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Felodipine and Vasomotion Physiology

Department of Pharmacology, Medical School, Aristotelian Univ of Tessaloniki, Greece

Constantinos Papadopoulos, MBBS, M.D., F.A.C.A.

Department of 2nd Cardiology, Medical School, Aristotelian Univ of Tessaloniki, Greece

Maria Kotoula, B.Pharm, M.D.

Department of Pharmacology, Medical School, Aristotelian Univ of Tessaloniki, Greece

Andreas Kouyoumtzis, B.Chem., M.D.

Department of Pharmacology, Medical School, Aristotelian Univ of Tessaloniki, Greece

Demetrios Kouvelas, B.Pharm., M.D.

Department of Pharmacology, Medical School, Aristotelian Univ of Tessaloniki, Greece

Demetrios Karatzas, MBBS, M.D.

Department of Nuclear Medicine, Medical School, Aristotelian University of Thessaloniki, Greece

Athanassios Paradelis, MBBS, M.D.

Department of Pharmacology, Medical School, Aristotelian Univ of Tessaloniki, Greece

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) Ca²⁺-entrance blocker with marked vascular selectivity. It was found that felodipine 1-10 µM presents a Ca²⁺ entrance-blocking activity when the bovine aortic smooth muscle is normal or stimulated by K⁺ 65.4 mM or the -adrenoceptor agonist phenylephrine 1 µM. 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 µM antagonizes the contraction of the bovine aortic ring that is induced by phenylephrine 10 µM or KCl 65.4 mM. On the contrary, felodipine 1-10 µM 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 (Ca²⁺-dependent) and reabsorption (mostly Na⁺-dependent) rates, the increase after felodipine may be attributed to a decreased secretion due to a Ca²⁺ entry inhibition. As felodipine is known to block L-channels, the active and remarkable functional role of the existing sympathetic presynaptic L-channels is confirmed.

Angiology, Vol. 44, No. 10, 803-809 (1993)
DOI: 10.1177/000331979304401007


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