Gordon R D, Küchel O, Liddle G W, Island D P
J Clin Invest. 1967 Apr;46(4):599-605. doi: 10.1172/JCI105561.
Several lines of evidence have been developed indicating that the sympathetic nervous system may play a role in mediating the renal and adrenocortical secretory responses to upright posture and sodium deprivation. Despite concurrent increases in arterial blood pressure, the plasma renin activity of normal subjects increased both in response to the infusion of catecholamines (norepinephrine: epinephrine, 10:1) and in response to stimulation of the sympathetic nervous system by cold. Aldosterone excretion was also increased by catecholamine infusion. In normal subjects the stimuli of upright posture and of sodium depletion both resulted in increases in urinary catecholamines, plasma renin activity, and urinary aldosterone. A patient with severe autonomic insufficiency did not experience normal elevations of urinary catecholamines, plasma renin activity, or urinary aldosterone in response to upright posture or sodium deprivation, despite a substantial fall in arterial blood pressure. When orthostatic hypotension was prevented by infusion of catecholamines, however, increases in plasma renin activity and in aldosterone excretion were observed. We suggest that both upright posture and sodium depletion lead to decreases in effective plasma volume and increases in sympathetic nervous system activity. This increase in sympathetic activity is then responsible for an increase in renal afferent arteriolar constriction, leading to an increase in renin secretion and, ultimately, an increase in aldosterone secretion.
已有多条证据表明，交感神经系统可能在介导肾脏和肾上腺皮质对直立姿势及钠缺乏的分泌反应中发挥作用。尽管动脉血压同时升高，但正常受试者的血浆肾素活性在输注儿茶酚胺（去甲肾上腺素：肾上腺素，10:1）以及因寒冷刺激交感神经系统时均会升高。输注儿茶酚胺也会使醛固酮排泄增加。在正常受试者中，直立姿势和钠缺乏这两种刺激均会导致尿儿茶酚胺、血浆肾素活性及尿醛固酮增加。一名患有严重自主神经功能不全的患者，尽管动脉血压大幅下降，但在直立姿势或钠缺乏时，其尿儿茶酚胺、血浆肾素活性或尿醛固酮并未出现正常升高。然而，当通过输注儿茶酚胺预防体位性低血压时，可观察到血浆肾素活性和醛固酮排泄增加。我们认为，直立姿势和钠缺乏均会导致有效血浆量减少以及交感神经系统活动增加。这种交感神经活动的增加进而导致肾入球小动脉收缩增强，从而使肾素分泌增加，最终使醛固酮分泌增加。
