The role of calcium in modulating the reactivity of the smooth muscle cells during ischemia/reperfusion. Part 1.

Background: Calcium ions regulate the function of cells in many ways, acting as first messengers of intercellular information and second messengers of intracellular information. Changes in cytoplasmic calcium levels depend on calcium influx from the extracellular space or calcium release from cellular stores. Increase in calcium ion concentration takes place in pathological situations, such as ischemia. In the present study the roles of calcium and G protein in contraction induced by angiotensin II (agonist of the metabotropic receptor AT1), phenylephrine (agonist of alpha1-adrenergic metabotropic receptor), and Bay K8644 (a calcium channel agonist) after ischemia/reperfusion were investigated.

Material/methods: Experiments were performed on perfused male Wistar rats' tail arteries. Contraction induced by angiotensin II, phenylephrine, and Bay K8644 mediated by intracellular or extracellular calcium after ischemia/reperfusion and in the presence of the blocker of G protein Bordetella pertussis toxin (P 7208) was analyzed.

Results: Ischemia reduced while reperfusion augmented the response of vascular smooth muscle cells to angiotensin II and phenylephrine, but they did not change the effects of Bay K8644. P 7208 decreased the effects of phenylephrine mediated by intracellular and extracellular calcium and reduced the reactions of angiotensin II mediated only by intracellular calcium, but did not change the effects of Bay K8644.

Conclusions: Ischemia/reperfusion modulates vascular contraction induced by angiotensin II and phenylephrine. Both intracellular and extracellular calcium ions mediate the contraction induced by angiotensin II and phenylephrine. The results suggests that G protein modulates the effects of angiotensin II mediated by intracellular calcium ions while it plays a role in the reactions of phenylephrine mediated by calcium coming from both sources, intracellular and extracellular.