Extracellular and intracellular calcium sources mediating contractile responses of smooth muscle in bovine ovarian follicle and ovarian artery
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The relative importance of extracellular and intracellular calcium sources mediating smooth muscle contraction in ovarian follicle and ovarian artery was assessed in experiments on the influence of nifedipine, D-600, amrinone, diethylstilbestrol (DES), lanthanum and/or calcium removal on contractions induced by K+ depolarization, by noradrenaline, histamine and acetylcholine. The K+-induced response was biphasic in the ovarian artery but not in the ovarian follicle. The K+-induced contraction in both preparations was greatly inhibited by nifedipine (1 μM), D-600 (10 μM) and lanthanum (2 mM). Although both phases of the responses in the ovarian artery appeared to be completely dependent on extracellular calcium, phase I was significantly more sensitive to nifedipine than phase II. Incubation in calcium-free medium for 15 min almost abolished the K+-induced contraction. Noradrenaline- and histamine-induced contractions of ovarian follicle were essentially unaffected by nifedipine (1 μM) and D-600 (10 μM) whereas the noradrenaline-induced contraction in ovarian artery was inhibited significantly by D-600 (1 and 10 μM) but not nifedipine (1 μM). In calcium-free medium containing EGTA (1 mM) the responses of ovarian follicle to noradrenaline and histamine were reduced by 26 and 22% respectively. When preparations were stimulated with noradrenaline more than one in calcium-free medium, the contraction decreased progressively compared to time-matched controls. The response was 34% of the control after 50 min in calcium-free medium containing EGTA. In the ovarian artery the response obtained (6% of control) was significantly smaller (P < 0.05) than that in the follicle. Amrinone (100 μM) inhibited both noradrenaline- and K+-induced contractions to a similar degree (about 40%) in the follicle wall. The results indicate that agonist-induced responses of ovarian follicle and artery are mediated by the release of calcium from intracellular stores in addition to influx of extracellular calcium. In contrast, the K+-induced contraction seems to be totally dependent on extracellular calcium. The difference in sensitivity to nifedipine of the two phases of the K+ response in ovarian artery strongly suggests the presence of two different types of K+-activated calcium channels in this smooth muscle.
|Enheter & grupper|
Ämnesklassifikation (UKÄ) – OBLIGATORISK
|Tidskrift||European Journal of Pharmacology|
|Status||Published - 1987 dec 15|
|Peer review utförd||Ja|