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  • Title: Attenuation of pressor responses to arginine vasopressin in right-sided congestive heart failure.
    Author: Stone CK, Imai N, Sladek CD, Liang CS.
    Journal: Am J Physiol; 1990 Jun; 258(6 Pt 2):H1882-8. PubMed ID: 2360676.
    Abstract:
    Although arginine vasopressin (AVP) is elevated in heart failure, inhibition of the vasopressinergic V1-receptor produces minimal changes in blood pressure. To determine whether the V1 vasoconstrictor effect is attenuated in heart failure, we randomly administered three increasing doses of AVP and methoxamine intravenously to 11 dogs with right-sided congestive heart failure (RHF) and 7 sham-operated dogs. Plasma AVP was elevated in RHF (21 +/- 3 pg/ml) compared with sham-operated dogs (3.8 +/- 0.6 pg/ml). While the pressor response to methoxamine was similar in the two groups, AVP caused a smaller increase in mean aortic pressure in RHF dogs than sham-operated dogs. To determine whether the difference in the pressor response to AVP was caused by greater reflex withdrawal of the sympathetic activity in RHF than sham-operated dogs, we also administered AVP after these animals had been pretreated with prazosin and propranolol. Adrenoceptor blockade exaggerated the pressor response to AVP; however, the increase in mean aortic pressure was still smaller in RHF than sham-operated dogs. The diminished pressor response in adrenoceptor-blocked RHF dogs was associated with a smaller increase in total peripheral vascular resistance compared with similarly treated sham dogs. Thus, although the pressor response to AVP was offset by baroreflex activation, the attenuated pressor effect of AVP in heart failure cannot be explained by sympathetic withdrawal alone. AVP probably exerts a smaller direct vasoconstrictor effect when the vasopressinergic system is chronically activated in heart failure.
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