Abstract
Renin, the so-called “renal pressor substance” is vaso-inactive unless permitted to interact with a pseudoglobulin present in blood plasma, which has tentatively been denominated “renin-activator.” 1 The interaction of renin and renin-activator yields a crystallizable, dialyzable, thermostable product, angiotonin. 2 Intravenous injections of this substance in normal animals cause sharp pressor responses which diminish slowly with repeated injections. Nephrectomized animals are highly sensitive to the pressor action of this substance and do not show tachyphylaxis with repeated injections. 3 Slow intravenous infusions of angiotonin in dogs increase arterial pressure and cause renal vasoconstriction, predominantly of the glomerular efferent arterioles, but do not alter cutaneous temperatures. 4 The effects of angiotonin infusion therefore simulate those of renin, 5 although they are not as long sustained.
The present report is concerned with observations of blood pressure and renal hemodynamics during single injections and intravenous infusions of angiotonin into human beings. Electrocardiographic records and observations of venous pressure and skin temperature were obtained in some instances. These, together with further observations of renal functional changes will form part of a subsequent report.
Arterial pressure was determined by auscultation. Effective renal blood flow was calculated from the hematocrit ratio and apparent plasma diodrast clearance and is equal to approximately 90% of total renal blood flow. 6 Diodrast was determined in blood and urine by a modification of the method of White and Rolf 7 and inulin by the method of Corcoran and Page. 8 A mixture of diodrast, phenol red and inulin in 0.9% NaCl was given intravenously at a slow rate during the observations of renal clearances. 9
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