Juxtaglomerular Cells in CCl 4 -Treated Experimental Hypertension. ∗

Abstract

Summary

Renal and DCA hypertension was produced in rats, and blood pressure was then reduced to normal levels with CCl₄ injections. The juxtaglomerular (JG) index of these Sprague-Dawley rats was determined. After CCl₄ treatment of the renal hypertensive animals, no significant decline in JG granulation appeared as the blood pressure fell to normal. In the DCA hpertensive and the normotensive rats, CCl₄ induced normotension was accompanied by a large increase in granulation. It is thus apparent that the blood pressure decline induced by CCl₄ is not accompanied by any decrease in renal renin secretion. DCA hypertensive rats rendered normotensive by CCl₄ treatment exhibit a normal blood pressure in combination with a high JG index. This paradoxical situation may be the experimental analogue of the clinical syndrome described by Bartter, and attributed by him to an unknown defect in the renin-angiotensin-aldosterone secreting mechanism. Experiments published elsewhere, suggest that, in our experiments, the defect is caused by an inhibition of the enzyme converting angiotensin I to angiotensin II, so that the normal feed back to the JG cell is prevented.