Felodipine and vasomotion physiology

This study concerns the investigation of felodipine's influence on some parameters of vasomotion physiology. Felodipine is a new generation 1,4 dihydropyridine (1,4 DHP) Ca(2+)-entrance blocker with marked vascular selectivity. It was found that felodipine 1-10 microM presents a Ca2+ entrance-blocking activity when the bovine aortic smooth muscle is normal or stimulated by K+ 65.4 mM or the alpha-adrenoceptor agonist phenylephrine 1 microM. The same action is observed after nifedipine, a first-generation 1,4 DHP derivative with less angioselectivity in clinical practice. It was also found that felodipine 1-10 microM antagonizes the contraction of the bovine aortic ring that is induced by phenylephrine 10 microM or KCl 65.4 mM. On the contrary, felodipine 1-10 microM increases the contraction of the rat aortic ring that is induced by the same substances. It is known that some 1,4 DHP derivatives that are Ca2+ activators can also behave as Ca2+ blockers and that their final action is dependent upon membrane potential. Now it is also proved that the kind of animal species may also influence the action of the 1,4 DHP derivatives. It was finally found that felodipine increases the catecholamine stores of the sympathetic nerve terminal at the mouse heart (H) and liver (L). Obtained values were as following: control 15.00 +/- 7.7 (H) and 17.72 +/- 3.5 (L). Felodipine 54.50 +/- 4.9 (H) and 41.54 +/- 10.4 (L). Since catecholamine stores depend on secretion (Ca(2+)-dependent) and reabsorption (mostly Na(+)-dependent) rates, the increase after felodipine may be attributed to a decreased secretion due to a Ca2+ entry inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)