Role of acetylcholine and calcium ions in three vascular contraction models: Angiotensin II, phenylephrine and caffeine.

The aim of this study was to determine the role of acetylcholine and calcium ions in modulating the vascular contraction induced by angiotensin II (ANG II), phenylephrine (PHE) and caffeine. The study was performed on perfunded Wistar rat tail arteries. The contraction caused by ANG II, PHE and caffeine with the participation of intracellular [in free physiological salt solution (FPSS)] and extracellular [in physiological salt solution (PSS), after emptying the cellular stores] pools of calcium ions and the addition of L-NNA (NOSe inhibitor) or ODQ (GC inhibitor) was studied. Then the effect of acetylcholine on the contraction responses was analyzed. ANG II, PHE and caffeine induced an increase in perfusion pressure in PSS and FPSS. Acetylcholine reduced the contraction resulting from the presence of ANG II and PHE, but not caffeine. L-NNA and ODQ abolished the spasmolytic action of acetylcholine. Both pools of calcium ions mediated the action of ANG II and PHE, and caffeine induced the contraction with the participation of calcium released from intracellular stores. The spasmolytic effect of acetylcholine on responses stimulated by ANG II and PHE indicates the participation of nitric oxide in modulating the reactivity of the arteries on the studied agonists of the metabotropic receptors. No observed acetylcholine effect on caffeine suggests that the pathway associated with nitric oxide does not interfere with the contraction induced by the ryanodin receptor.