FELODIPINE AND VASOMOTION PHYSIOLOGY

This study concerns the investigation of felodipine's influence on som e parameters of vasomotion physiology. Felodipine is a new generation 1,4 dihydropyridine (1,4 DHP) Ca2+-entrance blocker with marked vascul ar selectivity. It was found that felodipine 1-10 muM presents a Ca2entrance-blocking activity when the bovine aortic smooth muscle is nor mal or stimulated by K+ 65.4 mM or the alpha-adrenoceptor agonist phen ylephrine 1 muM. 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 muM antagonizes the c ontraction of the bovine aortic ring that is induced by phenylephrine 10 muM or KCl 65.4 mM. On the contrary, felodipine 1-10 muM increases the contraction of the rat aortic ring that is induced by the same sub stances. It is known that some 1,4 DHP derivatives that are Ca2+ activ ators 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 deriva tives. It was finally found that felodipine increases the catecholamin e 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 (Ca2+-dependent) and re absorption (mostly Na+-dependent) rates, the increase after felodipine may be attributed to a decreased secretion due to a Ca2+ entry inhibi tion. As felodipine is known to block L-channels, the active and remar kable functional role of the existing sympathetic presynaptic L-channe ls is confirmed.