The role of extracellular calcium in drug-induced contractile responses of the rabbit pulmonary artery.

Concentration-response relationships in rabbit pulmonary arteries to norepinephrine (NE), histamine (H) and potassium chloride (KC1) were determined in Ringer's solution containing 2.4, 1.2, 0.6, 0.1 or OmM CaCl2. The EC50 for NE and H did not vary with the extracellular calcium concentrations [Ca2+ ext], but the EC50 for KC1 was greatly increased in 0.1mM Ca2+. Maximum isometric contractile force in response to NE and H was significantly decreased in OmM Ca2+. Addition of 0.1 mM EGTA to the Ca2+-free solution further depressed the responses. KC1-induced maximum tension was decreased in 1.2mM, 0.6mM, 0.1mM and 0mM Ca2+. When a maximum concentration of NE (5 X 10(-5)M), H(5 X 10(-4)M) or KC1 (6 X 10(-2) was added to the bath the initial rapid phase of contraction induced by NE or H appeared to be dependent upon the release of internal Ca2+ from EGTA-sensitive and EGTA-resistant sites. The slow phase of contraction was dependent upon extracellular Ca2+. Both the fast and slow phase of contraction induced by KC1 (60 mM) was dependent upon extracellular Ca2+. In the presence of 0mM Ca2+ the tension response to NE (5 X 10(-5)M) was maintained, but the tension response to H (5 X 10(-4)M) was not maintained.