OBSERVATIONS UPON THE PRESSOR SUBSTANCE CAUSING THE RISE IN BLOOD PRESSURE FOLLOWING THE TERMINATION OF TEMPORARY, COMPLETE RENAL ISCHEMIA
- 31 October 1940
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Legacy Content
- Vol. 131 (1) , 18-26
- https://doi.org/10.1152/ajplegacy.1940.131.1.18
Abstract
The previous inj. of piperidomethyl-3-benzodioxane (933F) does not prevent the rise in blood pressure which results from the reestablishment of the circulation in the completely ischemic kidney, proving that the substance responsible for this rise is not of an epinephrine-like nature. The pressor reaction which follows the termination of complete renal ischemia is greatly reduced or abolished in animals rendered tachyphylactic to renin. This proves that the substance causing the rise in blood pressure is renin or a pressor principle having similar properties of tachyphylaxis. The pressor effect of extracts of completely ischemic kidneys is greater than that of extracts of control normal kidneys.This publication has 2 references indexed in Scilit:
- ANGIOTONIN-ACTIVATOR, RENIN- AND ANGIOTONIN-INHIBITOR, AND THE MECHANISM OF ANGIOTONIN TACHYPHYLAXIS IN NORMAL, HYPERTENSIVE, AND NEPHRECTOMIZED ANIMALSThe Journal of Experimental Medicine, 1940
- THE HEMODYNAMIC EFFECT OF THE DIOXANE DERIVATIVE 933 F ON TRAINED UNANESTHETIZED NORMAL AND RENAL HYPERTENSIVE DOGS AND ITS EFFECT ON THE PRESSOR ACTION OF RENINAmerican Journal of Physiology-Legacy Content, 1939