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|Title:||Neurohumoral responses to chronic myocardial infarction in rats.||Austin Authors:||Hodsman, G P;Kohzuki, M;Howes, L G;Sumithran, E;Tsunoda, K;Johnston, Colin I||Affiliation:||University of Melbourne Department of Medicine, Austin Hospital, Heidelberg, Australia||Issue Date:||1-Aug-1988||Publication information:||Circulation; 78(2): 376-81||Abstract:||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.||Gov't Doc #:||2899463||URI:||http://ahro.austin.org.au/austinjspui/handle/1/12886||Journal:||Circulation||URL:||https://pubmed.ncbi.nlm.nih.gov/2899463||Type:||Journal Article||Subjects:||Aldosterone.blood
Atrial Natriuretic Factor.blood
Rats, Inbred Strains
|Appears in Collections:||Journal articles|
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