Reaction of Endogenous Renin With Exogenous Renin Substrate Within the Isolated Perfused Rat Kidney

Hofbauer, K. G.; Zschiedrich, H.; Rauh, W; Orth, H.; Gross, F.

doi:10.3181/00379727-142-37119

Cited by 13 publications

(7 citation statements)

References 3 publications

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“…However, 10 min after the infusion of RS had been stopped, RPF had not returned to its previous value. This observation is consistent with our results in isolated rat kidneys perfused at constant flow (Hofbauer et al, 1973) and is suggestive of differences in action between infused and intrarenally released AI.…”

Section: Discussionsupporting

confidence: 93%

Conversion of Angiotensin I into Angiotensin II in the Isolated Perfused Rat Kidney

et al. 1973

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1. In the isolated rat kidney, perfused at constant pressure with a medium free from renin substrate, addition of angiotensin I to the perfusate decreases renal 'plasma' flow.2. A peptide inhibitor, SQ 20881, of converting enzyme reduces the vasoconstrictor effect of angiotensin I up to a maximum of 87%, the degree of inhibition being dose-dependent.3. The molar ratio of equi-effective doses of angiotensin I and angiotensin I1 was 50 : l ' , indkating a low rate of intrarenal conversion of the decapeptide..4. The vasoconstrictor effect elicited by the addition of renin substrate to the perfusate was not inhibited by SQ 20881, even if the concentration was fifteen times that which produced the maximum inhibition of conversion of angiotensin I..

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Section: Discussionsupporting

confidence: 93%

Conversion of Angiotensin I into Angiotensin II in the Isolated Perfused Rat Kidney

et al. 1973

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“…First, the present study demonstrates that the renin-angiotensin system is not physio logically intact in the isolated perfused rat kidney system. While previous studies have demonstrated an absence of renin substrate in artificial perfusion media [13], there have been no previous determinations of angio tensin converting enzyme. Our results dem onstrate clearly, for the first time, an ab sence of converting enzyme in the perfusate and a failure of release of this enzyme into the perfusate with time.…”

Section: Discussionmentioning

confidence: 95%

“…Previous evaluations of the dynamics of renin release with the recirculating perfused kidney technique have assumed that renin release is subtended by a linear function [8][9][10][11][12][13][20][21][22][23][24][25]. Furthermore, renal function was not examined concomitantly, rendering the interpretation of such renin data difficult.…”

Section: Introductionmentioning

confidence: 99%

Characterization of the Renin-Angiotensin System in the Isolated Perfused Rat Kidney

Epstein¹,

Flamenbaum²,

Loutzenhiser³

1979

Kidney Blood Press Res

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Most previous studies using the isolated perfused kidney model to assess the mechanisms governing renin release have utilized single-point determinations of media renin content as an estimate of renin release rate. In the present study the dynamics of renin release were examined under standardized conditions of perfusion, with simultaneous evaluations of changes in renal function. Media samples were collected at 5-min intervals. Renin release rate was characterized by an initial progressive increase which achieved a constant value of 67 ng/ h/min/g only after 45 min of perfusion. Consequently, the accumulation of renin within the media does not become linear until 45 min of perfusion. Simultaneous determinations of various parameters of renal function disclosed that neither GFR, renal sodium handling nor indices of distal delivery correlated with renin release. However, the renin-angiotensin system is not physiologically intact since the standard perfusate utilized in the present study was demonstrated to lack both renin substrate and converting enzyme. The present studies demonstrate that renin release is curvilinear and that experimental errors may occur if sampling is not restricted to the stable phase of perfusion.

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“…A crude preparation of rat plasma renin substrate induced a dose-dependent vasoconstriction (Hofbauer et al, 1973a). This effect could not be inhibited by SQ 20 881 (Hofbauer et al, 1973b), which suggests that no conversion of A1 to A11 was involved in the production of the effect.…”

Section: Intrarenal Formation Of Aiimentioning

confidence: 89%

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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Reaction of Endogenous Renin With Exogenous Renin Substrate Within the Isolated Perfused Rat Kidney

Cited by 13 publications

References 3 publications

Conversion of Angiotensin I into Angiotensin II in the Isolated Perfused Rat Kidney

Conversion of Angiotensin I into Angiotensin II in the Isolated Perfused Rat Kidney

Characterization of the Renin-Angiotensin System in the Isolated Perfused Rat Kidney

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

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