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.

scholarly journals Effect of beta adrenergic blockade on renin response to renal nerve stimulation.

1976 ◽  
Vol 57 (2) ◽  
pp. 459-465 ◽  
Author(s):  
M S Taher ◽  
L G McLain ◽  
K M McDonald ◽  
R W Schrier ◽  
L K Gilbert ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Adrenergic Blockade ◽  
Renal Nerve ◽  
Beta Adrenergic ◽  
Renal Nerve Stimulation

Effect of renal nerve stimulation on responsiveness of the rat renal vasculature

2002 ◽  
Vol 283 (5) ◽  
pp. F1056-F1065 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Sawin
Keyword(s):  
Nerve Stimulation ◽  
Low Frequency ◽  
Rectangular Pulse ◽  
Signal Frequency ◽  
Renal Nerves ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Renal Vasoconstriction ◽  
Low Frequency Oscillations ◽  
Renal Nerve Stimulation

When the renal nerves are stimulated with sinusoidal stimuli over the frequency range 0.04–0.8 Hz, low (≤0.4 Hz)- but not high (≥0.4 Hz)-frequency oscillations appear in renal blood flow (RBF) and are proposed to increase responsiveness of the renal vasculature to stimuli. This hypothesis was tested in anesthetized rats in which RBF responses to intrarenal injection of norepinephrine and angiotensin and to reductions in renal arterial pressure (RAP) were determined during conventional rectangular pulse and sinusoidal renal nerve stimulation. Conventional rectangular pulse renal nerve stimulation decreased RBF at 2 Hz but not at 0.2 or 1.0 Hz. Sinusoidal renal nerve stimulation elicited low-frequency oscillations (≤0.4 Hz) in RBF only when the basal carrier signal frequency produced renal vasoconstriction, i.e., at 5 Hz but not at 1 Hz. Regardless of whether renal vasoconstriction occurred, neither conventional rectangular pulse nor sinusoidal renal nerve stimulation altered renal vasoconstrictor responses to norepinephrine and angiotensin. The RBF response to reduction in RAP was altered by both conventional rectangular pulse and sinusoidal renal nerve stimulation only when renal vasoconstriction occurred: the decrease in RBF during reduced RAP was greater. Sinusoidal renal nerve stimulation with a renal vasoconstrictor carrier frequency results in a decrease in RBF with superimposed low-frequency oscillations. However, these low-frequency RBF oscillations do not alter renal vascular responsiveness to vasoconstrictor stimuli.

scholarly journals Cilnidipine Attenuates Renal Nerve Stimulation-Induced Renal Vasoconstriction and Antinatriuresis in Anesthetized Dogs

1997 ◽  
Vol 75 (1) ◽  
pp. 27-32
Author(s):  
Takahara Akira ◽  
Dohmoto Hideki ◽  
Hisa Hiroaki ◽  
Satoh Susumu ◽  
Yoshimoto Ryota
Keyword(s):  
Nerve Stimulation ◽  
Renal Nerve ◽  
Renal Vasoconstriction ◽  
Anesthetized Dogs ◽  
Renal Nerve Stimulation

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.

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.

Effect of renal nerve stimulation on NaCl and H2O transport in Henle's loop of the rat

1982 ◽  
Vol 243 (6) ◽  
pp. F576-F580 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin
Keyword(s):  
Nerve Stimulation ◽  
Isotonic Saline ◽  
Low Frequency ◽  
Sodium Reabsorption ◽  
Urinary Flow ◽  
Loop Of Henle ◽  
Renal Nerve ◽  
Henle's Loop ◽  
Chloride Excretion ◽  
Renal Nerve Stimulation

To assess the effect of renal nerve stimulation on sodium, chloride, and water transport in the loop of Henle, experiments were performed in anesthetized hydropenic and isotonic saline volume-expanded rats using renal clearance and Henle's loop microperfusion techniques (end-proximal convoluted tubule perfusion site, early distal convoluted tubule collection site). As compared with the control period values, low-frequency (less than 1.0 Hz) renal nerve stimulation decreased absolute and fractional urinary flow rate and sodium and chloride excretion without affecting mean arterial pressure, glomerular filtration rate, renal blood flow, or renal vascular resistance. In the loop of Henle, the absorptive transport of water was not affected, whereas the absorptive transport of sodium and chloride was increased in both hydropenic (Na 111 +/- 49 peq/min) and isotonic saline volume-expanded rats (Na 154 +/- 69 peq/min, Cl 180 +/- 52 peq/min) during low-frequency renal nerve stimulation. Low-frequency renal nerve stimulation decreases urinary sodium and chloride excretion via a direct effect of increasing renal tubular sodium and chloride reabsorption. In addition to the established effect of increasing proximal tubular sodium reabsorption, Henle's loop sodium and chloride absorption are also increased, supporting a physiological role for the adrenergic innervation of these structures.

scholarly journals Cilnidipine Attenuates Renal Nerve Stimulation-Induced Renal Vasoconstriction and Antinatriuresis in Anesthetized Dogs.

1997 ◽  
Vol 75 (1) ◽  
pp. 27-32 ◽  
Author(s):  
Akira Takahara ◽  
Hideki Dohmoto ◽  
Hiroaki Hisa ◽  
Susumu Satoh ◽  
Ryota Yoshimoto
Keyword(s):  
Nerve Stimulation ◽  
Renal Nerve ◽  
Renal Vasoconstriction ◽  
Anesthetized Dogs ◽  
Renal Nerve Stimulation

Mechanisms of antinatriuresis during low-frequency renal nerve stimulation in anesthetized dogs

1985 ◽  
Vol 249 (3) ◽  
pp. R360-R367
Author(s):  
J. L. Osborn ◽  
R. J. Roman ◽  
R. W. Harland
Keyword(s):  
Sodium Bicarbonate ◽  
Nerve Stimulation ◽  
Low Frequency ◽  
Acid Base Balance ◽  
Renal Nerve ◽  
Bicarbonate Reabsorption ◽  
Anesthetized Dogs ◽  
Renal Nerve Stimulation ◽  
Bicarbonate Infusion ◽  
Sodium Bicarbonate Infusion

The influence of 1.0 Hz renal nerve stimulation (RNS) on the renal excretion of sodium and bicarbonate was determined in anesthetized dogs before and during inhibition of renal bicarbonate reabsorption. RNS decreased both urinary sodium and bicarbonate excretion without changing arterial pressure, renal blood flow, or glomerular filtration rate. Pharmacological blockade of bicarbonate reabsorption with acetazolamide prevented RNS-induced decreases in bicarbonate excretion and reduced the antinatriuretic response. Physiological blockade of tubular bicarbonate reabsorption with intrarenal sodium bicarbonate infusion (1 M) abolished both the antinatriuretic response to RNS and the decrease in bicarbonate excretion. This physiological blockade of neurogenic antinatriuresis resulted from alkalinization of the urine and/or peritubular blood rather than an increase in filtered sodium load, because during intrarenal infusion of 1 M sodium chloride RNS concomitantly decreased sodium and urinary bicarbonate excretion. Since antinatriuretic responses and the decrease in bicarbonate excretion response to RNS were significantly decreased by blockade of bicarbonate reabsorption (with acetazolamide and intrarenal sodium bicarbonate infusion), antinatriuresis during RNS is partly mediated by a mechanism dependent on intact bicarbonate reabsorption. The data suggest that renal nerve activity may participate in the normal regulation of acid-base balance via changes in bicarbonate excretion.

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