Tranylcypromine induced hypertension is not mediated by the inhibition of prostacyclin synthesis.
Tranylcypromine (TCP) is a monoamine oxidase inhibitor used extensively in the treatment of patients with reactive depression. Hypertensive crisis can complicate drug therapy, but the mechanism through which TCP causes high blood pressure is unknown. The present study was undertaken because recent investigations have shown that TCP can inhibit production of a potent vasodilator hormone, prostacyclin (PGI2), by  blood vessels, possibly explaining the mechanism of pressor effects by the drug. Heart rate, left atrial, pulmonary artery and aortic pressures were monitored in dogs under control conditions and continuously following the IV infusion of TCP at the rate of 1 mg/kg over a period of one minute. Right femoral and the left internal mammary arteries were obtained during the control period and the left femoral and right internal mammary arteries resected between 6 and 30 minutes following drug infusion for PGI2 studies. Concentrations of the drug that caused significant elevation of the mean systemic pressure to 203 +/- 8 mmHg had no inhibitory effect on PGI2 production. Therefore, the influence of TCP on the hemodynamic parameters does not appear to be mediated through the inhibition of vascular PGI2 synthesis.
D000818:Animals; D001158:Arteries / Q000378:metabolism; D001792:Blood Platelets / Q000032:analysis; D004285:Dogs; D011464:Epoprostenol / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D006439:Hemodynamics / Q000187:drug effects; D006973:Hypertension / Q000139:chemically induced*; D011448:Prostaglandin Antagonists; D014191:Tranylcypromine / Q000009:adverse effects*
D011448:Prostaglandin Antagonists; D014191:Tranylcypromine; D011464:Epoprostenol