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What is the contribution of circulating catecholamines and angiotensin II to hindquarters' vascular resistance in guinea pigs with 30-day pulmonary artery constriction?
What is the contribution of circulating catecholamines and angiotensin II to hindquarters' vascular resistance in guinea pigs with 30-day pulmonary artery constriction?
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In a guinea pig model of right ventricular hypertrophy, increased humoral regulation of vascular resistance is primarily driven by circulating catecholamines and augmented vasoconstrictor responsiveness to norepinephrine.
In an earlier study of guinea pigs with constriction of the pulmonary artery (PA) for 30 days, hindquarters' vascular resistance was maintained primarily by humoral mechanisms. In the present study, we investigated the contribution of circulating catecholamines, angiotensin II, and other constrictor stimuli to hindquarters' vascular resistance by observing vasodilator responses to specific competitive antagonists. Pressure-flow curves indicated vascular resistances in isolated, perfused, sympathectomized hindquarters of anesthetized guinea pigs. Phentolamine produced significantly greater (P less than 0.05) vasodilatation in animals with constriction of pulmonary artery than in sham animals [Sar1-Ala8]angiotensin II produced no vasodilation in either group. After alpha-adrenergic blockade, papaverine produced similar vasodilatation and similar final perfusion pressures in both groups. It appears that circulating catecholamines and augmented vasoconstrictor responsiveness to norepinephrine are totally responsible for the increased humoral regulation of vascular resistance in this experimental model of right ventricular hypertrophy.
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McNamara et al. (1979) studied this question.
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