1. Pertussis toxin inactivates Gi‐protein, which mediates the inhibitory effects of receptors on adenylate cyclase. The effects of the toxin on endothelium‐dependent and independent relaxations were determined in porcine coronary arteries. 2. Arterial rings (with and without endothelium) were suspended for isometric tension recording in organ chambers filled with modified Krebs‐Ringer bicarbonate solution (maintained at 37 degrees C, gassed with 95% O2 and 5% CO2). 3. Incubation of the tissues with pertussis toxin (100 ng/ml for 60 min) virtually abolished the endothelium‐dependent relaxations produced by the alpha 2‐adrenergic agonist, UK 14304, and by 5‐hydroxytryptamine. Endothelium‐dependent relaxations to thrombin and to aggregating platelets were markedly reduced, whereas those produced by bradykinin were only minimally affected. Endothelium‐dependent responses produced by the calcium ionophore (A23187) and by adenosine diphosphate were not altered by pertussis toxin. 4. Pertussis toxin did not affect the direct, endothelium‐independent relaxations produced by nitric oxide, or by adenosine diphosphate. 5. These experiments demonstrate that pertussis toxin interferes with the release of endothelium‐derived relaxing factor(s) evoked by certain, but not all, endothelial activators. The release of endothelium‐derived relaxing factor(s) may occur through different pathways involving Gi‐protein‐dependent and independent mechanisms.
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