Comparison of the effects of pressor and depressor agents and influences on pulmonary and systemic pressures of normotensive and hypertensive subjects

Abstract

The comparative effects on the systemic and pulmonary arterial and capillary pressures of various pressor and depressor agents, including angiotonin, and psychogenic pressor influences have been studied. These measurements have been made on eleven patients with normal blood pressures and eleven patients with essential hypertension. Epinephrine, norepinephrine, Methedrine, ephedrine and angiotonin produced an elevation of systemic, pulmonary arterial, and pulmonary capillary pressures. The PA m-PC m gradient was not significantly changed as a result of any of the agents used. We interpret this to be due to either pulmonary vascular constriction beyond the tip of the catheter, pulmonary venous constriction, or both, rather than to an increased pulmonary blood volume secondary to left ventricular failure. We particularly wish to emphasize that angiotonin elevates the pulmonary artery and capillary pressures. It is further emphasized that pulmonary artery pressure in essential hypertension is normal. Pitressin does not cause an elevation of pulmonary artery pressure in either normotensive or hypertensive patients. All the depressor agents used caused a decrease in the systemic and pulmonary arterial pressures in both normotensive and hypertensive subjects. With the exception of Pitressin, the systemic and pulmonary arterial systems reacted similarly to both pressor and depressor drugs. The data presented do not support the concept that essential hypertension is due to angiotonin or epinephrine-like substances. The possibility that a humoral substance may cause essential hypertension is supported by the effects of Pitressin which causes selective elevation of systemic arterial pressure. The selective systemic hypertension produced under hypnosis is consistent with a possible central neurogenic mechanism for producing essential hypertension.