Cardiovascular Effects of Renin. ∗

Abstract

Renin, a pressor protein from the kidney which has been suggested as a cause of clinical hypertension, raises the blood pressure largely through generalized peripheral vasoconstriction. 1 , 2 During the pressor response, no significant changes have been observed in the skin temperature 3 , 4 nor cardiac output 5 of animals. Hessel 6 reported the production of permanent hypertension in rabbits by repeated intravenous injections of pig renin.

The effects of renin on human beings have not been extensively studied but it has been shown that hog renin is ineffective 7 , 8 while human renin raises the blood pressure. 7 Angiotonin, formed by the action of renin on blood globulins, has been shown to increase the arterial and venous pressure and to decrease the heart rate, cardiac output and blood flow in the limbs in human beings. 9 , 10

Methods. In the present investigation extracts of human and hog kidneys were prepared and assayed by methods described elsewhere. 11 , 12 A rabbit unit has been defined as the amount of renin (expressed as micrograms nitrogen) per kilogram of body weight which would cause an average rise in arterial blood pressure of 30 mm mercury. 11 A human unit is similarly defined as the amount of renin per kilogram of body weight required to produce in human beings a rise of 30 mm mercury in systolic arterial pressure. In unnesthetized dogs the blood pressure was measured by direct arterial puncture. In human beings the blood pressure was measured by the auscultatory method, blood flow in the hand or forearm by plethysmographic methods, 13 the venous pressure by the direct method of Moritz and von Tabora, 14 and cardiac output by the acetylene method. 15 All extracts were injected intravenously, the total dose being given during a period of one minute.