NEUROHUMORAL REGULATION OF THE PULMONARY CIRCULATION DURING CIRCULATORY HYPOTENSION IN CONSCIOUS DOGS

We investigated the effects of circulatory hypotension (HYPO) on the l eft pulmonary vascular pressure-flow relationship in chronically instr umented conscious dogs and the role of five neurohumoral mechanisms in either mediating or modulating the response to this stimulus. HYPO wa s induced by acute (approximately 15-min) inflation of a hydraulic occ luder implanted around the thoracic inferior vena cava, which decrease d systemic arterial pressure to approximately 55 mmHg. HYPO resulted i n active pulmonary vasoconstriction (53-66%; P < 0.01) in intact consc ious dogs. Sympathetic alpha1-adrenoreceptor block reduced (P < 0.01) the magnitude of HYPO-induced pulmonary vasoconstriction by 91-99%. Ne ither sympathetic beta-adrenoreceptor block nor cholinergic muscarinic receptor block had any significant effect on the magnitude of HYPO-in duced pulmonary vasoconstriction. Surprisingly, angiotensin II recepto r block increased (P < 0.05) HYPO-induced pulmonary vasoconstriction b y 69-91%. In contrast, arginine vasopressin V1-receptor block reduced (P < 0.05) HYPO-induced pulmonary vasoconstriction by 34-41%. These re sults indicate that the pulmonary circulation of intact conscious dogs is actively regulated by three distinct neurohumoral mechanisms durin g HYPO. Sympathetic alpha1-adrenoreceptor activation is the primary me diator of HYPO-induced pulmonary vasoconstriction. Angiotensin II and arginine vasopressin exert opposing pulmonary vasodilator and vasocons trictor effects during HYPO, whereas sympathetic beta-adrenoreceptor a nd cholinergic muscarinic receptor activation do not appear to modulat e the pulmonary vascular response to HYPO.