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.

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.

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.

Impaired neurogenic control of renal vasculature in renal hypertensive rats

1980 ◽  
Vol 238 (6) ◽  
pp. H770-H775 ◽  
Author(s):  
G. D. Fink ◽  
M. J. Brody
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Innervation ◽  
Renal Hypertension ◽  
Renal Nerves ◽  
Hypertensive Rats ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Renal Nerve Stimulation ◽  
Renal Vascular ◽  
Renal Sympathetic

Renal hypertension is accompanied by alterations in the renal sympathetic innervation involving reduced catecholamine content and histofluorescence. Because the renal nerves are a potentially important factor in the pathogenesis of renal hypertension, the functional significance of renal catecholamine depletion was evaluated. In rats with either one-kidney or two-kidney Grollman hypertension, renal vascular responses to renal nerve stimulation and intraarterial administration of vasoactive hormones were assessed in vivo at various times following renal compression. In the wrapped kidney of one-kidney hypertensive rats, vasoconstrictor responses to renal nerve stimulation were consistently reduced, compared to responses in uninephrectomized control rats, whereas responses to intra-arterial norepinephrine were slightly greater in kidneys from hypertensive animals. In the untouched kidney of rats with two-kidney renal hypertension, vasoconstrictor responses to nerve stimulation were also substantially reduced, although those to norepinephrine were only slightly altered. It was concluded that catecholamine depletion in the kidneys of renal hypertensive animals reflects a diminished capacity of renal sympathetic nerve impulses to produce vasoconstriction. Reduced neurogenic renal vascular resistance may serve to attenuate the rise in blood pressure in renal hypertension.

Basal norepinephrine overflow into the renal vein: effect of renal nerve stimulation

1980 ◽  
Vol 239 (4) ◽  
pp. F371-F377 ◽  
Author(s):  
Juan A. Oliver ◽  
John Pinto ◽  
Robert R. Sciacca ◽  
Paul J. Cannon
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Nerve Stimulation ◽  
Renal Vein ◽  
Renal Nerves ◽  
Plasma Norepinephrine ◽  
Renal Nerve ◽  
Sympathetic Nervous ◽  
Renal Nerve Stimulation ◽  
Renal Sympathetic

In order to determine whether the fraction of norepinephrine released from the renal nerves that escapes into the circulation can be used an an index of renal sympathetic nervous activity, arterial and renal vein plasma norepinephrine concentrations were measured by a radioenzymatic technique along with renal blood flow in anesthetized dogs under control conditions and during electrical renal nerve stimulation. In 25 animais studied under conditions of normal sodium balance, plasma norepinephrine in the renal vein, 198 ± 26 pg/ml, was significantly higher than in arterial blood, 102 ± 10 pg/ml (P < 0.001). In five dogs, electrical stimulation of the renal nerves (12 V, 3 ms) at frequencies of 0.5, 2,6, 12, and 18 Hz for 1 min was associated with increased norepinephrine concentration in renal venous plasma and an increase in the calculated renal norepinephrine overflow. There was a significant linear relationship between the frequency of stimulation and norepinephrine overflow into the renal vein in each animal, but there was also a significant interanimal variation in the slope of this relationship (P <0.01). Electrical stimulation at a frequency of 2 Hz significantly decreased renal blood flow (-24 ± 7 ml/min, P < 0.01). The maximal effect was achieved at 6 Hz (-66 ± 11 ml/min). The data indicate that there is a base-line overflow of norepinephrine into the renal venous blood of the dog that increases with increasing frequency of electrical nerve stimulation. They suggest that measurements of norepinephrine overflow into the renal vein may be used to assess the activity of the renal sympathetic nervous system. renal blood flow; catecholamines; renin; dog Submitted on January 10, 1980 Accepted on April 29, 1980

Selective renal denervation guided by renal nerve stimulation: mapping renal nerves for unmet clinical needs

2019 ◽  
Vol 33 (10) ◽  
pp. 716-724 ◽  
Author(s):  
Kunyue Tan ◽  
Yinchuan Lai ◽  
Weijie Chen ◽  
Hang Liu ◽  
Yanping Xu ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Renal Denervation ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Renal Nerve Stimulation

Ontogeny of renal hemodynamic response to renal nerve stimulation in sheep

1987 ◽  
Vol 252 (4) ◽  
pp. F605-F612 ◽  
Author(s):  
J. E. Robillard ◽  
K. T. Nakamura ◽  
M. K. Wilkin ◽  
O. J. McWeeny ◽  
G. F. DiBona
Keyword(s):  
Nerve Stimulation ◽  
Hemodynamic Response ◽  
Renal Nerve ◽  
Fetal Sheep ◽  
Adult Sheep ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Renal Hemodynamic ◽  
Renal Nerve Stimulation ◽  
Beta 2

The renal hemodynamic response to direct electrical stimulation of renal nerves was studied in conscious and chronically instrumented fetal (130-142 days gestation; term 145 days), newborn (7-12 days postnatal), and adult nonpregnant sheep. Renal nerve stimulation (RNS) produced a significant decrease in renal blood flow (RBF) velocity and a significant increase in renal vascular resistance (RVR) in all three groups of animals. The overall decline in RBF velocity and the overall rise in RVR was less pronounced in fetal than in adult sheep (P less than 0.05). Changes in RBF velocity and RVR using an RNS frequency of 16 Hz were -35 +/- 4 and 81 +/- 19% in fetal sheep, -61 +/- 10 and 374 +/- 128% in newborn lambs, and -84 +/- 12 and 540 +/- 94% in adult sheep, respectively. RNS during intrarenal infusion of the alpha-adrenoceptor antagonist phentolamine was associated with a significant increase in RBF velocity and decrease in RVR in both fetal sheep and newborn lambs, but not in adult sheep. Moreover, it was found that the rise in RBF velocity and the decrease in RVR associated with RNS during alpha-adrenoceptor antagonism were completely inhibited by intrarenal infusion of ICI 118,551, a beta 2-adrenoceptor antagonist and unaffected by either cholinergic or dopaminergic antagonists. Taken together, these results suggest that the overall renal vasoconstrictor response to RNS is age dependent. Furthermore, the present results demonstrate that, contrary to observations made in adult animals, RNS can produce renal vasodilation in immature animals that is mediated by beta 2-adrenoceptors.

Renal opiate receptor mediation of renin secretion to renal nerve stimulation in the dog

1986 ◽  
Vol 250 (6) ◽  
pp. R973-R979
Author(s):  
S. Koyama ◽  
H. Hosomi
Keyword(s):  
Nerve Stimulation ◽  
High Frequency ◽  
Opiate Receptor ◽  
Renal Hemodynamics ◽  
Renin Secretion ◽  
High Frequency Stimulation ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Frequency Stimulation ◽  
Renal Nerve Stimulation

The present study was designed to evaluate renal opiate receptor mediation of the renin secretion response to electrical stimulation of the renal nerves in the pentobarbital sodium-anesthetized dog by use of the opiate agonist leucine-enkephalin (Leu-enk) and the opiate antagonist naloxone. In all animals studied, left kidneys were pump perfused at a constant renal blood flow. Renal perfusion pressure (RPP) and glomerular filtration rate (GFR) were unaltered at a stimulation frequency of 1.0 Hz; however, renin secretion rate (RSR) increased significantly in the nontreated group. High-frequency renal nerve stimulation (10 Hz) increased RPP and decreased GFR. RSR at the high-frequency stimulation was significantly augmented in the nontreated group. Renal arterial infusion of either Leu-enk (25 micrograms X kg-1 X min-1) or naloxone (7 micrograms X kg-1 X min-1) did not alter base-line levels of renal hemodynamics and RSR and did not produce significant changes in these variables even when renal nerves were stimulated at the low frequency; however, Leu-enk inhibited RPP and RSR responses to the high-frequency stimulation, and naloxone augmented these responses. Phentolamine (13 micrograms X kg-1 X min-1) prevented renal hemodynamic responses to the renal nerve stimulation, whereas RSR responses to the stimulation were unaffected. Propranolol (8 micrograms X kg-1 X min-1) resulted in decreases in RSR at the renal nerve stimulation despite the presence of changes in renal hemodynamics similar to the other groups. The results indicate that intrarenal opiate receptors may participate in inhibiting renal secretion of renin mediated by the renal nerves when renal vasoconstriction and reduction of GFR occurred at the high-frequency stimulation.

Effect of catecholamines and the renal nerves on renin secretion in anesthetized dogs

1965 ◽  
Vol 209 (3) ◽  
pp. 659-662 ◽  
Author(s):  
Arthur J. Vander
Keyword(s):  
Nerve Stimulation ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Pressor Activity ◽  
Renal Nerve Stimulation

Intravenous infusion of either epinephrine (5–6 µg/min) or norepinephrine (12–16 µg/min) during maintenance of a constant renal arterial blood pressure by means of suprarenal aortic constriction, or stimulation of the renal nerves produced essentially the same effects on renal function and renal venous plasma renin concentration, the latter being measured indirectly by bioassaying the pressor activity produced by plasma incubation under standardized conditions. Glomerular filtration rate (GFR), renal plasma flow (RPF), and sodium excretion were decreased, and renin concentration was increased. The induction of osmotic diuresis during catecholamine infusion or renal nerve stimulation reversed or prevented the increase in renin secretion but did not alter the changes in GFR or RPF. It is suggested that the increased renin secretion induced by catecholamines and renal nerve stimulation in nondiuretic dogs might be the indirect result of the decrease in filtered sodium produced by these procedures. However, a direct effect of the catecholamines and renal nerves on the renin-secreting cells cannot be ruled out.

Role of macula densa in renal nerve modulation of renin secretion

1982 ◽  
Vol 242 (3) ◽  
pp. R367-R371 ◽  
Author(s):  
J. L. Osborn ◽  
M. D. Thames ◽  
G. F. DiBona
Keyword(s):  
Nerve Stimulation ◽  
Low Frequency ◽  
Renal Perfusion ◽  
Macula Densa ◽  
Renin Secretion ◽  
Renal Nerves ◽  
Aortic Constriction ◽  
Renal Nerve ◽  
Anesthetized Dogs ◽  
Renal Nerve Stimulation

Low-frequency renal nerve stimulation (0.25 Hz) augments the renin secretion response to reduction of renal perfusion pressure to 50 mmHg by aortic constriction. The present experiments determined whether this modulating influence could be demonstrated when the macula densa receptor was inoperative. In 10 anesthetized dogs with a nonfiltering kidney and sectioned renal nerves, aortic constriction to 52 mmHg decreased renal blood flow and increased renin secretion from 126 +/- 94 to 192 +/- 55 ng/min. During low-frequency renal nerve stimulation and aortic constriction to 50 mmHg, renin secretion was not augmented (37 +/- 13 to 81 +/- 42 ng/min). In four anesthetized dogs with nonfiltering kidneys, aortic constriction to 52 mmHg increased renin secretion similarly before (16 +/- 8 to 68 +/- 17 ng/min) and after renal denervation (14 +/- 14 to 78 +/- 18 ng/min). Therefore, the augmentation of the renin secretion response to aortic constriction to 50 mmHg by low-frequency renal nerve stimulation in filtering kidneys does not result from an interaction with the renal vascular baroreceptor or the juxtaglomerular granular cells. Since neural augmentation of renin secretion during aortic constriction was not observed in the nonfiltering kidney where the macula densa is inoperative, we conclude that the macula densa is the probable site for the neural modulation of renin secretion.

Sign in / Sign up

Export Citation Format

Share Document