ENDOGENOUS ETA-RECEPTORS DO NOT MODULATE ACUTE HYPOXIC VASOCONSTRICTION

The hypothesis that endogenous endothelin (ET) via ET(A) receptors is one of the endothelium derived constricting factors (EDCF) contributin g to acute hypoxic pulmonary vasoconstriction (HPV) was tested using i solated pulmonary arterial rings derived from normoxic and chronically hypoxic rats and isolated perfused lungs (IPL). The effect of the two novel ET(A) receptor antagonists, BQ123 and FR139317, on the acute hy poxic presser response and the presser response to phenylephrine and a ngiotensinII (AII) were assessed. Neither ET(A) receptor antagonist al tered the presser response to hypoxic air and phenylephrine in isolate d pulmonary arterial rings from normoxic and hypoxic rats whereas the dose of the antagonists used was effective in suppressing the response to exogenously applied ET1. Therefore, we conclude that the ET/ET(A) receptor interaction does not play a role during acute HPV.