Abstract
Summary
During restoration of normotension by giving CCI4 to experimental renal and post-DCA hypertensive rats, serum incubated with renin yields predominantly angiotensin I. This suggests a deficit in hepatogenous converting enzyme. However, incubation of post-CC14 normotensive serum with normal serum containing this enzyme still yielded angio-tensins I and II. This suggests that CCI4 liver injury is associated with formation of a substance that inhibits circulating converting enzyme. Adrenal failure, angiotensinase excess and decreased pressor responsiveness to angiotensin do not participate in the pressure lowering effect of CCI4.
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