Dopaminergic modulation of aldosterone secretions on changes of sodium intake in aldosterone-producing adenoma.
BACKGROUND
Impairment of renal dopamine excretion on high-salt diet (HS) may account for increased blood pressure (BP) in hypertensive subjects. Whether such impairment of dopaminergic activity exists in the adrenal gland is unknown. The purpose of this study was to differentiate degrees of dopaminergic inhibition of aldosterone secretion in patients with aldosterone-producing adenoma (APA).


METHODS
A total of 15 patients with unilateral APA were fed a low-salt diet (LS) for 1 week, followed by another week on HS. At the end of each diet period, 24-h ambulatory BP recording, daily urine catecholamine measurement, and a metoclopramide test were performed.


RESULTS
A high-salt diet increased both daytime and nighttime BP (P < .001), and urine dopamine excretion (P < .01). Intravenous injection of 10-mg metoclopramide increased plasma aldosterone concentrations (PAC) on both diets. The areas-under-the-curve for PAC between LS and HS were not different, but the area-under-the-curve for PAC increment was greater on HS (P < .05). Six patients with increment areas on HS greater than those on LS by 50% were termed "suppressible," and the remainders as "nonsuppressible." On HS, the so-called suppressible subjects had greater urine dopamine and less urine norepinephrine excretions (P < .05). The nonsuppressible subjects had greater percentage increase of nighttime BP by HS than the suppressible (for systolic BP, 13.1% v 4.5%, P < .01; for mean BP, 12.0% v 5.1%, P < .01, respectively), but no difference in daytime BP.


CONCLUSIONS
Two subtypes of APA were defined according to their responses to metoclopramide during salt manipulation. On HS, the nonsuppressible subjects, with less dopaminergic inhibition of aldosterone secretion, had less urinary DA excretion and greater BP elevation. The renal and adrenal dopaminergic activities are regulated in a parallel fashion.
Department of Internal Medicine, National Taiwan University Hospital, Taipei.
Kwan-Dun
KD
Wu
Yung-Ming
YM
Chen
Tzong-Shinn
TS
Chu
Shih-Chieh
SC
Chueh
Gen-Chen
GC
Tsai
Yung-Zu
YZ
Tseng
Bor-Shen
BS
Hsieh
D000306:Adrenal Cortex Neoplasms / Q000378:metabolism*; D018246:Adrenocortical Adenoma / Q000378:metabolism*; D000328:Adult; D000450:Aldosterone / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects; D004039:Diet, Sodium-Restricted; D004298:Dopamine / Q000652:urine*; D018492:Dopamine Antagonists; D004837:Epinephrine / Q000652:urine; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000175:diagnosis / Q000378:metabolism; D006973:Hypertension / Q000378:metabolism; D008297:Male; D008787:Metoclopramide; D009638:Norepinephrine / Q000652:urine; D012982:Sodium, Dietary / Q000008:administration & dosage* / Q000652:urine
D018492:Dopamine Antagonists; D012982:Sodium, Dietary; D000450:Aldosterone; D008787:Metoclopramide; D004298:Dopamine; D009638:Norepinephrine; D004837:Epinephrine