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

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Abstract
Vasoconstrictory and vasodilatory hormone systems may be important in the regulation of peripheral vascular resistance and renal hemodynamics in the carly 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<0.05), oxygen saturation of the mixed venous blood (−13%; p<0.05), and mean arterial pressure (−24 mm Hg; p<0.05) on the 4th day. Mean pulmonary arterial pressure and mean pulmonary capillary wedge pressure increased (+4 mm Hg; p<0.05 and +7 mm Hg, respectively; p<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<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<0.05), and plasma aldosterone levels were decreased (from 108±12 pg/ml to 76±12 pg/ml; p<0.05). ANP increased 3-fold (p<0.05) and 6-keto-prostaglandin F1 alpha increased in 4 out of 6 dogs. Since ANP is known to inhibit renin release and aldosteronc production, the suppressed RAAS may be an effect of the highly elevated plasma levels of ANP in the early phase of heart failure. The depressor systems such as ANP and prostacyclin may balance the stimulated sympathetic system, resulting in no change of renal blood flow and renal vascular resistance and preventing a considerable increase of peripheral vascular resistance.