  
pp. 96
Author(s):  
Toshiyuki Matsuoka ◽  
Yoshiharu Hayashi ◽  
Mizue Suzuki-Kusaba ◽  
Susumu Satoh
Keyword(s):  
Angiotensin Ii ◽  
Nerve Stimulation ◽  
Norepinephrine Release ◽  
Renal Nerve ◽  
Renal Nerve Stimulation

Differential Efect of Noradrenaline and Renal Nerve Stimulation on Vascular Resistance in the Dog Kidney and the Release of a Prostaglandin E-Like Substance

1972 ◽  
Vol 42 (2) ◽  
pp. 223-233 ◽  
Author(s):  
J. C. McGiff ◽  
K. Crowshaw ◽  
N. A. Terragno ◽  
K. U. Malik ◽  
A. J. Lonigro
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Nerve Stimulation ◽  
Venous Blood ◽  
Urine Flow ◽  
Rapid Recovery ◽  
Prostaglandin E ◽  
Early Recovery ◽  
Renal Nerve ◽  
Renal Nerve Stimulation

1. The concentrations of prostaglandin E(PGE)- and prostaglandin F(PGF)-like substances in renal venous blood were determined by parallel bioassay of extracts of renal venous effluent before and during adrenergic stimulation of the kidney and were related to simultaneous measurements of renal blood flow and urine flow. 2. When noradrenaline was infused continuously into the renal artery, its initial vasoconstrictor and antidiuretic effects diminished on seven of eight occasions in six dogs. Rapid recovery of renal blood flow and urine flow was invariably associated with increasing concentration in renal venous blood of a substance having the physicochemical, chromatographic and biological properties of a prostaglandin of the E series. In the one instance when rapid early recovery of renal blood flow was not observed the concentration of PGE-like substance was not increased. 3. In contrast, during renal nerve stimulation early rapid recovery of renal blood flow and urine flow did not occur and the concentration of a PGE-like substance in renal venous blood did not increase. The concentration of a PGF-like substance in renal venous effluent did not increase in response to either stimulus. 4. Since PGE2, unlike PGF2α, is a potent renal vasodilator and diuretic, the intrarenal release of this substance by noradrenaline in concentrations similar to those determined for a PGE-like substance (>0·50 ng/ml assayed as PGE2 equivalents) would account for the changes in renal blood flow and urine flow in these experiments when the renal actions of noradrenaline were attenuated. 5. These results support the proposal that renal prostaglandins function in an intrarenal negative feedback control system which regulates antidiuretic and vasoconstrictor systems.

Role of prostaglandin in norepinephrine and renin release in canine kidney

1987 ◽  
Vol 253 (5) ◽  
pp. F929-F934
Author(s):  
Y. Hayashi ◽  
H. Hisa ◽  
S. Satoh
Keyword(s):  
Secretion Rate ◽  
The Other ◽  
Renin Secretion ◽  
Renal Nerve ◽  
Anesthetized Dogs ◽  
Renal Nerve Stimulation ◽  
Pg E2 ◽  
Secretion Rates ◽  
Canine Kidney

We investigated renin and norepinephrine (NE) release during electrical renal nerve stimulation (RNS) in relation to prostaglandin (PG) E2 concomitantly produced by the kidney in anesthetized dogs. During 10 min of continuous RNS (2.5-4 Hz), the increases in renin, NE, and PGE2 secretion rates were determined at 1 and 10 min after the start of stimulation. Under control conditions, almost the same extent of increase in the NE secretion rate was observed at 1 and 10 min of RNS, whereas the increase in renin secretion rate at 1 min of RNS was followed by a further increase at 10 min of RNS. On the other hand, an upward but not significant trend of increase in PGE2 secretion at 1 min of RNS was followed by a substantial level at 10 min of RNS. After administration of indomethacin, the increase in NE secretion rates at both 1 and 10 min of RNS were not altered, but the increase in renin secretion rate at 10 min of RNS was suppressed by approximately 50%, without any reduction of the increase in the renin secretion rate at 1 min of RNS. Consequently, the time-related change in the renin secretion rate during RNS was abolished. These results suggest that renin response to continuous RNS is enhanced by concomitantly generated PGs but not by NE, and furthermore, that endogenously generated PGs do not inhibit the release of NE from canine renal nerve endings.

Renal nerve stimulation augments effect of intraluminal angiotensin II on proximal tubule transport

2002 ◽  
Vol 282 (6) ◽  
pp. F1043-F1048 ◽  
Author(s):  
Albert Quan ◽  
Michel Baum
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Nerve Stimulation ◽  
Filtration Rate ◽  
Renin Angiotensin System ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Angiotensin System ◽  
Renal Nerve Stimulation

The proximal tubule synthesizes and secretes angiotensin II into the lumen, where it regulates transport. Renal denervation abolishes the effect of angiotensin II on proximal tubule transport. Using in vivo microperfusion, we examined whether renal nerve stimulation modulates the effect of angiotensin II on transport. The effect of angiotensin II was assessed by measuring the decrease in volume reabsorption with the addition of 10−4M luminal enalaprilat. Luminal enalaprilat did not alter volume reabsorption (2.80 ± 0.18 vs. 2.34 ± 0.14 nl · mm−1 · min−1). However, with renal nerve stimulation, enalaprilat decreased volume reabsorption (3.45 ± 0.22 vs. 1.67 ± 0.20 nl · mm−1 · min−1, P < 0.0005). The absolute and percent decrements in volume reabsorption with luminal enalaprilat were higher with renal nerve stimulation than with native innervation (1.78 ± 0.19 vs. 0.46 ± 0.23 nl · mm−1 · min−1, P < 0.02, and 51.8 ± 5.0 vs. 14.6 ± 7.4%, P < 0.05, respectively). Renal nerve stimulation did not alter the glomerular filtration rate or renal blood flow. Renal nerve stimulation augments the stimulatory effect of intraluminal angiotensin II. The sympathetic renal nerves modulate the proximal tubule renin-angiotensin system and thereby regulate proximal tubule transport.

Renal nerve stimulation leads to the activation of the Na+/H+ exchanger isoform 3 via angiotensin II type I receptor

2015 ◽  
Vol 308 (8) ◽  
pp. F848-F856 ◽  
Author(s):  
Roberto B. Pontes ◽  
Renato O. Crajoinas ◽  
Erika E. Nishi ◽  
Elizabeth B. Oliveira-Sales ◽  
Adriana C. Girardi ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Low Frequency ◽  
Renin Angiotensin System ◽  
Receptor Activation ◽  
Sodium Reabsorption ◽  
Urinary Flow ◽  
Type I ◽  
Ang Ii ◽  
Renal Nerve ◽  
Renal Nerve Stimulation

Renal nerve stimulation at a low frequency (below 2 Hz) causes water and sodium reabsorption via α1-adrenoreceptor tubular activation, a process independent of changes in systemic blood pressure, renal blood flow, or glomerular filtration rate. However, the underlying mechanism of the reabsorption of sodium is not fully understood. Since the sympathetic nervous system and intrarenal ANG II appear to act synergistically to mediate the process of sodium reabsorption, we hypothesized that low-frequency acute electrical stimulation of the renal nerve (ESRN) activates NHE3-mediated sodium reabsorption via ANG II AT1 receptor activation in Wistar rats. We found that ESRN significantly increased urinary angiotensinogen excretion and renal cortical ANG II content, but not the circulating angiotensinogen levels, and also decreased urinary flow and pH and sodium excretion via mechanisms independent of alterations in creatinine clearance. Urinary cAMP excretion was reduced, as was renal cortical PKA activity. ESRN significantly increased NHE3 activity and abundance in the apical microvillar domain of the proximal tubule, decreased the ratio of phosphorylated NHE3 at serine 552/total NHE3, but did not alter total cortical NHE3 abundance. All responses mediated by ESRN were completely abolished by a losartan-mediated AT1 receptor blockade. Taken together, our results demonstrate that higher NHE3-mediated proximal tubular sodium reabsorption induced by ESRN occurs via intrarenal renin angiotensin system activation and triggering of the AT1 receptor/inhibitory G-protein signaling pathway, which leads to inhibition of cAMP formation and reduction of PKA activity.

Losartan corrects abnormal frequency response of renal vasculature in congestive heart failure

2003 ◽  
Vol 285 (5) ◽  
pp. H1857-H1863 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Sawin
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Angiotensin Ii ◽  
Frequency Response ◽  
Nerve Stimulation ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Pass Filter ◽  
Vasoconstrictor Response ◽  
Renal Nerve Stimulation

In congestive heart failure, renal blood flow is decreased and renal vascular resistance is increased in a setting of increased activity of both the sympathetic nervous and renin-angiotensin systems. The renal vasoconstrictor response to renal nerve stimulation is enhanced. This is associated with an abnormality in the low-pass filter function of the renal vasculature wherein higher frequencies (≥0.01 Hz) within renal sympathetic nerve activity are not normally attenuated and are passed into the renal blood flow signal. This study tested the hypothesis that excess angiotensin II action mediates the abnormal frequency response characteristics of the renal vasculature in congestive heart failure. In anesthetized rats, the renal vasoconstrictor response to graded frequency renal nerve stimulation was significantly greater in congestive heart failure than in control rats. Losartan attenuated the renal vasoconstrictor response to a significantly greater degree in congestive heart failure than in control rats. In control rats, the frequency response of the renal vasculature was that of a first order (–20 dB/frequency decade) low-pass filter with a corner frequency (–3 dB, 30% attenuation) of 0.002 Hz and 97% attenuation (–30 dB) at ≥0.1 Hz. In congestive heart failure rats, attenuation did not exceed 45% (–5 dB) over the frequency range of 0.001–0.6 Hz. The frequency response of the renal vasculature was not affected by losartan treatment in control rats but was completely restored to normal by losartan treatment in congestive heart failure rats. The enhanced renal vasoconstrictor response to renal nerve stimulation and the associated abnormality in the frequency response characteristics of the renal vasculature seen in congestive heart failure are mediated by the action of angiotensin II on renal angiotensin II AT1 receptors.

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