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.

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.

Effects of afferent renal nerve stimulation on renal hemodynamic and excretory functions

1984 ◽  
Vol 247 (4) ◽  
pp. H576-H583
Author(s):  
A. Stella ◽  
R. Golin ◽  
I. Busnardo ◽  
A. Zanchetti
Keyword(s):  
Glomerular Filtration ◽  
Nerve Stimulation ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Nerve ◽  
Blood Flows ◽  
Renal Perfusion Pressure ◽  
Afferent Fibers ◽  
Renal Nerve Stimulation ◽  
Reflex Control

In anesthetized cats (n = 9) renal afferent fibers were electrically stimulated for 11 min, and the response of the contralateral innervated kidney was compared with that of the ipsilateral denervated one. Before stimulation, renal blood flow, glomerular filtration rate, and water and sodium excretions were significantly lower in the innervated kidney than in the denervated one. Afferent renal nerve stimulation augmented arterial pressure and also increased sodium and water excretions from both kidneys without concomitant changes in glomerular filtration rates and renal blood flows. Absolute and percent changes in sodium and water excretions from the innervated kidney were similar to those observed in the denervated one. The same results were obtained in cats (n = 4) which underwent bilateral adrenalectomy to avoid the effect of circulating catecholamines. In another group of cats (n = 5), the increase in renal perfusion pressure due to the stimulation was prevented by an aortic snare: this resulted in a slight but equal decrease of all variables in both kidneys. These experiments do not show a reflex control of renal function from renal afferents.

Effects of meclofenamate on the renin response to aortic constriction in the rat

1984 ◽  
Vol 247 (3) ◽  
pp. R546-R551 ◽  
Author(s):  
D. Villarreal ◽  
J. O. Davis ◽  
R. H. Freeman ◽  
W. D. Sweet ◽  
J. R. Dietz
Keyword(s):  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Release ◽  
Aortic Constriction ◽  
Renal Perfusion Pressure ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Intact Kidney ◽  
Stimulus Secretion Coupling

This study examines the role of the renal prostaglandin system in stimulus-secretion coupling for renal baroreceptor-dependent renin release in the anesthetized rat. Changes in plasma renin activity (PRA) secondary to suprarenal aortic constriction were evaluated in groups of rats with a single denervated nonfiltering kidney (DNFK) with and without pretreatment with meclofenamate. Suprarenal aortic constriction was adjusted to reduce renal perfusion pressure to either 100 or 50 mmHg. In addition, similar experiments were performed in rats with a single intact filtering kidney. Inhibition of prostaglandin synthesis with meclofenamate failed to block or attenuate the increase in PRA in response to the decrement in renal perfusion pressure after both severe and mild aortic constriction for both the DNFK and the intact-kidney groups. The adequacy of prostaglandin inhibition was demonstrated by complete blockade with meclofenamate of the marked hypotensive and hyperreninemic responses to sodium arachidonate. The results in the DNFK indicate that in the rat, renal prostaglandins do not function as obligatory mediators of the isolated renal baroreceptor mechanism for the control of renin release. Also the findings in the intact filtering kidney suggest that prostaglandins are not essential in the renin response of other intrarenal receptor mechanisms that also are stimulated by a reduction in renal perfusion pressure.

scholarly journals Role of the endothelium-dependent relaxing factor nitric oxide on renal function.

1992 ◽  
Vol 2 (9) ◽  
pp. 1371-1387 ◽  
Author(s):  
J C Romero ◽  
V Lahera ◽  
M G Salom ◽  
M L Biondi
Keyword(s):  
Nitric Oxide ◽  
Renal Function ◽  
Perfusion Pressure ◽  
Sodium Intake ◽  
Systemic Circulation ◽  
Renal Perfusion ◽  
Renin Release ◽  
High Sodium ◽  
Renal Perfusion Pressure

The role of nitric oxide in renal function has been assessed with pharmacologic and physiologic interventions. Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins. However, prostaglandins and nitric oxide do not participate in the renal effects produced by endothelium-independent vasodilators such as atrial natriuretic peptide, prostaglandin I2, and nitroprusside. Physiologically, nitric oxide and prostaglandins exert a strong regulation on the effects produced by changes in renal perfusion pressure. Increments in renal perfusion pressure within the range of RBF autoregulation appear to inhibit prostaglandin synthesis while simultaneously enhancing the formation of nitric oxide. Nitric oxide modulates autoregulatory vasoconstriction and at the same time inhibits renin release. Conversely, a decrease of renal perfusion pressure to the limit of or below RBF autoregulation may inhibit the synthesis of nitric oxide but may trigger the release of prostaglandins, whose vasodilator action ameliorates the fall in RBF and stimulates renin release. Nitric oxide and prostaglandins are also largely responsible for mediating pressure-induced natriuresis. However, unlike prostaglandins, mild impairment of the synthesis of nitric oxide in systemic circulation produces a sustained decrease in sodium excretion, which renders blood pressure susceptible to be increased during high-sodium intake. This effect suggests that a deficiency in the synthesis of nitric oxide could constitute the most effective single disturbance to foster the development of a syndrome similar to that seen in salt-sensitive hypertension.

Neural and vascular interaction in renin response to graded renal nerve stimulation

1982 ◽  
Vol 242 (5) ◽  
pp. R552-R562 ◽  
Author(s):  
W. S. Ammons ◽  
S. Koyama ◽  
J. W. Manning
Keyword(s):  
Nerve Stimulation ◽  
Control Level ◽  
Low Frequency ◽  
Adrenergic Blockade ◽  
Renal Nerve ◽  
Beta Adrenergic ◽  
Renal Vasoconstriction ◽  
Alpha Adrenergic Receptors ◽  
Alpha Receptors ◽  
Renal Nerve Stimulation

The effect of a 1-min period of renal nerve stimulation was studied in alpha-chloralose-anesthetized cats, whose left kidneys were pump perfused. Renal hemodynamics and filtration parameters were unaltered at stimulation frequencies of 2.0 Hz or less; however, renin secretion rates (RSR) increased with frequency reaching 3 times the control level. At higher frequencies renal vasoconstriction occurred and glomerular filtration rate (GFR) fell. RSR was increased but little more than at 2.0 Hz. The RSR response plots were similar to constant-flow and constant-pressure perfused preparations. beta-Adrenergic blockade with propranolol abolished low-frequency responses and resulted in progressive decreases in RSR at higher frequencies. alpha-Adrenergic blockade with phentolamine prevented renal vascular and GFR changes, whereas RSR continually increased up to 12.0 Hz (13.5 times control). Papaverine treatment, to prevent vascular-GFR changes without blocking alpha-receptors, resulted in similar renin responses. The results indicate that the beta-adrenergic receptor mediates increases in RSR in proportion to frequency when vascular-GFR factors are constant. When renal vasoconstriction occurs at high frequencies the beta-receptor mechanism interacts with an inhibiting mechanism indirectly mediated by alpha-adrenergic receptors.

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.

Role of the Renal Nerves in Renin Release during Suprarenal Aortic Stenosis in Cats

1976 ◽  
Vol 51 (s3) ◽  
pp. 85s-87s
Author(s):  
A. Stella ◽  
F. Calaresu ◽  
A. Zanchetti
Keyword(s):  
Aortic Stenosis ◽  
Time Course ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renin Release ◽  
Renal Nerves ◽  
Renal Perfusion Pressure ◽  
The Difference

1. Renin release from an intact, innervated kidney and from the contralateral denervated kidney was measured before and during a period of suprarenal aortic stenosis. 2. Aortic stenosis of 10 min duration reduced renal perfusion pressure to 50 mmHg and increased renin release from both kidneys, but the response from the innervated kidney was greater. 3. A study of the time-course of the response during 30 min of aortic stenosis showed that the difference in rate of renin release between the innervated and the denervated kidney is greatest during the first few minutes of aortic stenosis.

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.

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