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Induction of hypovolaemia by thirst‐inducing doses of renin or angiotensin II
Author(s) -
HAEFELI LISETTE,
PETERS G.
Publication year - 1971
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.1476-5381.1971.tb07083.x
Subject(s) - thirst , renin–angiotensin system , plasma volume , medicine , endocrinology , plasma renin activity , blood volume , chemistry , angiotensin ii , receptor , sed , blood pressure
Summary1 Intravenous injection of five Goldblatt units (Gbl.U) of renin, or intravenous infusion of 2·5 μg of angiotensin into nephrectomized rats decreased plasma volume by 22 ± 2% (calculated from the increase of the haematocrit) or by 14 ± 2% (calculated from the increase in protein concentration) within 2 minutes. Fifteen minutes and 60 min after injection or infusion, the plasma volume (calculated from both parameters) was still 10% lower than initially. 2 The initial discrepancy between haematocrit values and plasma protein concentration was neither due to mobilization of red blood cells (r.b.c.) from the spleen, nor to an increase in r.b.c. volume. 3 The observed decrease in plasma volume was large enough to explain the drinking response to renin and angiotensin. Renin may thus induce or aggravate hypovolaemia rather than signalling its occurrence to hypothalamic receptors.