Cannabinoid CB1 receptor and endothelium‐dependent hyperpolarization in guinea‐pig carotid, rat mesenteric and porcine coronary arteries

摘要: 1. The purpose of these experiments was to determine whether or not the endothelium-dependent hyperpolarizations vascular smooth muscle cells (observed in presence inhibitors nitric oxide synthase and cyclo-oxygenase) can be attributed production an endogenous cannabinoid. 2. Membrane potential recorded guinea-pig carotid, rat mesenteric porcine coronary arteries by intracellular microelectrodes. 3. In artery, cannabinoid receptor antagonist, SR 141716 (1 microM), did modify either resting membrane hyperpolarization induced acetylcholine microM) (17.3 +/- 1.8 mV, n = 4 17.8 2.6 4, control 141716, respectively). Anandamide (30 a (12.6 1.4 13 2.0 3.0 6 vessels with without endothelium, respectively) which could repeated same tissue, whereas still able hyperpolarize preparation. anandamide significantly influenced microM). HU-210 synthetic CB1 agonist, palmitoylethanolamide CB2 influence cells. 4. (19.0 1.7 6) altered glibenclamide microM; 17.7 2.3 3). However, combination charybdotoxin (0.1 plus apamin (0.5 abolished acetylcholine-induced under conditions, evoked depolarization (7.7 2.7 13) inhibited (4.0 0.4 4) but affected 4). 5. carotid (18.8 0.7 15). (10 nM 10 caused direct, concentration-dependent (up mV at significant inhibition hyperpolarization. 3 potential. At concentration 30 microM, agonist non-reproducible (5.6 1.3 10) slow onset. affect microM (5.3 1.5 6. up relax relaxation bradykinin were 7. These results indicate that hyperpolarizations, observed arteries, are related activation receptors.