Abnormal Cardiac Norepinephrine Storage in Isoproterenol-Treated Rats
Repeated administration of large doses of isoproterenol to rats produced myocardial enlargement and a fall in blood pressure. A defect in storage of norepinephrine (NE) was manifested by a decrease in endogenous NE, unimpaired uptake of 3H-NE, and an accelerated rate of loss of accumulated 3H-NE. This accelerated loss of 3H-NE was characterized by a more rapid disappearance of 3H-NE from the granular or microsomal than from the supernatant NE fraction. The increased rate of loss of 3H-NE could be reversed by treatment with a ganglionic blocking agent, chlorisondamine, by salt restriction and mercurial diuresis, and by withholding isoproterenol treatment for 7 days. The NE storage defect resembled that previously described in the hearts of rats made hypertensive by administration of desoxycorticosterone and NaCl. It is possible that the NE storage defect in the hearts of isoproterenol-treated rats is the result of a combination of changes in sympathetic nervous activity and altered neuronal electrolytes.
- DOCA and salt hypertension
- systolic blood pressure
- uptake and binding of 3H-norepinephrine
- myocardial enlargement
- Accepted October 18, 1968.
- © 1968 American Heart Association, Inc.