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 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.

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.

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.

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.

Angiotensin II in adrenergic-induced alterations in glomerular hemodynamics

1984 ◽  
Vol 247 (5) ◽  
pp. F799-F807 ◽  
Author(s):  
J. C. Pelayo ◽  
M. G. Ziegler ◽  
R. C. Blantz
Keyword(s):  
Angiotensin Ii ◽  
Nerve Stimulation ◽  
Critical Factor ◽  
Functional Expression ◽  
Ang Ii ◽  
Functional Responses ◽  
Renal Nerve ◽  
Renal Nerve Stimulation ◽  
Glomerular Ultrafiltration ◽  
Glomerular Hemodynamics

Micropuncture analysis of glomerular ultrafiltration (SNGFR) was conducted in Munich-Wistar rats to assess the functional responses to moderate-frequency (3-Hz) renal nerve stimulation. Angiotensin II inhibition (ANG II-inhib) was produced by the intravenous administration of [Sar1, Ala8] angiotensin II or MK 421 to investigate whether it modulates the effects of renal nerve stimulation. Micropuncture measurements were obtained before and during renal nerve stimulation. Renal nerve stimulation decreased SNGFR approximately 25% (from 49.9 +/- 2.3 to 38.0 +/- 1.4 nl X min-1 X g kidney wt-1), the result of decreased glomerular capillary hydrostatic pressure gradient and nephron plasma flow. These decreases were due to increased afferent (approximately 43%) and efferent (approximately 30%) arteriolar resistances, since the glomerular ultrafiltration coefficient remained unaffected. The effects of renal nerve stimulation during ANG II-inhib were less in magnitude than in renal nerve stimulation alone: SNGFR decreased from 48.0 +/- 1.5 to 44.8 +/- 2.0 nl X min-1 X g kidney wt-1 after renal nerve stimulation. The net renal production of norepinephrine was augmented by renal nerve stimulation but it was not influenced by ANG II-inhib. In conclusion: renal nerve stimulation can regulate glomerular ultrafiltration by altering vascular resistances, and angiotensin II appears to be a critical factor for the full functional expression of renal nerve stimulation at the glomerulus.

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.

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.

Differentiated sympathetic neural control of the kidney

1996 ◽  
Vol 271 (1) ◽  
pp. R84-R90 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin ◽  
S. Y. Jones
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Nerve Stimulation ◽  
Nerve Fibers ◽  
Urinary Flow ◽  
Renal Nerve ◽  
Renal Vasoconstriction ◽  
Central Chemoreceptors ◽  
Renal Nerve Stimulation ◽  
Stimulation Of

Anatomic and neurophysiological methods were used to identify functionally specific subgroups of renal sympathetic nerve fibers. The distribution of diameters of the predominating unmyelinated fibers showed a major mode at 1.1 microns and a minor mode at 1.6 microns. The conduction velocity was 2.10 +/- 0.10 m/s, consistent with unmyelinated C fibers. Analysis of strength-duration relationships during renal nerve stimulation showed that both rheobase and chronaxie values for renal blood flow were greater than those for urinary flow rate and were independent of stimulation frequency. This difference suggests a higher stimulation threshold (smaller diameter) for those renal nerve fibers involved in the renal blood flow response (renal vasoconstriction) compared with those for the urinary flow rate response (antidiuresis) to renal nerve stimulation. Single renal units that responded to preganglionic splanchnic nerve stimulation were studied. Those with spontaneous activity (88%) responded to stimulation of arterial baroreceptors, arterial and central chemoreceptors, and peripheral thermoreceptors, whereas those that lacked spontaneous activity (12%) responded only to stimulation of peripheral thermoreceptors (known to produce renal vasoconstriction). A minority population of single renal units has been identified that, although renal vasoconstrictor, does not exhibit other characteristic features of vasoconstrictor neurons (i.e., responsiveness to stimulation of arterial baroreceptors and arterial and central chemoreceptors). These findings suggest the existence of functionally specific subgroups of renal nerve fibers.

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.

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