Hemodynamic changes and renal plasma flow in early heart failure: implications for renin, aldosterone, norepinephrine, atrial natriuretic peptide and prostacyclin.

Vasoconstrictory and vasodilatory hormone systems may be important in the regulation of peripheral vascular resistance and renal hemodynamics in the early phase of heart failure. The activity of the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous activity, and, as possible counterregulating systems, the activity of prostacyclin and atrial natriuretic peptide (ANP) were studied in 6 conscious dogs during the first 4 days of congestive heart failure in relation to hemodynamic changes and renal plasma flow. Congestive heart failure was induced by rapid right ventricular pacing, which caused a considerable decrease of cardiac output (-38%; p less than 0.05), oxygen saturation of the mixed venous blood (-13%; p less than 0.05), and mean arterial pressure (-24 mm Hg; p less than 0.05) on the 4th day. Mean pulmonary arterial pressure and mean pulmonary capillary wedge pressure increased (+4 mm Hg; p less than 0.05 and +7 mm Hg, respectively; p less than 0.05). Renal plasma flow was slightly reduced (N.S.), renal vascular resistance did not change. Peripheral vascular resistance showed a significant increase only on the 1st day. Sympathetic nervous activity was stimulated (from 175 +/- 31 pg/ml to 391 +/- 100 pg/ml; p less than 0.05), while plasma renin concentration was significantly suppressed on the 4th day (from 3.3 +/- 0.4 ngAI/ml/h to 1.9 +/- 0.5 ngAI/ml/h; p less than 0.05), and plasma aldosterone levels were decreased (from 108 +/- 12 pg/ml to 76 +/- 12 pg/ml; p less than 0.05). ANP increased 3-fold (p less than 0.05) and 6-keto-prostaglandin F1 alpha increased in 4 out of 6 dogs.(ABSTRACT TRUNCATED AT 250 WORDS)