Intrarenal Action of Angiotensin

Thurau, Klaus

doi:10.1007/978-3-642-65600-2_26

Cited by 28 publications

(7 citation statements)

References 56 publications

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“…The calculated FPRN, and FDRN, were both reduced by ANP infusion. A11 increases FPRN, by a direct action on the proximal tubules, and also causes an increase in FDRN, mediated by stimulation of aldosterone secretion (Thurau 1974). Recently, Harris et al (1 987), using a micropuncture technique in rats, demonstrated that ANP inhibits AII-stimulated proximal tubular reabsorption of sodium and water (Harris et al 1987).…”

Section: Discussionmentioning

confidence: 99%

“…A11 is believed to have an antinatriuretic action mediated by stimulation of sodium reabsorption in the proximal tubules (Thurau 1974) or by stimulation of aldosterone secretion (Davis 1974). ANP has been reported to antagonize the actions of A11 in a variety of tissues (Burnett et al 1984;De Lean et al 1984;Garcia et al 1984;Nakamaru et al 1986;Vierhapper et al 1986).…”

Section: Discussionmentioning

confidence: 99%

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Renal Interaction of Atrial Natriuretic Peptide With Angiotensin Ii: Glomerular and Tubular Effects

Rakugi

Ogihara

Nakamaru

et al. 1989

Clin Exp Pharma Physio

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1. The possible interactions between the renal effects of atrial natriuretic peptide (ANP) and angiotensin II (AII) were studied in normal sodium-replete human subjects. Recent investigations have suggested that ANP inhibits the pressor and volume-retaining effects of activation of the renin-angiotensin system. Thus, ANP may attenuate the effects of AII on renal haemodynamics or tubular transport. 2. ANP (0.1 micrograms/kg per min, 60 min) was intravenously infused into eight normal human subjects with and without pretreatment with enalapril (20 mg, per oral), an inhibitor of the converting enzyme, and during infusion of AII (10 mg/kg per min). 3. ANP infusion alone caused increases in the urine volume (from 96 +/- 23 to 229 +/- 44 mL/h, P less than 0.05) and urinary sodium excretion (from 11.5 +/- 1.6 to 20.9 +/- 4.2 mEq/h, P less than 0.05). These changes were accompanied by an increase in the glomerular filtration rate (from 127 +/- 9 to 158 +/- 9 mL/min, P less than 0.05). ANP infusion after enalapril administration lowered the mean blood pressure (from 76 +/- 2 to 71 +/- 3 mmHg, P less than 0.05) to a level similar to that observed during ANP infusion alone (from 84 +/- 2 to 74 +/- 2 mmHg, P less than 0.01), but did not result in a significant diuresis (from 139 +/- 23 to 174 +/- 51 mL/h) or natriuresis (from 19.7 +/- 2.5 to 14.3 +/- 3.4 mEq/h, P less than 0.05). This combined treatment with a converting enzyme inhibitor and ANP reduced both the glomerular filtration rate (160 +/- 9 to 141 +/- 10 mL/min) and the renal plasma flow (from 775 +/- 49 to 570 +/- 45 mL/min, P less than 0.01). 4. The antinatriuretic effects of exogenous AII were reversed by superimposed ANP infusion (urinary sodium excretion: from 4.8 +/- 1.0 to 24.3 +/- 5.2 mEq/h, P less than 0.01). Under these conditions, the glomerular filtration rate increased (from 114 +/- 6 to 156 +/- 7 mL/min, P less than 0.05) to levels similar to those observed with ANP infusion alone. In addition the increased tubular sodium reabsorption induced by AII was inhibited by concomitant ANP infusion (fractional proximal tubular sodium reabsorption: from 90.7 +/- 3.5 to 80.3 +/- 16.6%, P less than 0.05, fractional post-proximal tubular sodium reabsorption: from 91.5 +/- 9.8 to 87.6 +/- 8.8%, P less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Renal Interaction of Atrial Natriuretic Peptide With Angiotensin Ii: Glomerular and Tubular Effects

Rakugi

Ogihara

Nakamaru

et al. 1989

Clin Exp Pharma Physio

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“…25 These observations, plus the fact that converting enzyme activity has been demonstrated to be present in the juxtaglomerular apparatus, 28 provide the basis for the hypothesis that the renin-angiotensin system participates in the regulation of cortical blood flow. Thurau et al 27 proposed that the renin-angiotensin system mediates autoregulation of GFR and RBF by a feedback mechanism involving the macula densa and afferent arteriole. We have previously reported our studies 14 which provide indirect support for the reninangiotensin hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of prostaglandin E2 secretion. Failure to abolish autoregulation in the isolated dog kidney.

Kaloyanides¹,

Ahrens²,

Shepherd³

et al. 1976

Circulation Research

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We studied the role of renal prostaglandins in the regulation of glomerular filtration rate (GFR) and renal blood flow (RBF) in the isolated dog kidney. Indomethacin or meclofenamate, 2 mg/kg of body weight, suppressed renal prostaglandin E2 (PGE2) secretion, measured by radioimmunoassay, to zero within 20 minutes; the effect persisted for the duration of the study. When renal arterial pressure (PRA) was maintained at 104 mm Hg both drugs caused a sharp decrease in sodium excretion and RBF with redistribution of flow from inner to outer cortes we examined autoregulation of GFR and RBF over the pressure ranges of 150-100 and 150-75 mm Hg, respectively, after inhibition of PGE2 secretion and under control conditions. deltaGFR/deltaPRA (ml/min per mm Hg) was 0.020 +/- 0.017 in the indomethacin group, 0.152 +/- 0.055 in the meclofenamate group, and 0.086 +/- 0.017 in the control group. The change in GFR for the indomethacin group was significantly less than that for meclofenamate (P less than 0.01) and control groups (P less than 0.025); the latter two groups were not statistically different from each other (P greater than 0.1). There was no significant difference (P greater than 0.1) between the three groups with respect to deltaRBF/deltaPRA, which measured 0.288 +/- 0.046, 0.370 +/- 0.112, and 0.438 +/- 0.123 ml/min per mm Hg in the indomethacin, meclofenamate and control groups, respectively. Renal was lowered from 150 to 75 mm Hg. The observation that inhibition of prostaglandin synthesis promotes a redistribution of RBF from inner to outer cortex suggests that renal prostaglandins may participate in the regulation of medullary blood flow. However, since autoregulation of GFR and RBF remained intact despite inhibition of prostaglandin secretion, these data argue against a role for renal prostaglandins in regulating whole kidney GFR and RBF.

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“…Kidney was chosen as a model tissue because of evidence that A11 might be locally formed and serve a physiologically important role in this organ (Thurau, 1974).…”

Section: Introductionmentioning

confidence: 99%

A Method for Measurement of Angiotensin II in Tissues and its Application to Rat Kidney

Mendelsohn¹

1976

Clinical Science

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1. A method for extraction, partial purification and radioimmunoassay of angiotensin II in tissues and application of the method to the kidneys of sodium-deficient rats are described. 2. Angiotensin in acid-ethanol extracts of kidney were adsorbed on to a cation-exchange resin, eluted and further purified with an immobilized angiotensin II antiserum, before radioimmunoassay. 3. Thin-layer chromatography was used, in some experiments, to separate fmol amounts of angiotensin II from its immunoreactive peptide fragments before radioimmunoassay. 4. Angiotensin II-immunoreactive material isolated from rat kidney resembled angiotensin II in many of its physicochemical properties and chromatographic mobility. 5. The concentration of immunoreactive material in kidney greatly exceeded that which could be accounted for by trapped blood and suggests that the peptide may have a local role in the organ.

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Intrarenal Action of Angiotensin

Cited by 28 publications

References 56 publications

Renal Interaction of Atrial Natriuretic Peptide With Angiotensin Ii: Glomerular and Tubular Effects

Renal Interaction of Atrial Natriuretic Peptide With Angiotensin Ii: Glomerular and Tubular Effects

Inhibition of prostaglandin E2 secretion. Failure to abolish autoregulation in the isolated dog kidney.

A Method for Measurement of Angiotensin II in Tissues and its Application to Rat Kidney

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