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.

scholarly journals Effect of angiotensin II on renal nerve stimulation-induced norepinephrine release in dogs

1987 ◽  
Vol 43 ◽  
pp. 96
Author(s):  
Toshiyuki Matsuoka ◽  
Yoshiharu Hayashi ◽  
Mizue Suzuki-Kusaba ◽  
Susumu Satoh
Keyword(s):  
Angiotensin Ii ◽  
Nerve Stimulation ◽  
Norepinephrine Release ◽  
Renal Nerve ◽  
Renal Nerve Stimulation

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 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.

Losartan corrects abnormal frequency response of renal vasculature in congestive heart failure

2003 ◽  
Vol 285 (5) ◽  
pp. H1857-H1863 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Sawin
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Angiotensin Ii ◽  
Frequency Response ◽  
Nerve Stimulation ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Pass Filter ◽  
Vasoconstrictor Response ◽  
Renal Nerve Stimulation

In congestive heart failure, renal blood flow is decreased and renal vascular resistance is increased in a setting of increased activity of both the sympathetic nervous and renin-angiotensin systems. The renal vasoconstrictor response to renal nerve stimulation is enhanced. This is associated with an abnormality in the low-pass filter function of the renal vasculature wherein higher frequencies (≥0.01 Hz) within renal sympathetic nerve activity are not normally attenuated and are passed into the renal blood flow signal. This study tested the hypothesis that excess angiotensin II action mediates the abnormal frequency response characteristics of the renal vasculature in congestive heart failure. In anesthetized rats, the renal vasoconstrictor response to graded frequency renal nerve stimulation was significantly greater in congestive heart failure than in control rats. Losartan attenuated the renal vasoconstrictor response to a significantly greater degree in congestive heart failure than in control rats. In control rats, the frequency response of the renal vasculature was that of a first order (–20 dB/frequency decade) low-pass filter with a corner frequency (–3 dB, 30% attenuation) of 0.002 Hz and 97% attenuation (–30 dB) at ≥0.1 Hz. In congestive heart failure rats, attenuation did not exceed 45% (–5 dB) over the frequency range of 0.001–0.6 Hz. The frequency response of the renal vasculature was not affected by losartan treatment in control rats but was completely restored to normal by losartan treatment in congestive heart failure rats. The enhanced renal vasoconstrictor response to renal nerve stimulation and the associated abnormality in the frequency response characteristics of the renal vasculature seen in congestive heart failure are mediated by the action of angiotensin II on renal angiotensin II AT1 receptors.

Interaction Between Norepinephrine Release and Intrarenal Angiotensin II Formation During Renal Nerve Stimulation in Dogs

2000 ◽  
Vol 35 (6) ◽  
pp. 831-837 ◽  
Author(s):  
Naoki Yamaguchi ◽  
Mizue Suzuki-Kusaba ◽  
Hiroaki Hisa ◽  
Yoshiharu Hayashi ◽  
Makoto Yoshida ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Nerve Stimulation ◽  
Norepinephrine Release ◽  
Renal Nerve ◽  
Renal Nerve Stimulation

Renal adrenergic effector mechanisms: glomerular sites for prostaglandin interaction

1988 ◽  
Vol 254 (2) ◽  
pp. F184-F190 ◽  
Author(s):  
J. C. Pelayo
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Wistar Rats ◽  
Filtration Rate ◽  
Renal Nerve ◽  
Single Nephron ◽  
Marked Decline ◽  
Renal Nerve Stimulation ◽  
Glomerular Ultrafiltration ◽  
Hydrostatic Pressure Difference

Micropuncture experiments were performed in Munich-Wistar rats to ascertain the renal microcirculatory sites at which prostaglandins interact with the renal nerve and angiotensin II. Renal nerve stimulation (RNS) of 3 Hz alone decreased single-nephron glomerular filtration rate (SNGFR) by 30%, the consequence of 10 and 35% reductions in the glomerular capillary hydrostatic pressure difference (delta P) and the single-nephron plasma flow (SNPF), respectively. Pre- and postglomerular vascular resistances increased. RNS during prostaglandin inhibition (indomethacin) resulted in a 70% reduction in SNGFR, secondary to 1) a further diminution in delta P and in SNPF, via heightened pre- and postglomerular vasoconstriction and 2) a marked decline in the glomerular ultrafiltration coefficient (LpA), from 0.058 +/- 0.006 to 0.027 +/- 0.002 nl.s-1.mmHg-1.g kidney wt-1 (P less than 0.005). Acute angiotensin II inhibition (MK-421 and [Sar1,Ala8]angiotensin II) in rats pretreated with indomethacin partially attenuated the effects of RNS on vascular resistances and therefore on delta P, SNPF, and SNGFR and prevented the reduction in LpA. Thus vasodilatory prostaglandins act as local modulators of both renal nerve and angiotensin II constrictive actions on glomeruli and renal microcirculation.

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.

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