What does this research mean for the field?

Atrial natriuretic peptide (ANP) antagonizes the antinatriuretic effects of angiotensin II by increasing glomerular filtration rate and inhibiting tubular sodium reabsorption, while its own diuretic and natriuretic effects are blunted when the renin-angiotensin system is inhibited. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

February 1, 1989

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

Structured PICO

Does atrial natriuretic peptide (ANP) interact with angiotensin II to alter renal hemodynamics and tubular transport in normal human subjects?

Population

8 normal sodium-replete human subjects

Intervention

Intravenous infusion of atrial natriuretic peptide (ANP) (0.1 micrograms/kg per min for 60 min) under three conditions: alone, after pretreatment with oral enalapril (20 mg), and during infusion of angiotensin II (10 mg/kg per min)

Comparator

Baseline measurements and comparison between the different infusion conditions (ANP alone vs. ANP + enalapril vs. ANP + angiotensin II)

Outcome

Changes in urine volume, urinary sodium excretion, and glomerular filtration ratesurrogate

ANP interacts significantly with the renin-angiotensin system, reversing the sodium-retaining effects of angiotensin II while requiring baseline angiotensin II activity for its own full natriuretic effect.

Abstract

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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