Sıçan Izole Mezenter Arterinde Kalsiyumsuz Ortamda Elektriksel Alan Uyarısı Ile Elde Edilen Kasılmaların Mekanizmasının Incelenmesi
Özet
In the present study, we aimed to examine the effect of blockade of L-type calcium channels (LTCC) and in addition the removal of extracellular calcium, on EFS-induced relaxations in rings of rat mesenteric artery. EFS (30 V, 0.3 ms, 5 s, 0.5-8 Hz) applied to the tissues precontracted with phenylephrine caused relaxations which were markedly inhibited by nifedipine (100 nM) and tetraethylammonium (1 mM). Upon removal of calcium, EFS with the same stimulation parameters produced frequency-dependent transient contractions. Tetrodotoxin (1 μM), capsaicin (10 μM) and removal of endothelium did not alter these contractions suggesting that they were not neural in origin and endothelium-derived contracting factors were unlikely to be involved. However, they were markedly increased by BAY K 8644 (100 nM) and were inhibited by nifedipine (100 nM), indicating that activation of the LTCCs was essential. 2-APB (100 μM) significantly reduced, and high concentration of caffeine (20 mM) almost totally suppressed the contractions. When tissues incubated with thapsigargin (1 μM) and cyclopiazonic acid (20 μM) contractions significantly reduced as well. In the presence of U 73122 (10 μM) and Y 27632 (10 μM) responses were significantly reduced. These results suggest that in the absence of extracellular calcium EFS through membrane depolarization, evokes the opening of the LTCCs which subsequently leads to the release of calcium from internal stores via IP3 receptors, a phenomenon known as “calcium channel-induced calcium release”, to trigger vasoconstriction. That activation of LTCCs causes arterial relaxation or contraction depending on the calcium status apparently exemplifies how the same messenger fulfils opposing physiological functions in a given cell.
