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HYPOTENSION‐INDUCED HYPOKALAEMIA IN SHEEP
Author(s) -
Dallemagne Catherine,
Cross R. B.,
Law Sandra,
Verschuer Louise,
Wholohan Therese,
Yesberg Nancy E.
Publication year - 1986
Publication title -
quarterly journal of experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0144-8757
DOI - 10.1113/expphysiol.1986.sp003017
Subject(s) - plasma renin activity , aldosterone , furosemide , sodium nitroprusside , medicine , endocrinology , verapamil , isoprenaline , chemistry , blood pressure , mineralocorticoid , nifedipine , renin–angiotensin system , sodium , calcium , nitric oxide , organic chemistry , stimulation
Plasma K + was measured in Merino ewes during 50‐90 min periods of hypotension induced by sodium nitroprusside, isoprenaline, verapamil or nifedipine. Doses were adjusted to produce falls in systemic blood pressure of approximately 20 mmHg. All of these drugs caused decreases in plasma K + which could not be attributed to increased urinary excretion of K + . In all cases plasma renin activity increased during the hypotension. Plasma aldosterone concentration which was measured in some sodium nitroprusside experiments also increased during the hypotension. However, enhancement of the plasma renin activity and plasma aldosterone concentration responses by prior sodium depletion of the sheep by furosemide administration or suppression of the plasma renin activity and plasma aldosterone concentration responses by prior salt loading did not influence the magnitude of the hypotension‐induced hypokalaemia.