Falckh P H, de la Lande I S, Stitzel R E, Mano M, Head R J
CSIRO, Division of Human Nutrition, Adelaide, South Australia.
J Pharmacol Exp Ther. 1990 May;253(2):432-6.
Experiments were designed to characterize the nature of the epinephrine-induced potentiation of responses to sympathetic nerve stimulation in the Hooded Wistar rat. The responses to sympathetic nerve stimulation were determined in the isolated perfused mesenteric vascular bed preparation before and after infusion of epinephrine (at 0.27 or 2.7 microM); at the conclusion of the experiment the content of epinephrine in the mesenteric artery was determined. The intraluminal infusion of epinephrine at both high and low concentrations potentiated the responses of the preparation to sympathetic nerve stimulation. Mesenteric artery concentrations of this catecholamine were unchanged at the lower concentration (0.27 microM), but were increased after perfusion of epinephrine at the higher concentration (2.7 microM). The beta adrenoceptor antagonist propranolol (0.5 microM) did not prevent the epinephrine-associated potentiation of responses to sympathetic nerve stimulation, nor did it influence the pressor effects of exogenous norepinephrine. The results suggest that beta adrenoceptors do not play a role in the epinephrine-induced potentiation of responses to sympathetic nerve stimulation in the rat mesenteric vascular bed preparation. This potentiation may, however, be related to a desensitization of presynaptic inhibitory alpha adrenoceptors.
实验旨在表征肾上腺素诱导的Wistar大鼠对交感神经刺激反应增强的本质。在灌注肾上腺素（0.27或2.7微摩尔）前后，通过分离灌注的肠系膜血管床制备来测定对交感神经刺激的反应；在实验结束时，测定肠系膜动脉中肾上腺素的含量。高浓度和低浓度的肾上腺素腔内灌注均增强了制备物对交感神经刺激的反应。低浓度（0.27微摩尔）时，肠系膜动脉中这种儿茶酚胺的浓度未变，但高浓度（2.7微摩尔）肾上腺素灌注后浓度增加。β肾上腺素能受体拮抗剂普萘洛尔（0.5微摩尔）并未阻止肾上腺素相关的对交感神经刺激反应的增强，也未影响外源性去甲肾上腺素的升压作用。结果表明，β肾上腺素能受体在大鼠肠系膜血管床制备中对肾上腺素诱导的对交感神经刺激反应的增强不起作用。然而，这种增强可能与突触前抑制性α肾上腺素能受体的脱敏有关。
