Phentolamine-resistant neurogenic constriction occurs in small arteries at higher frequencies

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Abstract
The effect of the .alpha.1, .alpha.2-antagonist phentolamine (PTA) on neuromuscular transmission and exogenous norepinephrine (NE) was assessed in arteries of diminishing diameter possessing a substantial adventitiomedial junction adrenergic innervation in the rabbit ear, i.e., central ear artery (CEA), unstretched lumen diameter (ULD) .simeq. 300 .mu.m; main side branch (MSB) off the CEA (ULD .simeq. 150 .mu.m); and terminal branch (TB) off the MSB (ULD .simeq. 75 .mu.m). With increasing PTA concentrations, contractile responses to transmural nerve stimulation (TNS) were decreased proportionately less in TB than in MSB and CEA. PTA (4 .times. 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 .times. 10-5 and 3 .times. 10-5 M PTA, respectively. PTA (3 .times. 10-5 M) possessed nonspecific depressant properties in addition to its .alpha.-antagonist properties. The sympathetic nervous system evidently influences tone through .alpha.-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 .alpha.-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 .alpha.-adrenoceptors and/or a high threshold site cannot be distinguished.

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