de Champlain J
Department of Physiology, Faculty of Medicine, University of Montreal, Canada.
J Hypertens Suppl. 1990 Dec;8(7):S77-85.
Numerous experimental and clinical studies, using various approaches to evaluate the release of sympathetic transmitters and to obtain sympathetic nerve microneurographic recordings, have shown clearly that sympathetic system activity and reactivity is increased in experimental models of hypertension [deoxycorticosterone acetate (DOCA) salt and spontaneously hypertensive rats (SHR)] and in an important subgroup of essential hypertensive patients. This finding may reflect dysfunctions in the baroreflex blood pressure regulation, since an elevated blood pressure should normally inhibit sympathetic activity. This abnormality may arise from a variety of dysfunctions occurring at various sites along the baroreflex arc, including presynaptic modulatory adrenergic autoreceptors, where reduced sensitivity of presynaptic alpha 2 inhibitory receptors and enhanced sensitivity of beta 2 presynaptic receptors have been demonstrated. Although it has been possible to correlate the blood pressure elevation with various indices of sympathetic activity in experimental and human hypertension, the functional implications of that abnormality can be fully understood only in the light of concomitant alterations occurring in postsynaptic mechanisms. Pharmacologic, physiologic and biochemical studies strongly suggest that postsynaptic alpha 1 adrenergic functions become dominant while beta adrenergic functions are attenuated in hypertension. In experimental hypertension, this phenomenon is associated with a reduction in the number of beta adrenoceptors and in the production of its second messenger, cyclic AMP, whereas the number of alpha 1 adrenoceptors remained unchanged or increased, but the production of their second messengers, inositol triphosphate and diacylglycerol, is enhanced in cardiac and vascular tissues. These observations suggest the presence of an imbalance in postsynaptic adrenoceptor functions, which promotes the pressor effects of the sympathetic system.(ABSTRACT TRUNCATED AT 250 WORDS)
众多实验和临床研究采用各种方法评估交感递质的释放并获取交感神经微神经图记录，结果清楚显示，在高血压实验模型（醋酸脱氧皮质酮盐和自发性高血压大鼠）以及重要的原发性高血压患者亚组中，交感神经系统的活性和反应性增强。这一发现可能反映了压力反射性血压调节功能障碍，因为血压升高通常应抑制交感神经活动。这种异常可能源于压力反射弧各部位出现的多种功能障碍，包括突触前调节性肾上腺素能自身受体，在这些受体处已证实突触前α2抑制性受体敏感性降低，而β2突触前受体敏感性增强。尽管在实验性和人类高血压中已将血压升高与交感神经活动的各种指标相关联，但只有结合突触后机制中同时发生的改变，才能充分理解这种异常的功能意义。药理、生理和生化研究强烈表明，在高血压中突触后α1肾上腺素能功能占主导，而β肾上腺素能功能减弱。在实验性高血压中，这种现象与β肾上腺素能受体数量及其第二信使环磷酸腺苷生成减少有关，而α1肾上腺素能受体数量保持不变或增加，但其第二信使三磷酸肌醇和二酰甘油在心脏和血管组织中的生成增强。这些观察结果表明突触后肾上腺素能受体功能存在失衡，这促进了交感神经系统的升压作用。（摘要截断于250字）
