Possible mechanism of high calcium-induced relaxation of rabbit thoracic aorta.
1. The present study examined the effects of various agents on high calcium-induced relaxation of the rabbit thoracic aorta precontracted by phenylephrine (0.1 microM) or KCl (30 mM). 2. The vascular smooth muscle relaxation caused by high calcium was not changed in the presence of endothelium, glibenclamide (3 microM), TEA (5 mM), verapamil (1 microM), lidocaine (0.1 mM) and vanadate (0.1 mM). 3. In the presence of ouabain (0.1 mM) or potassium-free medium, high calcium-induced relaxation was completely abolished. 4. When rings were precontracted by high concentrations of phenylephrine (1 microM, 10 microM) and KCl (30 mM, 45 mM, 60 mM), calcium-induced relaxation was gradually decreased. 5. A low concentration of calcium ionophore A-23187 (0.1 microM) did not change calcium-induced relaxation, but A-23187 at a high concentration (1 microM) depressed this relaxation. 6. These results suggest that Na-K-ATPase activation could be responsible for high calcium-induced relaxation.
Yildirim
S
S
Department of Pharmacology, Medical Faculty of Ankara University, Turkey.
Kamoy
H
H
Demirel-Yilmaz
E
E
D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects* / Q000502:physiology; D002118:Calcium / Q000494:pharmacology*; D015220:Calcium Channels / Q000502:physiology; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D015221:Potassium Channels / Q000502:physiology; D011817:Rabbits; D015222:Sodium Channels / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology*; D014664:Vasodilation
D015220:Calcium Channels; D015221:Potassium Channels; D015222:Sodium Channels; D000254:Sodium-Potassium-Exchanging ATPase; D002118:Calcium