Contribution of vasopressin to vasoconstriction in patients with congestive heart failure: Comparison with the renin-angiotensin system and the sympathetic nervous system

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Ten patients with advanced congestive heart failure were treated with an arginine vasopressin VIantagonist during hemodynamic monitoring to determine the contribution of vasopressin to vasoconstriction in this disorder. The vasopressin antagonist caused a decrease in systemic vascular resistance in the three patients whose plasma vasopressin was greater than 4.0 pg/ml (average for the group was 2.4 ± 0.6). Plasma vasopressin concentration correlated with the percent decrease of systemic vascular resistance (r = 0.70, p < 0.025), serum sodium (r = 0.72, p < 0.02) and serum creatinine (r = 0.85, p < 0.005). To compare the relative roles of vasopressin, the renin-angiotensin system and the sympathetic nervous system, these patients also received captopril and phentolamine. Captopril decreased systemic vascular resistance by 20% (p < 0.05), mostly in patients with high plasma renin activity. Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 ± 5.7) and correlated with serum sodium (r = 0.77, p < 0.025), serum creatinine (r = 0.73, p < 0.025) and right atrial pressure (r =0.67, p < 0.05). Phentolamine decreased systemic vascular resistance in all patients (average 34%, p < 0.01), but the decrease did not correlate with the pretreatment norepinephrine concentration. Norepinephrine levels were elevated in all patients (694 ± 110 pg/ml) and correlated with baseline stroke volume index (r =0.75, p < 0.025) and plasma renin activity (r =0.67, p < 0.05).

It is concluded that vasopressin and the renin-angiotensin system each contribute to systemic vasoconstriction in some patients with heart failure, whereas the sympathetic nervous system consistently contributes to vasoconstriction in these patients.

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Assistance in data organization and analysis was provided by the CLINFO data management and analysis system at Brigham and Women's Hospital, Boston, supported by General Clinical Research Center Grant 5 MO 1 RROO888-IOCLR.