Cabral A M, Vasquez E C
Pharmacol Res Commun. 1984 Oct;16(10):1031-40. doi: 10.1016/s0031-6989(84)80067-3.
The chronotropic reactivity to beta-adrenergic stimulation was studied in isolated perfused hearts from sinoaortic baroreceptors denervated (SAD) rats in the phases of maximal tachycardia (5 h) and normalized heart rate (15 days) or after repeated injection of isoproterenol (1 mg/kg, 3 times daily for 10 days). The threshold doses of isoproterenol needed to cause a significant acceleration of heart rate were significantly higher in acute SAD (1.6 X 10(-7)M), chronic SAD (3.2 X 10(-7)M), and isoproterenol-pretreated (6.4 X 10(-7)M) rats than in control rats (0.8 X 10(-7)M). The maximal increment in basal heart rate was lower in acute (59%) and chronic (48%) SAD rats and in isoproterenol-pretreated rats (26%) than in control rats (78%). These results suggest that the increased efferent sympathetic outflow to the heart induced by SAD causes desensitization of cardiac beta-adrenoceptors and may explain the gradual tachycardia disappearance in this SAD hypertensive rats.
在去窦主动脉压力感受器（SAD）大鼠的离体灌注心脏中，研究了在最大心动过速阶段（5小时）、心率恢复正常阶段（15天）或反复注射异丙肾上腺素（1毫克/千克，每日3次，共10天）后，心脏对β-肾上腺素能刺激的变时反应性。急性SAD大鼠（1.6×10⁻⁷M）、慢性SAD大鼠（3.2×10⁻⁷M）和异丙肾上腺素预处理大鼠（6.4×10⁻⁷M）引起心率显著加快所需的异丙肾上腺素阈值剂量，显著高于对照大鼠（0.8×10⁻⁷M）。急性SAD大鼠（59%）、慢性SAD大鼠（48%）和异丙肾上腺素预处理大鼠（26%）基础心率的最大增幅低于对照大鼠（78%）。这些结果表明，SAD引起的心脏传出交感神经输出增加导致心脏β-肾上腺素能受体脱敏，这可能解释了SAD高血压大鼠心动过速逐渐消失的原因。
