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.
Drummond
R M
RM
Department of Physiology and Pharmacology, University of Strathclyde, Glasgow, Scotland.
Wadsworth
R M
RM
D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000502:physiology; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D002536:Cerebral Arteries / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology; D003331:Coronary Vessels / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology; D015232:Dinoprostone / Q000494:pharmacology; D066298:In Vitro Techniques; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D011450:Prostaglandin Endoperoxides, Synthetic / Q000494:pharmacology; D011651:Pulmonary Artery / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology; D011817:Rabbits; D012701:Serotonin / Q000494:pharmacology; D012756:Sheep; D013928:Thromboxane A2 / Q000031:analogs & derivatives / Q000494:pharmacology; D014662:Vasoconstrictor Agents / Q000494:pharmacology
D011450:Prostaglandin Endoperoxides, Synthetic; D014662:Vasoconstrictor Agents; D012701:Serotonin; D013928:Thromboxane A2; D011189:Potassium Chloride; D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D015232:Dinoprostone; D002118:Calcium; D009638:Norepinephrine