The effect of the Î±1, Î±2-antagonist phentolamine (PTA) on neuromuscular transmission and exogenous norepinephrine (NE) was assessed in arteries of diminishing diameter posessing a substantial adventitiomedial junction adrenergic innervation in the rabbit ear, i/.e., central ear artery (CEA), unstretched lumen diameter (ULD) â‰ƒ 300 Î¼m; main side branch (MSB) off the CEA (ULD â‰ƒ 150 Î¼m); and terminal branch (TB) off the MSB (ULD â‰ƒ 75 Î¼m). With increasing PTA concentrations, contractile response to transmural nerve stimulation (TNS) were decreased proportionately less in TB than in MSB and CEA. PTA (4 x 10-6 M, a competitive antagonist concentration) blocked the tetrodotoxin-sensitive TNS-induced contractions of CEA segments at 2, 4, and 8 Hz. The response at 8 Hz was reduced at least 98% in MSB and 86% in TB. However, responses to 8 Hz were not abolished in MSB and TB until 2 x 10-5 and 3 x 10-5 M PTA, respectively. PTA (3 x 10-5 M) possessed nonspecific depressant properties in addition to its Î±-antagonist properties. We conclude that the sympathetic nervous system influences tone through Î±-adrenoceptors in the CEA and in the MSB and TB at lower frequencies. Responses in the MSB and TB at higher frequencies of nerve stimulation are mediated predominately through Î±-receptors. If the possibility of a nonadrenergic transmitter is discounted, the possibilities that the small PTA-resistant component of the neurogenic response is due to a high concentration of NE acting on Î±-adrenoceptors and/or a high threshold site cannot be distinguished.
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