Dynamics of intrarenal pressures and glomerular filtration rate after acetazolamide

Leyssac, P. P.; Karlsen, Finn Michael; Skøtt, Ole

doi:10.1152/ajprenal.1991.261.1.f169

Cited by 19 publications

(20 citation statements)

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“…In other studies (31,37,38), we employed the proximal tubular diuretic acetazolamide to enhance tubular salt load to the macula densa and thereby stimulate TGF. Although acetazolamide exerted its desired action, as evidenced by a marked increase in urinary excretion and a presumed TGF-mediated decrease in steady-state RBF, RBF autoregulation was unaffected and the relative contribution of the myogenic and TGF mechanisms were unchanged.…”

Section: Discussionmentioning

confidence: 99%

Dynamics and contribution of mechanisms mediating renal blood flow autoregulation

Just

Arendshorst

2003

American Journal of Physiology-Regulatory, Integrative and Comp

139

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-We investigated dynamic characteristics of renal blood flow (RBF) autoregulation and relative contribution of underlying mechanisms within the autoregulatory pressure range in rats. Renal arterial pressure (RAP) was reduced by suprarenal aortic constriction for 60 s and then rapidly released. Changes in renal vascular resistance (RVR) were assessed following rapid step reduction and RAP rise. In response to rise, RVR initially fell 5-10% and subsequently increased ϳ20%, reflecting 93% autoregulatory efficiency (AE). Within the initial 7-9 s, RVR rose to 55% of total response providing 37% AE, reaching maximum speed at 2.2 s. A secondary RVR increase began at 7-9 s and reached maximum speed at 10-15 s. Response times suggest that the initial RVR reflects the myogenic response and the secondary tubuloglomerular feedback (TGF). During TGF inhibition by furosemide, AE was 64%. The initial RVR rise was accelerated and enhanced, providing 49% AE, but it represented only 88% of total. The remaining 12% indicates a third regulatory component. The latter contributed up to 50% when the RAP increase began below the autoregulatory range. TGF augmentation by acetazolamide affected neither AE nor relative myogenic contribution. Diltiazem infusion markedly inhibited AE and the primary and secondary RVR increases but left a slow component. In response to RAP reduction, initial vasodilation constituted 73% of total response but was not affected by furosemide. The third component's contribution was 9%. Therefore, RBF autoregulation is primarily due to myogenic response and TGF, contributing 55% and 33-45% in response to RAP rise and 73% and 18-27% to RAP reduction. The data imply interaction between TGF and myogenic response affecting strength and speed of myogenic response during RAP rises. The data suggest a third regulatory system contributing Ͻ12% normally but up to 50% at low RAP; its nature awaits further investigation. renal circulation; afferent arteriole; glomerular arterioles; myogenic mechanism; tubuloglomerular feedback; vascular smooth muscle cells; macula densa cells; calcium channel blocker; furosemide; acetazolamide AUTOREGULATION OF RENAL blood flow (RBF) has been well characterized under steady-state conditions (2, 28, 36).Less is known about the dynamics and the relative contribution of the responsible mechanisms. Since the underlying mechanisms differ in their response times, the relative contributions affect the speed of overall regulation. Because of the continuous fluctuations of arterial pressure over a wide range of frequencies (33), the efficiency of autoregulation determines the size and range of pressure changes reaching glomeruli, peritubular capillaries, and medullary perfusion and will thus have an important bearing on fluid homeostasis and hypertensive renal damage.There is general agreement that renal autoregulation is mediated by at least two mechanisms, the tubuloglomerular feedback (TGF) and the myogenic response (36), and perhaps by a third (24). Although TGF participates, it appears that a d...

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Section: Discussionmentioning

confidence: 99%

Dynamics and contribution of mechanisms mediating renal blood flow autoregulation

Just

Arendshorst

2003

American Journal of Physiology-Regulatory, Integrative and Comp

139

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“…These studies were motivated in part by reports that have questioned TGF as a dominant mechanism in the reduction of GFR by CA inhibitors [14]. Further investigations of this question are important because CA inhibitors are often used as a systemic approach to activate the TGF mechanism [10,27].…”

Section: Discussionmentioning

confidence: 99%

“…Careful and detailed studies exploring the role of proximal tubular pressure in the GFR reduction caused by acetazolamide have led to the conclusion that even small changes in proximal pressure could contribute to the reduction in ultrafiltration pressure, and that this effect may be more important than the reduction in glomerular capillary pressure under some circumstances [14,15]. Micropuncture studies have examined the role of TGF in the GFR-reducing effect of CA inhibition by comparing SNGFR measurements in the distal tubule, where TGF is functional, with measurements in the proximal tubule where TGF regulation is abolished.…”

Section: Discussionmentioning

confidence: 99%

Effect of carbonic anhydrase inhibition on GFR and renal hemodynamics in adenosine-1 receptor-deficient mice

Hashimoto

Huang

Castrop

et al. 2004

Pflugers Arch - Eur J Physiol

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The reduction of glomerular filtration rate (GFR) caused by inhibitors of carbonic anhydrase (CA) is thought to be initiated by activation of the tubuloglomerular feedback (TGF) mechanism. We determined the effect of the CA inhibitor benzolamide (Bz) on renal hemodynamics in adenosine-1 receptor (A1AR) knockout mice that have been shown previously to lack a TGF response. In A1AR(+/+) mice, Bz (150 microg plus 2 microg/min) reduced RBF by 19.8% (from 829+/-42 to 666+/-44 microl/min; n=7), and GFR by 19.8% (from 396+/-43 to 324+/-46 microl/min; n=9, P=0.001). In A1AR(-/-) mice, RBF fell by 15.9 % (from 809+/-24 to 680+/-40 microl/min; n=7), and GFR by 21.1% (from 358+/-27 to 287+/-32 microl/min; n=10, P=0.0003; NS compared with A1AR(+/+)). The absence of TGF responses both before and during Bz infusion in A1AR(-/-) mice was confirmed by micropuncture. Following angiotensin II-receptor blockade with candesartan, Bz did not alter RBF (1.4+/-0.2 vs. 1.4+/-0.15 ml/min in A1AR(+/+), and 1.4+/-0.22 vs. 1.39+/-0.2 ml/min in A1AR(-/-); n=5/genotype) while GFR changed by -8.9 % in A1AR(+/+) mice ( n=7), and by -1% in A1AR(-/-) mice ( n=9; NS compared with A1AR(+/+)). Bz caused a significant rise of plasma renin concentration in both A1AR(+/+) and A1AR(-/-) mice. Our data show that the absence of a functional TGF mechanism does not prevent the reduction in GFR or RBF caused by CA inhibition. Acute angiotensin II receptor blockade, on the other hand, diminishes the effect of CA inhibition on GFR and RBF. The causes for the GFR reduction appear to be complex and include an effect of the renin-angiotensin system.

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“…The left femoral vein was cannulated for the administration of [51Cr]-EDTA solution (i.v. bolus at 13.8 yCi in 1.75 ml over 2 min followed by infusion at 0.16 yCi min' at 20 yl min') (Stacy & Thorburn, 1966;Leyssac et al, 1991). The abdominal cavity was opened through a ventral midline incision.…”

Section: Introductionmentioning

confidence: 99%

Effects of calcitonin gene‐related peptide receptor antagonists on renal actions of adrenomedullin

Elhawary

Poon

Pang

1995

British J Pharmacology

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1 Adrenomedullin is a novel vasoactive peptide which is produced in the lungs, ventricle, kidneys, heart and adrenal medulla. Adrenomedullin shows homology to calcitonin gene-related peptide (CGRP) and has similar pharmacological actions to CGRP. 2 This study examined the dose-response effects of adrenomedullin (rat, 11-50) on mean arterial pressure (MAP), heart rate (HR), renal blood flow (RBF), glomerular filtration rate (GFR) and renal tubular electrolyte excretion in Inactin-anaesthetized Sprague Dawley rats. The possible involvement of CGRP receptors in actions of adrenomedullin was also examined via renal arterial injection of a CGRP receptor antagonist, CGRP (8-37) (1 or 10 nmol kg-') or [TyrICGRP(28-37) (3 or 30 nmol kg-'), starting 15 min prior to the administration of adrenomedullin. 3 Renal arterial infusion (0.001 to 1 nmol kg-') of adrenomedullin did not alter MAP, HR and renal K+ excretion but dose-dependently increased RBF and arterial conductance, GFR, urine flow and Na+ excretion. 4 The renal actions of adrenomedullin were not blocked by either the low or the high dose of or . 5 The results show that adrenomedullin causes renal vasodilatation, increments in GFR, diuresis and natriuresis. The renal actions of adrenomedullin are not mediated via the activation of CGRPI receptors.

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Dynamics of intrarenal pressures and glomerular filtration rate after acetazolamide

Cited by 19 publications

References 0 publications

Dynamics and contribution of mechanisms mediating renal blood flow autoregulation

Dynamics and contribution of mechanisms mediating renal blood flow autoregulation

Effect of carbonic anhydrase inhibition on GFR and renal hemodynamics in adenosine-1 receptor-deficient mice

Effects of calcitonin gene‐related peptide receptor antagonists on renal actions of adrenomedullin

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