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ROLE OF ANGIOTENSIN II AND BRADYKININ IN THE DIURESIS CAUSED BY STIMULATION OF ATRIAL RECEPTORS
Author(s) -
Knapp M. F.,
Linden R. J.,
Mary D. A. S. G.,
Pearson M. J.
Publication year - 1981
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.1981.sp002577
Subject(s) - bradykinin , angiotensin ii , diuresis , medicine , stimulation , diuretic , endocrinology , angiotensin receptor , renin–angiotensin system , blockade , chemistry , atrium (architecture) , receptor , pharmacology , kidney , blood pressure , atrial fibrillation
The diuretic response to stimulation of left atrial receptors, by distending balloons located either at the pulmonary vein‐left atrial junctions or in the body of the left atrium, was studied during blockade of the generation of angiotensin II using a continuous infusion of angiotensin converting enzyme inhibitor, SQ 14,225, in anaesthetized dogs. Despite blockade of angiotensin conversion, known also to potentiate the activity of bradykinin, a diuretic response was obtained in each dog; the response was similar to that observed in dogs without blockade of angiotensin conversion. Angiotensin II and bradykinin did not significantly influence the rate of secretion of Malpighian tubules of Rhodnius prolixus, which have been shown capable of detecting the blood‐borne agent known to mediate the diuretic response. It is concluded that neither angiotensin II nor bradykinin is likely to be the blood‐borne agent released by stimulation of atrial receptors.