Autoregulation of Glomerular Filtration in Renin-Depleted Dogs

Potkay, S; Gilmore, J. P.

doi:10.3181/00379727-143-37354

Cited by 9 publications

(5 citation statements)

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“…It has been shown that infusions o f angiotensin II do not prevent normal autoregulatory adjustments in renal vascular resistances following reduc tions in arterial pressure [8,21]. Also, several studies have indicated that R B F and G F R autoregulatory behavior is not impaired in renin-depleted animals [9,22] or following angiotensin blockade in high-renin models [14], Findings by other investigators, how ever, have indicated that there is a dissocia tion between RBF autoregulatory' behavior and G F R autoregulalion in renin-depleted animals [ 11] and following angiotensin block ade during high-renin states [7,12], These latter observations have led to the hypothesis that intrarenally formed angiotensin acts pre ferentially on efferent resistance vessels and exerts a progressively increasing influence on postglomerular resistance, as the RAP is reduced [23]. This issue was also evaluated recently in a micropuncture study on rats [24].…”

Section: Discussionmentioning

confidence: 99%

“…Most studies have demonstrated that autoregulatory effi ciency for renal blood flow (RBF) remains basically intact during angiotensin II infu sions, administration o f angiotensin II antag onists or converting enzyme inhibitors, or during chronic renin depletion [5,[7][8][9][10][11][12][13][14], However, the glomerular filtration rate (G FR ) responses to reductions in arterial pressure have remained uncertain; in partic ular, the G F R autorcgulatory efficiency un der these conditions has not been clearly established. Some studies have observed au toregulation o f G F R along with R B F follow ing blockade o f the renin-angiotensin system [5,8,9,14]. Other studies have indicated that there is an uncoupling in antoregulation of G F R and R BF during inhibition of the renin-angiotensin system [11,13,15].…”

Section: Introductionmentioning

confidence: 99%

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Renal Autoregulatory Efficiency during Angiotensin-Converting Enzyme Inhibition in Dogs on a Low Sodium Diet

Rosivall

Youngblood

Navar

1986

Kidney Blood Press Res

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Autoregulatory efficiency of renal blood flow (RBF) and glomerular filtration rate (GFR) was evaluated in 12 anesthetized dogs that had been maintained on low-sodium diet during control conditions and following infusion of an angiotensin-converting enzyme inhibitor (captopril). Converting enzyme inhibition (CEI) decreased systemic blood pressure by 15.5 ± 3.5%, increased RBF by 36.3 ± 6.5%, and increased GFR by 25.9 ± 10.7%. In response to reductions in renal arterial pressure, RBF was efficiently autoregulated and did not change significantly until the 89- to 75-mm Hg range during the control period and the 74- to 54-mm Hg range during CEI. Overall GFR autoregulatory efficiency was generally well maintained during CEI; however, evaluation of the coupled autoregulatory efficiency of RBF and GFR indicated that during angiotensin blockade, there was a greater incidence of a dissociation between RBF and GFR autoregulatory efficiency. Six of the 12 dogs showed reduced GFR autoregulatory efficiency at renal arterial pressures where RBF was still well maintained. Thus, while the data indicate that blockade of the renin-angiotensin system does not abolish the basic capability of the kidney to autoregulate either RBF or GFR efficiently, more subtle influences on the coupling of RBF and GFR autoregulatory efficiency were observed at the lower level of the autoregulatory range.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Renal Autoregulatory Efficiency during Angiotensin-Converting Enzyme Inhibition in Dogs on a Low Sodium Diet

Rosivall

Youngblood

Navar

1986

Kidney Blood Press Res

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“…Several recent studies have examined the role of the renin-angiotensin system in the control of autoregulation of kidney hemodynamics (4-7), and although conflicting, these reports have failed to establish a pivotal role for the renin-angiotensin system in the mediation of autoregulatory adjustments in renal vascular resistance (4,6,7). The possible influence of the renin-angiotensin system on the base-line control setting of renal hemodynamics has received somewhat greater support (3,8,9).…”

Section: Introductionmentioning

confidence: 99%

Tubuloglomerular Feedback and Single Nephron Function after Converting Enzyme Inhibition in the Rat

Ploth¹,

Rudulph²,

Lagrange³

et al. 1979

J. Clin. Invest.

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A B S T R A C T Experiments were done in normal rats to assess kidney, single nephron, and tubuloglomerular feedback responses during renin-angiotensin blockade with the converting enzyme inhibitor (CEI) SQ 20881 (E. R. Squibb & Sons, Princeton, N. Y.) (3 mg/kg, per h). Converting enzyme inhibition was documented by complete blockade of vascular responses to infusions of angiotensin I (600 ng/kg). Control plasma renin activity was 12.5+2.7 ng angiotensin I/ml per h (mean±SEM) and increased sevenfold with CEI (n = 7). There were parallel increases in glomerular filtration rate from 1.08±0.05 to 1.26±0.05 ml/min and renal blood flow from 6.7±0.4 to 7.5±0.5 ml/min. During CEI infusion absolute and fractional sodium excretion were increased 10-fold. Proximal tubule and peritubular capillary pressures were unchanged. Single nephron glomerular filtration rate (SNGFR) was measured from both proximal and distal tubule collections; SNGFR based only on distal collections was significantly increased by CEI. A significant difference was observed between SNGFR values measured from proximal and distal tubule sites (6.0±1.6 nl/min) and this difference remained unchanged after CEI administration. Slight decreases in fractional absorption were suggested at micropuncture sites beyond the late proximal tubule, whereas early distal tubule flow rate was augmented by CEI. Tubuloglomerular feedback activity was assessed by measuring changes in proximal tubule stop-flow pressure (SFP) or SNGFR in response to alterations in orthograde microperfusion rate from late proximal tubule sites. During control periods, SFP was decreased 11.2±0.4This work was presented in part at the Fall American Physiological Society Meetings in Miami, Florida, 1977, and at the VII International Congress of Nephrology in Montreal, Canada, 1978. Dr. Navar is the recipient of a National Heart and Lung Institute Research Career Development Award.Received for publication 7 August 1978 and in revised form 27 June 1979. mm Hg when the perfusion rate was increased to 40 nl/min; during infusion of CEI, the same increase in perfusion rate resulted in a SFP decrement of 6.7+0.5 mm Hg (P< .001). When late proximal tubule perfusion rate was increased from 0 to 30 nl/min, SNGFR was decreased by 15.0±+1.2 nl/min during control conditions, and by 11.3+1.3 nl/min during CEI infusion. Attenuation of feedback responsiveness during CEI was also observed at lower perfusion rates with both techniques. These results indicate that blockade of the renin-angiotensin system with CEI reduces the activity of the tubuloglomerular feedback mechanism which may mediate the observed renal vasodilation.

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“…In red blood cell-perfused kidneys we observed an almost complete autoregulation of perfusate flow at pressures above 90 mmHg, provided that the perfusion pressure was changed rapidly (Zschiedrich et al, 1975b). Since there is no evidence that during the perfusion A11 is formed within the renal vascular bed (experiments with saralasin and SQ 20 88 1, discussed below), our findings suggest that the capacity of the kidney to autoregulate is independent of the intrarenal reninangiotensin system (Belleau & Earley, 1967;Kid, Kjekshus & Lsyning, 1969;Eide et al, 1973a;Potkay & Gilmore, 1973). However, the renin-angiotensin system might modify, rather than mediate, autoregulation.…”

Section: Autoregulationmentioning

confidence: 73%

Regulation of Renin Release and Intrarenal Formation of Angiotensin. Studies in the Isolated Perfused Rat Kidney

Hofbauer

Zschiedrich

Gross

1976

Clin Exp Pharmacol Physiol

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1. Isolated rat kidneys were perfused at a constant pressure of 90 mmHg in a single-pass system with either a cell-free medium or a suspension of washed bovine red blood cells, free of the components of the renin-angiotensin system. In red blood cell perfused kidneys renal haemodynamics and sodium reabsorption corresponded closer to values observed in the intact rat than in cell-free perfused kidneys. 2. In red blood cell-perfused kidneys in the absence of plasma renin substrate autoregulation of renal blood flow was almost complete at pressures above 90 mmHg, provided that perfusion pressure was changed rapidly. 3. Renin release varied inversely with perfusion pressure within a pressure range from 50 to 150 mmHg; the greatest changes of renin release occurred, when perfusion pressure was reduced from 90 to 70 mmHg; maximal stimulation of renin release was observed at 50 mmHg. After reduction of perfusion pressure, renin release immediately started to rise and reached a new level within 5 min. Local reduction of perfusion pressure in small arteries and arterioles by the injection of microspheres induced a short-lasting decrease in renal plasma flow and a transient stimulation of renin release. 4. High concentrations of furosemide stimulated renin release by a direct intrarenal mechanism. 5. Isoproterenol stimulated renin release in low concentrations without a concomitant vasodilation, whereas high concentrations induced an increase in both renal plasma flow and renin release. The effects of isoproterenol were completely blocked by propranolol. 6. Sodium nitroprusside induced similar increases in renal plasma flow, as did high concentrations of isoproterenol, but only a small and slow increase in renin release was observed. 7. Angiotensin II (AII) suppressed renin release in concentrations corresponding to plasma levels measured in the intact rat independently of its vasoconstrictor effects, whereas vasopressin in antidiuretic concentrations did not affect renin release. 8. AII, AI, synthetic tetradecapeptide renin substrate (TDP), crude and purified rat plasma renin substrate induced a dose-dependent reduction in renal plasma flow. SQ 20 881, a competitive inhibitor of converting enzyme, and low doses of 1-Sar-8-Ala-AII (saralasin), a competitive antagonist of AII, did not change renal plasma flow, whereas high concentrations of saralasin had a vasoconstrictor effect on their own. 9. Saralasin inhibited the vasoconstrictor effects of AII and TDP to a similar degree. SQ 20 881 inhibited the vasoconstrictor effects of AI and purified renin substrate, but did not influence the actions of TDP and the crude renin substrate preparation. 10. From these data it is concluded, that AI is converted into AII within the kidney at a rate of 1-2%. The vasoconstriction induced by the crude renin substrate probably does not involve the AII receptors. TDP may act by itself on the AII receptors or via the direct intrarenal formation of AII...

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Autoregulation of Glomerular Filtration in Renin-Depleted Dogs

Cited by 9 publications

References 0 publications

Renal Autoregulatory Efficiency during Angiotensin-Converting Enzyme Inhibition in Dogs on a Low Sodium Diet

Renal Autoregulatory Efficiency during Angiotensin-Converting Enzyme Inhibition in Dogs on a Low Sodium Diet

Tubuloglomerular Feedback and Single Nephron Function after Converting Enzyme Inhibition in the Rat

Regulation of Renin Release and Intrarenal Formation of Angiotensin. Studies in the Isolated Perfused Rat Kidney

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