The role of adrenergic receptor blockade in serotonin‐induced changes in the pulmonary circulation.

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Abstract
In dogs, i.v. injection of serotonin caused a rise in pulmonary artery pressure and pulmonary arteriocapillary resistance that persisted even after .alpha.- and .beta.-adrenergic receptor blockade; pulmonary venous resistance also increased, but this was abolished by pretreatment with either propranolol or phenoxybenzamine. The injection of serotonin into the ascending aorta produced an immediate rise in systemic, pulmonary arterial and pulmonary venous pressures and pulmonary venous resistance. After phenoxybenzamine, the rise in systemic and pulmonary arterial pressures remained unchanged, but previously observed increases in pulmonary venous pressure and resistance were blocked. In contrast, propranolol failed to abolish the rise in pulmonary venous resistance after serotonin injection into the ascending aorta. The vasoconstrictor effect attributed to i.v. injected serotonin on the arterial side of the pulmonary circulation is apparently independent of the known sympathetic pathways. The data suggest that the pulmonary venoconstriction induced by i.v. serotonin is of reflex origin, abolished by .alpha. and .beta. receptor blockade, but the efferent arm of the reflex pulmonary venoconstriction following injection of serotonin into the ascending aorta is mediated via .alpha.-adrenergic receptors.