TY - JOUR
T1 - Dietary protein increases plasma renin and reduces pressor reactivity to angiotensin II
AU - Paller, Mark S
AU - Hostetter, T. H.
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 1986
Y1 - 1986
N2 - The effect of dietary protein on the renin-angiotensin system was studied in rats. Rats were fed isocaloric, 50% (high protein, HP), or 6% (low protein, LP) protein diets with identical electrolyte content for 10 days. Food intake and electrolyte excretion were equivalent on the two diets. Plasma renin activity (PRA) was higher in HP (10.0 ± 2.5 vs 3.5 ± 0.5 ng ANG I·ml-1·h-1, P<0.02) as was plasma aldosterone. However, in conscious rats mean arterial pressure (MAP) was not different between groups. The pressor response to graded doses of angiotensin II (ANG II) was diminished by 30-60% with HP (all doses, P<0.05). ANG II binding by mesenteric artery smooth muscle particles did not differ between HP and LP. Chronic administration of captopril did not normalize the pressor response in HP. Urinary prostaglandin (PG) E and 6-keto-PGF(1α) excretion was markedly increased by the HP diet. Acute inhibition of prostaglandin synthesis with meclofenamate restored the pressor response to ANG II in HP to that LP. In summary, a HP diet increased PRA, plasma aldosterone, urinary PGE, and 6-keto-PGF(1α) and decreased pressor responsiveness to ANG II. Resistance to ANG II was not reversed by chronic converting enzyme inhibition but was abolished by inhibition of prostaglandin synthesis.
AB - The effect of dietary protein on the renin-angiotensin system was studied in rats. Rats were fed isocaloric, 50% (high protein, HP), or 6% (low protein, LP) protein diets with identical electrolyte content for 10 days. Food intake and electrolyte excretion were equivalent on the two diets. Plasma renin activity (PRA) was higher in HP (10.0 ± 2.5 vs 3.5 ± 0.5 ng ANG I·ml-1·h-1, P<0.02) as was plasma aldosterone. However, in conscious rats mean arterial pressure (MAP) was not different between groups. The pressor response to graded doses of angiotensin II (ANG II) was diminished by 30-60% with HP (all doses, P<0.05). ANG II binding by mesenteric artery smooth muscle particles did not differ between HP and LP. Chronic administration of captopril did not normalize the pressor response in HP. Urinary prostaglandin (PG) E and 6-keto-PGF(1α) excretion was markedly increased by the HP diet. Acute inhibition of prostaglandin synthesis with meclofenamate restored the pressor response to ANG II in HP to that LP. In summary, a HP diet increased PRA, plasma aldosterone, urinary PGE, and 6-keto-PGF(1α) and decreased pressor responsiveness to ANG II. Resistance to ANG II was not reversed by chronic converting enzyme inhibition but was abolished by inhibition of prostaglandin synthesis.
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U2 - 10.1152/ajprenal.1986.251.1.f34
DO - 10.1152/ajprenal.1986.251.1.f34
M3 - Article
C2 - 3524265
AN - SCOPUS:0022517924
SN - 0363-6143
VL - 251
SP - F34-F39
JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
IS - 1 (20/1)
ER -