Impaired vasopressin suppression and enhanced atrial natriuretic hormone release following an acute water load in primary aldosteronism

Abstract

The release of arginine vasopressin (AVP) and atrial natriuretic hormone (ANH) and their involvement in renal water and electrolyte metabolism in primary aldosteronism in humans were studied. An oral acute water load (20 ml/kg body weight) was given to each of 12 patients before and after surgical removal of their aldosterone-producing adenoma(s). Plasma AVP and ANH were measured simultaneously, and renal water and electrolyte metabolism and tubular functions were determined. The same water load was given to seven normal subjects and the same parameters were determined. In the presence of mineralocorticoid excess before the operation, plasma AVP was relatively low compared with plasma osmolality (Posm), but was not suppressed in response to decreases in Posm after the water load. Baseline plasma ANH was high and increased further after the water load; urinary dilution and diuresis both remained normal. After the operation, baseline plasma AVP was normal and decreased in response to the decrease in Posm after the water load, with normal urinary dilution and diuresis. Baseline plasma ANH was normal, and did not increase after the water load. The ratio of urinary K and Na clearances and distal tubular reabsorption of Na increased before the operation. These results suggest that there are perturbations of AVP and ANH release in primary aldosteronism, despite the normal urinary dilution after a water load. European Journal of Endocrinology 137 154-161

Glucocorticoidal Regulation of Pituitary Vasopressin Content in Rats.

“…In this model of hypertension, the release of AVP is elevated, pressor responsiveness to AVP is increased, and AVP antiserum reduces mean arterial blood pressure (16). Consistent with these findings, we recently found that the suppression of AVP was impaired after water load in patients with primary aldosteronism (17). During glucocorticoid excess, on the other hand, AVP may play a minor role in the blood pressure increase, since glucocorticoids inhibit AVP bio- synthesis and secretion as shown in this and other studies (3, 4), Consequently, other systems, including the renin-angiotensin unit, may be responsible for glucocorticoid-induced hypertension (1, 2).…”

Genetic polymorphisms in the beta-subunit of the epithelial sodium channel (βENaC) gene in the Japanese population

“…In essential hypernatremia, altered regulation of AVP secretion in response to plasma sodium concentration has been reported in some patients. 14, 15 Kimura and coworkers 16 investigated AVP secretion in response to changes in plasma osmolality in patients with primary aldosteronism, in which condition ENaC function is considered to be promoted. The results demonstrated altered regulation of AVP secretion, which was normalized after the surgical excision of adrenal tumor.…”