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Control of canine renin release: macula densa requires prostaglandin synthesis.
Author(s) -
Gerber J G,
Nies A S,
Olsen R D
Publication year - 1981
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1981.sp013918
Subject(s) - macula densa , renin–angiotensin system , endocrinology , medicine , chemistry , perfusion , plasma renin activity , juxtaglomerular apparatus , sodium nitroprusside , papaverine , vasodilation , excretion , kidney , blood pressure , nitric oxide
1. The macula densa mechanism of renin release was functionally isolated in uninephrectomized, anaesthetized dogs by producing renal denervation, beta‐adrenoceptor blockade, and maximum renal vasodilation with an infusion of papaverine into the renal artery. 2. A suprarenal aortic clamp was adjusted to reduce renal perfusion pressure by 50% which resulted in a 90% reduction in urinary sodium excretion and a two to threefold increase in plasma renin activity within 10 min. 3. Indomethacin (8 mg/kg) or meclofenamic acid (10 mg/kg) inhibited the rise plasma renin activity produced by the decrease in renal perfusion pressure in this model, although a comparable decrease in urinary sodium excretion was achieved. 4. We conclude that the macula densa mechanism of renin release is blocked by inhibition of prostaglandin synthesis.