Role of the Sympathetic Nervous System in Regulating Renin and Aldosterone Production in Man *

Gordon, Richard D.; Kuchel, O; Liddle, Grant W.; Island, Donald P.

doi:10.1172/jci105561

Cited by 302 publications

(105 citation statements)

References 25 publications

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“…in patients with orthostatic hypotension due to other neurological disorders have produced conflicting evidence for the role of the sym pathetic nervous system in renin release. It has been suggested that an integrated sympathetic nervous system is necessary (Gordon, Kuchel, Liddle & Island, 1967;Chokroverty, Barron, Katz, Del Greco & Sharp, 1969) but our present observations fail to support this view. Corbett, Frankel and Harris (1971C) have investigated the cardiovascular responses to change of posture in tetraplegic man and considered that any blood pressure overshoot they observed immediately after return to the supine position was associated with a spasm of skeletal muscles.…”

contrasting

confidence: 99%

Orthostatic hypotension and the renin-angiotensin system in paraplegia

1971

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contrasting

confidence: 99%

Orthostatic hypotension and the renin-angiotensin system in paraplegia

1971

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“…Both in man [11,28] and experimental animals [30,35], renin release has been shown with activation of the sympathetic nervous system.…”

Section: Discussionmentioning

confidence: 99%

Response to 2-Deoxy-D-glucose and to Glucagon in “Ketotic Hypoglycemia” of Childhood: Evidence for Epinephrine Deficiency and Altered Alanine Availability

et al. 1973

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ExtractThe commonest clinical type of hypoglycemia in childhood presents as "ketotic hypoglycemia," a syndrome which typically remits spontaneously before adolescence. In young children with the severe form of this syndrome, deficient catecholamine secretion and, recently, decreased mobilization of gluconeogenic substrate (alanine) have been shown. The present study concerns five children with ketotic hypoglycemia, aged 2.5 to 9.5 years, and six control children, of similar ages. Each received (7) an infusion of 2-deoxy-D-glucose (2-DG) to test the catecholamine response and (2) intravenous glucagon before and after a 26-28-hr fast, to define possible difference in the response of substrates and hormones, with particular reference to alanine. In the control group, the infusion of 2-DG, 50 mg/kg body wt over 30 min, induced anxiety, hunger or thirst and sweating, as well as a sustained rise in plasma glucose from 78 ± 5 (mean ± SEM) to 156 ± 13.5 mg/100 ml from 1-3 hr after beginning the infusion. There was a transient rise in renin activity in plasma (PRA) from 2.0 ± 0.5 to a peak of 5.8 ± 1.2 ng/ml/hr. By contrast, in the children with hypoglycemia, no clinical response was observed, and there was no change in either glucose in plasma, which remained at 77 ± 6 mg/100 ml, or in PRA (1.3 ± 0.3 to 1.0 ± 0.5 ng/ml/hr). After a period of unrestricted diet, and after an overnight fast, values of plasma glucose, insulin, glucagon, /3-hydroxybutyrate, and alanine were the same in the two groups. In both groups intravenous glucagon, 30 yug/kg, was followed by a comparable rise in glucose in plasma and immunoreactive insulin and a comparable fall in alanine in plasma. During the subsequent fast, glucose and insulin in plasma declined similarly. Ketonuria appeared at the same time and /S-hydroxybutyrate in plasma rose to equivalent values. The response to a second glucagon infusion was smaller after fasting both as to glucose in blood and plasma insulin, but once again similar for control and hypoglycemia groups. However, the fall in alanine in plasma was significantly greater in the hypoglycemic group during fasting (to 200 ± 13 /*M for the control group compared with 151 ± 13 ^Mforthe hypoglycemia group, P < 0.05) and at five time points (10,30, 60, 90, and 120 min) after the second glucagon administration. Absence of hyperglycemic response to 2-DG in ketotic hypoglycemia suggests 983 984 SlZONENKO ET AL. impaired catecholamine response. Further, after provocation by fasting and subsequent glucagon administration, the hypoalaninemia which resulted was more marked. Because epinephrine has been shown to raise alanine levels in plasma in man, it is hypothesized that a connection may exist between defective catechol secretion and alanine mobilization in ketotic hypoglycemia. SpeculationDecreased availability of alanine in so-called ketotic hypoglycemia probably represents a defective metabolic system by which neoglucogenic substrates are not readily mobilized, rather than an absolute absence of substrate. One of the poss...

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“…39 Others noted increases in blood levels or secretion rates of aldosterone following the combined stimulus on norepinephrine and epinephrine. 5 ' * Angiotensin II being the major regulator of aldosterone secretion, 40 it is probable that aldosterone activation in our subjects was at least partly due to the concomitant increase in PRA. Nevertheless, the absence of a significant correlation between norepinephrine-induced increases in PRA and those in plasma aldosterone suggest that additional factors may be involved.…”

Section: Discussionmentioning

confidence: 89%

Effects of short-term norepinephrine infusion on plasma catecholamines, renin, and aldosterone in normal and hypertensive man.

Beretta-Piccoli¹,

Weidmann²,

Meier³

et al. 1980

Hypertension

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SUMMARYThe acute responsiveness of plasma catecbolamine, renln (PRA), and aldosterone levels to exogenous norepinephrine was studied under placebo conditions and following renin-angiotensin activation by diuretic pretreatment in 25 normal subjects and 34 patients with borderllne-to-moderate essential hypertension. Norepinephrine infusion caused increases in plasma norepinephrine (PNE) that correlated with the infused norepinephrine dose (p < 0.001); this relationship was similar in normal and hypertensive subjects and unaltered by diuretic therapy. Plasma eplnephrine and dopamine levels were unchanged during norepinephrine infusion. Norepinephrine infusion at pressor doses stimulated PRA (p < 0.01). The PRA responses correlated with the dose of infused norepinephrine [p < 0.0025), and norepinephrlne-stimolated PRA correlated with basal PRA (p < 0.001). These norepinephrine-PRA relationships were unaltered by diuretic treatment and similar in normal and hypertensive subjects. In both groups, norepinephrine also caused a similar Increase in plasma aldosterone (p < 0.05) under placebo conditions, but not following diuretic therapy. These findings demonstrate that an acute increase in the blood levels of the adrenergic neurotransmittor, norepinephrine, causes mild but distinct stimulation of plasma renin and aldosterone levels. Renin release in response to exogenous norepinephrine is not enhanced following renin-angiotensin activation by diuretic pretreatment. The responsiveness of the renin-angiotensin-aldosterone system to an acute norepinephrine input seems to be intact in essential hypertension.

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Role of the Sympathetic Nervous System in Regulating Renin and Aldosterone Production in Man *

Cited by 302 publications

References 25 publications

Orthostatic hypotension and the renin-angiotensin system in paraplegia

Orthostatic hypotension and the renin-angiotensin system in paraplegia

Response to 2-Deoxy-D-glucose and to Glucagon in “Ketotic Hypoglycemia” of Childhood: Evidence for Epinephrine Deficiency and Altered Alanine Availability

Effects of short-term norepinephrine infusion on plasma catecholamines, renin, and aldosterone in normal and hypertensive man.

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