Adenosine inhibits beta-adrenoceptor but not DBcAMP-induced renin release

1987 ◽  
Vol 252 (1) ◽  
pp. F46-F52 ◽  
Author(s):  
G. Deray ◽  
R. A. Branch ◽  
W. A. Herzer ◽  
A. Ohnishi ◽  
E. K. Jackson
Keyword(s):  
Nerve Stimulation ◽  
Initial Study ◽  
Renin Release ◽  
Base Line ◽  
Renal Nerve ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Renal Nerve Stimulation ◽  
Canine Kidney

The purpose of these studies was to assess the direct effect of adenosine on the renin release response to beta-adrenoceptor activation in vivo in the canine kidney. In an initial study, innervated, intrarenal beta-adrenoceptors were activated selectively via renal nerve stimulation in kidneys in which the alpha-adrenoceptor response to renal nerve stimulation had been blocked with phentolamine. Adenosine, infused directly into the renal artery (10 and 30 micrograms/min), significantly blunted the renin release response to renal nerve stimulation. However, adenosine also caused significant reductions in base-line glomerular filtration rate, sodium excretion rate, and filtration fraction. To eliminate these confounding effects of adenosine on renal function and to prevent changes in norepinephrine release due to prejunctional inhibition by adenosine, we also studied the effect of intrarenal infusions of adenosine on norepinephrine-induced renin release in the nonfiltering, alpha-adrenoceptor-blocked, canine kidney. In this model of beta-adrenoceptor activation, adenosine abolished the renin release response to intrarenal infusions of norepinephrine. In a final series of experiments, the effect of adenosine on the renin response to dibutyryl-adenosine 3',5'-cyclic monophosphate (cAMP) was examined in the nonfiltering, beta-adrenoceptor-blocked, canine kidney. In this model of cAMP-induced renin release, adenosine was ineffective in attenuating the renin release response. These data demonstrate that in vivo adenosine directly inhibits beta-adrenoceptor-mediated renin release by a mechanism that does not involve a reduction in the ability of cAMP to activate intracellular mechanisms leading to renin release.

Atrial natriuretic factor reduces renin release by opposing alpha-adrenoceptor activity

1991 ◽  
Vol 261 (2) ◽  
pp. E240-E245
Author(s):  
P. A. Naess ◽  
G. Christensen ◽  
F. Kiil
Keyword(s):  
Nerve Stimulation ◽  
Atrial Natriuretic Factor ◽  
Renin Release ◽  
Renal Nerve ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Natriuretic Factor ◽  
Stimulation Experiments ◽  
Ureteral Occlusion ◽  
Atrial Natriuretic

To examine how atrial natriuretic factor (ANF) inhibits renin release during renal sympathetic nerve stimulation, experiments were performed in barbiturate-anesthetized dogs. In five dogs, intravenous ANF infusion (50 ng.min-1.kg body wt-1) reduced renin release induced by renal nerve stimulation (1 Hz) from 16.8 +/- 8.4 to 3.5 +/- 2.1 micrograms angiotensin I (ANG I)/min. In two groups, renin release was raised by ureteral occlusion, which enhances the effects of beta-adrenoceptor stimulation and increased prostaglandin synthesis. During ureteral occlusion, intrarenal infusion of isoproterenol (0.2 micrograms.min-1.kg body wt-1) increased renin release in eight dogs to 82.6 +/- 10.9 micrograms ANG I/min, which was not significantly reduced by ANF infusion (81.1 +/- 10.1 micrograms ANG I/min). Similarly, intrarenal infusion of arachidonic acid (80 micrograms.min-1.kg body wt-1) during ureteral occlusion increased renin release in five dogs to 22.2 +/- 3.0 micrograms ANG I/min, which was not significantly reduced by ANF infusion (22.5 +/- 3.5 micrograms ANG I/min). Finally, in six dogs examined at free urine flow, intrarenal infusion of phenylephrine, an alpha-adrenergic agonist, raised renin release from 0.5 +/- 0.3 to 20.1 +/- 6.8 micrograms ANG I/min, which was reduced to 10.6 +/- 3.9 micrograms ANG I/min by intravenous ANF infusion (100 ng.min-1.kg body wt-1). These results indicate that ANF does not counteract stimulation of renin release by beta-adrenoceptors and prostaglandins but reduces nerve-stimulated renin release by opposing alpha-adrenoceptor activity.

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 venous outflow and urinary excretion of norepinephrine, epinephrine, and dopamine during graded renal nerve stimulation

1983 ◽  
Vol 244 (1) ◽  
pp. E52-E60 ◽  
Author(s):  
U. Kopp ◽  
T. Bradley ◽  
P. Hjemdahl
Keyword(s):  
Urinary Excretion ◽  
Nerve Stimulation ◽  
Renal Nerves ◽  
Similar Degree ◽  
Venous Outflow ◽  
Renal Nerve ◽  
Concentration Difference ◽  
Alpha Adrenoceptor ◽  
Renal Nerve Stimulation ◽  
High Level

The effect of renal nerve stimulation (RNS) on renal venous outflow and urinary excretion of endogenous norepinephrine, epinephrine, and dopamine was examined in anesthetized dogs. In the unstimulated denervated kidney, there was a negative venoarterial concentration difference for all catecholamines. Low-level RNS (LLRNS) caused small changes in renal hemodynamics and renal venous outflow of dopamine and increased norepinephrine outflow by 3.22 +/- 0.95 pmol X min-1 X g-1 (n = 5, P less than 0.05). High-level RNS (HLRNS) reduced renal blood flow by 50% and increased renal venous outflow of norepinephrine and dopamine by 9.58 +/- 0.67 and 0.46 +/- 0.05 pmol X min-1 X g-1, respectively (n = 27, P less than 0.01 for both). Renal uptake of epinephrine was unchanged by HLRNS. The urinary excretion of norepinephrine but not dopamine was increased to a similar degree following RNS at both levels. HLRNS caused a similar increase of the urinary norepinephrine excretion from the contralateral denervated and unstimulated kidney. This could be explained by the increase in arterial norepinephrine (from 0.74 +/- 0.08 to 1.20 +/- 0.14 nM, P less than 0.01) caused by HLRNS as shown by experiments with intravenous infusions of norepinephrine. The alpha-adrenoceptor antagonist phenoxybenzamine counteracted the hemodynamic response to HLRNS and enhanced the renal venous outflow and urinary excretion of norepinephrine and dopamine. Our results indicate that renal nerves release dopamine as well as norepinephrine and that urinary catecholamine excretion is a poor indicator of intrarenal catecholamine release.

Effect of low-level renal nerve stimulation on renin release from nonfiltering kidneys

1981 ◽  
Vol 241 (2) ◽  
pp. F156-F161 ◽  
Author(s):  
H. Holdaas ◽  
G. F. DiBona ◽  
F. Kiil
Keyword(s):  
Nerve Stimulation ◽  
Perfusion Pressure ◽  
Low Frequency ◽  
Renal Perfusion ◽  
Renin Release ◽  
Aortic Constriction ◽  
Renal Nerve ◽  
Low Level ◽  
Renal Perfusion Pressure ◽  
Renal Nerve Stimulation

The mechanism whereby renal nerves influence the renin-release response to aortic constriction was examined in a nonfiltering ureter-occluded kidney preparation in anesthetized dogs. The kidney was rendered nonfiltering by a combination of mannitol infusion and ureteral occlusion. Suprarenal aortic constriction reduced renal perfusion pressure to 61 +/- 7 mmHg and increased renin release from 16.7 +/- 4.1 to 26.1 +/- 6.0 U/min. At normal renal perfusion pressure, low-frequency renal nerve stimulation (0.25 Hz) increased renin release by 11.6 +/- 4.2 to 25.1 +/- 7.6 U/min. The effect of combined low-level renal nerve stimulation and aortic constriction on renin release was additive; renin release increased by 24.6 +/- 6.5 to 39.5 +/- 7.3 U/min. Propranolol or metoprolol, administered intrarenally at 2 microgram . min-1 . kg-1, abolished the renin-release response to low-level renal nerve stimulation at normal renal perfusion pressure. These data provide evidence that low-frequency renal nerve stimulation influences the renin-release response to reduction in renal perfusion pressure in a nonfiltering ureter-occluded kidney with an inoperative macula densa receptor mechanism. The neural effect on renin release at normal renal perfusion pressure is mediated via beta 1-adrenoceptors probably located on the juxtaglomerular granular cells.

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