Circulation, Vol 78, 376-381, Copyright © 1988 by American Heart Association
GP Hodsman, M Kohzuki, LG Howes, E Sumithran, K Tsunoda and CI Johnston
In chronic cardiac failure, various neurohumoral mechanisms are activated
to sustain blood volume, blood pressure, and organ perfusion. Using the
coronary artery ligation model of heart failure in the rat, we have
measured changes in vasoactive hormone secretion and related these changes
to salt and water status during a 1-month period. When compared with
controls, rats with infarction had a marked rise in plasma atrial
natriuretic peptide (294 +/- 59 vs. 79 +/- 10 pg/ml, p less than 0.001)
although there was no increase in total exchangeable body sodium. Plasma
renin activity and plasma aldosterone concentrations were the same for both
rats with infarction and controls. Similarly, there were no significant
differences in plasma arginine vasopressin, plasma osmolality, or plasma
sodium concentration in rats with infarction. Ventricular norepinephrine
levels were reduced in animals with infarction (p less than 0.01). Plasma
atrial natriuretic peptide levels were raised in this model of chronic left
ventricular failure. However, there was no salt retention and little
stimulation of the renin-angiotensin-aldosterone system or vasopressin. The
results suggest that high circulating atrial natriuretic peptide levels may
prevent or limit salt and water retention, either directly or indirectly,
by inhibiting the renin-angiotensin-aldosterone system.
ARTICLES
Neurohumoral responses to chronic myocardial infarction in rats
University of Melbourne Department of Medicine, Austin Hospital, Heidelberg, Australia.
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