Calcium-induced pulmonary vasodilation: modification by meclofenamate and ouabain

Based on work with isolated arteries, we hypothesized that elevation of the extracellular calcium concentration would cause pulmonary vasodilation by stimulation of the Na+K+ATPase. If so, ouabain should inhibit the "membrane stabilizing" effect of a high calcium concentration. Addition of CaCl2 to the perfusate of rat isolated lungs to give a final concentration of 10(-2)M caused vasodilation when the lungs were vasoconstricted by KCl, angiotensin II or hypoxia. Ouabain addition to the perfusate increased pulmonary artery perfusion pressure and the magnitude of angiotensin II-induced vasoconstriction delayed vasodilation and transformed the CaCl2-induced vasodilation into rapid vasoconstriction accompanied by edema formation. Meclofenamate reduced the calcium-induced vasodilation suggesting that part of the high calcium vasodilation may be due to the action of a vasodilator prostaglandin. The vasodilation due to prostacyclin was blocked in lungs treated with ouabain. The results taken together suggest that high calcium vasodilation operates by mechanisms which may be prostaglandin-dependent and prostaglandin-independent, both of which can be blocked by ouabain.