Experiments were designed to determine the effects of the vasoactive drug naftidrofuryl on vascular smooth muscle, endothelial cells and adrenergic nerves in isolated canine blood vessels. Naftidrofuryl inhibited contractions of basilar arteries (in a decreasing order of potency), evoked by 5-hydroxytryptamine > KCl = anoxia (in rings with endothelium) > prostaglandin F(2α) = uridine-5'-triphosphate. Naftidrofuryl antagonized competitively the contractions evoked by 5-hydrixytryptamine in the femoral artery and the saphenous vein. Naftidrofyryl caused the release of an endothelium-derived relaxing factor(s) from the endothelium of femoral arteries. The compound depressed contractions of saphenous weins evoked by electrical stimulation of the adrenergic nerve endings, but not those caused by the indirect sympathomimetic amine tyramine or exogenous norepinephrine. In saphenous veins incubated previously with [3H]norepinephrine, the drug inhibited the contractions and the release of transmitter evoked by electrical stimulation. Thus, naftidrofuryl acts at different levels in the blood vessel wall to cause: release of an endothelium-derived relaxing factor(s); inhibition of S2-serotonergic receptors on vascular smooth muscle; prejunctional inhibition of adrenergic neurotransmission; and nonselective inhibition of the contractile process in vascular smooth muscle, which is particularly pronounced in cerebral arteries.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Pharmacology and Experimental Therapeutics|
|State||Published - Dec 1 1986|
ASJC Scopus subject areas
- Molecular Medicine