Valet P, Damase-Michel C, Montastruc J L, Montastruc P
Laboratoire de Pharmacologie Médicale et Clinique, INSERM U 317, Faculté de Médecine, Toulouse, France.
Fundam Clin Pharmacol. 1989;3(3):307-20. doi: 10.1111/j.1472-8206.1989.tb00459.x.
Chronic sinoaortic denervation (SAD) performed by section of both carotid and aortic nerves induced a significant and sustained increase in blood pressure and heart rate in conscious dogs; under our experimental conditions, the values of systolic blood pressure and heart rate were never lower than 190 mmHg and 120 beats/min, respectively. The present long-term study (8 mo) investigated the time-course of plasma catecholamine levels and circulating blood cell adrenoceptor (leukocyte beta 2 and platelet alpha 2) number. Catecholamine plasma levels were highly correlated with the variations of leukocyte beta adrenoceptors (measured by [125I]cyanopindolol binding and characterized as a beta 2 receptor in dogs). These two parameters followed a biphasic pattern after SAD: during the first 2 mo, significant increases in noradrenaline and adrenaline levels were associated with a decrease in leukocyte beta 2 adrenoceptor number; from the 4th month, they slowly returned to normal values, although blood pressure remained elevated. By contrast, platelet alpha 2 adrenoceptor number (measured by [3H]yohimbine binding) did not follow this pattern since it remained lower than before SAD during the whole experiment. Finally, the development (but not the maintenance) of SAD-induced hypertension is associated with an increase in sympathetic tone. Only leukocyte beta 2 (and not platelet alpha 2) adrenoceptors are directly regulated by the endogenous levels of catecholamines.
通过切断颈动脉和主动脉神经进行慢性窦主动脉去神经支配（SAD），可使清醒犬的血压和心率显著且持续升高；在我们的实验条件下，收缩压和心率值分别从未低于190 mmHg和120次/分钟。本长期研究（8个月）调查了血浆儿茶酚胺水平和循环血细胞肾上腺素能受体（白细胞β2和血小板α2）数量的时间进程。儿茶酚胺血浆水平与白细胞β肾上腺素能受体的变化高度相关（通过[125I]氰吲哚洛尔结合测定，并在犬中鉴定为β2受体）。SAD后这两个参数呈现双相模式：在最初的2个月内，去甲肾上腺素和肾上腺素水平显著升高，同时白细胞β2肾上腺素能受体数量减少；从第4个月起，尽管血压仍升高，但它们缓慢恢复到正常值。相比之下，血小板α2肾上腺素能受体数量（通过[3H]育亨宾结合测定）并未遵循此模式，因为在整个实验过程中它一直低于SAD前的水平。最后，SAD诱导的高血压的发展（而非维持）与交感神经张力增加有关。只有白细胞β2（而非血小板α2）肾上腺素能受体直接受儿茶酚胺内源性水平的调节。
