The present study was designed to characterize the neurogenic contraction of rat radial artery. Electrical field stimulation (EFS) evoked frequency-dependent contraction that was abolished by tetrodotoxin (neuronal Na
+ channel blocker), guanethidine (sympathetic neuron blocker), or phentolamine (α-adrenoceptor blocker). The α
1-adrenoceptor antagonist prazosin inhibited endothelium-independent contractions to EFS, noradrenaline (NA), and the α
1-adrenoceptor agonist phenylephrine. Rauwolscine, an α
2-adrenoceptor antagonist, augmented nerve-mediated contractions and reduced sensitivity to NA and the α
2-adrenoceptor agonist BHT-920. The β-adrenoceptor antagonist propranolol diminished EFS-elicited contractions, while sensitivity to NA was enhanced by propranolol. Relaxations evoked by isoproterenol, a β-adrenoceptor agonist, were abolished by propranolol.
NG-Nitro-
L-arginine (
L-NOARG), a nitric oxide (NO) synthase inhibitor, increased both nerve-mediated and NA-induced responses in endothelium-intact, but not in endothelium-denuded arteries. Moreover, endothelium-dependent responses to BHT-920 and isoproterenol were modified by
L-NOARG. Tetraethylammonium (TEA) or 4-amynopyridine, the Ca
2+-activated (K
Ca) or voltage-dependent K
+ (K
V) channel blockers, respectively, enhanced the neurogenic contractions observed. TEA but not 4-amynopyridine increased NA-induced contractions. The ATP-sensitive K
+ (K
ATP)–channel blocker glibenclamide failed to modify adrenergic contractions. Blockade of capsaicin-sensitive primary afferents increased EFS-induced contractions. In conclusion, adrenergic contractions are predominantly mediated by muscular α
1-adrenoceptors, while endothelial α
2- and β-adrenoceptors play a minor role. Presynaptic α
2- and β-adrenoceptors cannot be precluded. Noradrenergic neurotransmission in rat radial artery seems to be modulated by both stimulation of endothelial NO, K
Ca, and K
V channels and sensory C-fiber activation.
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