Modulation of Plasma Aldosterone Concentration by Plasma Potassium in Anephric Man in the Absence of a Change in Potassium Balance

Cooke, Colin R.; Horvath, John S.; Moore, Michael A.; Bledsoe, Turner; Walker, W. Gordon

doi:10.1172/jci107501

Cited by 57 publications

(20 citation statements)

References 23 publications

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“…Moreover, in three volunteers whose potassium levels were equal during the two studies, carboxydopa pretreatment resulted in the same prominent enhancement of 5HTP-induced aldosterone secretion. None of these features is consistent with potassium-mediated stimulation of aldosterone (26)(27)(28)(29). The increase in plasma aldosterone after administration of 5HTP is unlikely to be a result of spontaneous variation (6,30).…”

Section: Discussionmentioning

confidence: 89%

Central serotonergic stimulation of aldosterone secretion.

Shenker¹,

Gross²,

Grekin³

1985

J. Clin. Invest.

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Serotonin stimulates aldosterone secretion both in vitro and in vivo, and serotonin antagonism decreases plasma aldosterone levels in patients with idiopathic aldosteronism. This study was designed to assess the effects of the serotonin precursor, 5-hydroxytryptophan (5HTP), upon aldosterone secretion in man, and to determine whether stimulatory effects of SHTP are mediated through the central nervous system. Oral 5HTP, administered as a single 200-mg dose, increased plasma aldosterone levels from 4.7±0.6 to 13.3±2.8 ng/dl in dexamethasone-pretreated, normal volunteers. Peripheral inhibition of decarboxylation of 5HTP, achieved by pretreatment with carboxydopa, 25 mg three times daily for 3 d, significantly increased the stimulatory effects of 5HTP on aldosterone levels (P < 0.001). No change in aldosterone levels occurred in subjects who received placebo after pretreatment with dexamethasone and carboxydopa. Increased aldosterone was not accompanied by increases in plasma levels of renin activity, potassium, or ACITH. Plasma levels of 5HTP were markedly increased by carboxydopa pretreatment, but peak plasma levels of serotonin were not significantly altered. Four patients with idiopathic aldosteronism all had an increase in plasma aldosterone levels after 5HTP administration, whereas the response in four patients with aldosterone-producing adenoma was variable.Incubation of isolated human and rat adrenal glomerulosa cells with serotonin resulted in increased aldosterone secretion by both sets of cells, whereas 5HTP was ineffective in stimulating aldosterone secretion in vitro. We conclude that central serotonergic pathways are involved in the stimulation of aldosterone induced by administration of 5HTP. This mechanism may be an important etiologic factor in the hypersecretion of aldosterone that occurs in patients with idiopathic aldosteronism.

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Section: Discussionmentioning

confidence: 89%

Central serotonergic stimulation of aldosterone secretion.

Shenker¹,

Gross²,

Grekin³

1985

J. Clin. Invest.

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“…Aldosterone plays an important role in controlling plasma K + levels by increasing renal K + excretion [23,24]. The levels of aldosterone are controlled both by the plasma K + levels and by the renin-angiotensin system [23][24][25].…”

Section: Discussionmentioning

confidence: 99%

“…The levels of aldosterone are controlled both by the plasma K + levels and by the renin-angiotensin system [23][24][25]. In hypoglycaemia, aldosterone levels increase due to the activation of the renin-angiotensin system [26,27], and this increase appears to be an effect by hypoglycaemia and not of insulin, as euglycaemic hyperinsulinaemia leads to a decrease of aldosterone.…”

Section: Discussionmentioning

confidence: 99%

Dynamics of blood electrolytes in repeated hyper- and/or hypoglycaemic events in patients with type 1 diabetes

et al. 2011

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Aims/hypothesis Electrolyte disturbances are well-known consequences of the diabetic pathology. However, less is known about the cumulative effects of repeated changes in glycaemia, a characteristic of diabetes, on the electrolyte balance. We therefore investigated the ionic profiles of patients with type 1 diabetes during consecutive hyper-and/or hypoglycaemic events using the glucose clamp. Methods In protocol 1, two successive hyperglycaemic excursions to 18 mmol/l were induced; in protocol 2, a hypoglycaemic excursion (2.5 mmol/l) was followed by a hyperglycaemic excursion (12 mmol/l) and another hypoglycaemic episode (3.0 mmol/l). Results Blood osmolarity increased during hyperglycaemia and was unaffected by hypoglycaemia. Hyperglycaemia induced decreases in plasma Na + Cl − and Ca 2+ concentrations and increases in K + concentrations. These changes were faithfully reproduced during a second hyperglycaemia. Hypoglycaemia provoked rapid and rapidly reversible increases in Na + , Cl − and Ca 2+ . In sharp contrast, K + levels displayed a rapid and substantial fall from which they did not fully recover even 2 h after the re-establishment of euglycaemia. A second hypoglycaemia caused an additional fall. Conclusions/interpretation Repeated hyperglycaemia events do not lead to any cumulative effects on blood electrolytes. However, repeated hypoglycaemias are cumulative with respect to K + levels due to a very slow recovery following hypoglycaemia. These results suggest that recurring hypoglycaemic events may lead to progressively lower K + levels despite rapid re-establishment of euglycaemia. This warrants close monitoring of plasma K + levels combined with continuous glucose monitoring particularly in patients under intensive insulin therapy who are subject to repeated hypoglycaemic episodes.Trial registration: Clinicaltrial.gov NCT01060917. Funding:

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“…The N--N bond exhibits partial doublebond character which leads to restricted rotation about the bond as also found from solution NMR studies (Cooney & Brownstein, 1974). The nitroso group has a coplanar orientation with respect to atoms C(2)and C(7), as is evident from the torsion angles C (2) The dihedral angle between the phenyl rings is 145.3 ° .…”

Section: Ci7hi7n302mentioning

confidence: 55%