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Stimulation and suppression of renin release from incubations of rat renal cortex by factors affecting calcium flux
Author(s) -
May Clive N.,
Peart W.S.
Publication year - 1986
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1986.tb11133.x
Subject(s) - isoprenaline , endocrinology , egta , medicine , chemistry , ouabain , verapamil , renin–angiotensin system , stimulation , calcium , secretion , aldosterone , biology , sodium , organic chemistry , blood pressure
1 Inhibition of renin secretion from incubations of rat kidney cortex by angiotensin II (AII), ouabain and K + depletion, depended on the presence of external Ca 2+ . 2 AII inhibition of isoprenaline‐stimulated renin secretion was only partially dependent on external Ca 2+ . 3 Ouabain and K + depletion inhibited isoprenaline‐stimulated renin release but only in the presence of external Ca 2+ . Since, in Ca 2+ ‐free medium, isoprenaline stimulated renin release when the Na + /K + ‐ATPase was blocked, isoprenaline probably does not act through the Na + /K + ‐ATPase. 4 Lanthanum blocked the stimulation of renin release by isoprenaline. 5 Ethylenediamine tetra‐acetic acid (EDTA) and ethyleneglycol‐ bis ‐(β‐amino‐ethyl ether) N,N'‐tetra‐acetic acid (EGTA) increased renin secretion to a similar degree in Ca 2+ ‐ and Mg 2+ ‐free buffer. When Mg 2+ was present the effect of EGTA, but not EDTA, was considerably reduced. 6 Verapamil reduced the fall in basal renin secretion in normal but not Ca 2+ ‐free buffer. Verapamil did not block the inhibitory effects of AII or ouabain and did not alter the stimulation of renin secretion by isoprenaline. 7 Bay K 8644 inhibited renin secretion from cortex incubated in medium containing 15 mM K + and this was dependent on extracellular Ca 2+ . In normal buffer (5.9 mM K + ) Bay K 8644 increased renin secretion.

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