Midbrain‐renal dopaminergic axis and control of venous capacitance: Pathological and therapeutic significance in hypertension

Abstract

AbstractAcute intravenous infusion of methyldopa in anesthetized normotensive dogs produced a hemodynamic profile which indicates that the decrease in arterial blood pressure occurs secondary to venous pooling. The methyldopa‐mediated venous pooling is blocked by prior treatment with indomethacin. Both acute administration of methyldopa and L‐dopa mediate venous pooling from the midbrain as reactivity to the carotid occlusion reflex is intact. The venous pooling occurs in the cutaneous venous capacitance bed. Chronic treatment with methyldopa causes venoconstriction with a secondary increase in cardiac output. The venoconstriction is accompanied by a significant decrease in plasma renin activity without any effect on plasma aldosterone secretion, cortisol secretion, or serum electrolytes (Na+, K+, Cl−). Renal denervation abolished both the chronic methytldopa venoconstriction and endocrine effects; only venodilation was evident. Chronic treatment with L‐dopa caused only venodilation with a significant increase in plasma aldosterone secretion, but without an effect on plasma renin activity, cortisol secretion, or serum electrolyte values. The primary neuroeffector in the kidney which communicates with the midbrain venomotor center appears to be mediated by a prostaglandins. It is postulated that the alterations in plasma renin activity and aldosterone secretion reported in this investigation are mediated by the brain isorenin‐angiotensin system since alterations in plasma renin activity and aldosterone secretion do not occur in parallel, cortisol secretion is not altered, and the blood pressure‐pressor response to angiotensin I and II is not blocked.