Contraction of the sheep middle cerebral, pulmonary and coronary arteries initiated by release of intracellular calcium.

The aim of the study was to compare contraction initiated by intracellular Ca2+ release in the middle cerebral, coronary and pulmonary arteries of the sheep. With all three arteries from the sheep, incubation in Ca(2+)-free physiological salt solution (PSS) reduced agonist-induced contraction much more than occurred with the rabbit aorta. The intracellular Ca2+ store appeared to be of limited capacity, since contraction was transient in Ca(2+)-free conditions with most agonists. In the middle cerebral artery, contraction in Ca(2+)-free conditions was much reduced if a previous contraction had been obtained (for 5-hydroxytryptamine, 5-HT, from 11 +/- 4 to 1 +/- 0.5% of control contraction in 2.5 mM Ca2+), suggesting that the previous contraction had partly discharged the intracellular Ca2+ store. Contraction was less affected in the pulmonary artery and almost unaffected in the coronary artery (for 5-HT, from 15 +/- 1 to 11 +/- 1%) by a previous contraction in Ca(2+)-free conditions. Rings prepared from small branches of the pulmonary and coronary arteries were affected by Ca2+ deprivation in a similar manner to large diameter pulmonary and coronary artery rings. In Ca(2+)-free PSS, contraction induced by prostaglandin E2 was almost eliminated (3 +/- 1% of control contraction in 2.5 mM Ca2+), contractions induced by 5-HT and noradrenaline were reduced, and contraction induced by the thromboxane mimetic U46619 was least affected (up to 73 +/- 8%). Increasing agonist concentration from EC50 to the maximally effective concentration raised the percentage contraction remaining in the middle cerebral artery (for noradrenaline from 7 +/- 2% to 12 +/- 3%) but not in the pulmonary artery (for noradrenaline from 22 +/- 2% to 24 +/- 6%). The present study has revealed notable differences, in coupling to intracellular Ca2+ release between the three vascular territories studied.