Inhibition of hypoxic pulmonary vasoconstriction by calcium antagonists in isolated rat lungs.

摘要: The role of a transmembrane calcium influx in hypoxic pulmonary vasoconstriction was studied isolated, blood-perfused, rat lungs. We reasoned that, if the extracellular mediated mechanism, pressor responses to alveolar hypoxia (2.5% O2) would be susceptible inhibition by antagonists verapamil (2 X 10(-5) 2 10(-1) mM) and SKF 525A (2.6 260 mM). Susceptibility these contrasted that elicited humoral vasoconstrictors angiotensin II(1 or 0.5 mug) prostaglandin F2alpha (10 myg). Since neither saralasin (0.5 muM), competitive antagonist II, nor meclofenamate (6.8 an inhibitor synthesis, depressed responses, it concluded transmitters were not directly involved therefore served as independent reference agonists. order susceptibility greater than II F2alpha. also reduced more readily those II. both suggested mechanism critically dependent on calcium. Mediation response this type excitation-contraction coupling is consistent with idea has direct depolarizing effect vascular smooth muscle. It provides unifying explanation for various agents have depressant stabilizing actions membranes addition other pharmacological effects.