Renal Dopaminergic Activity in Patients with Primary Aldosteronism

DOI 18 References
  • Ishiguro Toshiya
    the Second Department of Internal Medicine, Sapporo Medical University School of Medicine
  • Shimamoto Kazuaki
    the Second Department of Internal Medicine, Sapporo Medical University School of Medicine
  • Sakamoto Takashi
    the Second Department of Internal Medicine, Sapporo Medical University School of Medicine
  • Hayashi Manabu
    the Second Department of Internal Medicine, Sapporo Medical University School of Medicine
  • Torii Takaaki
    the Second Department of Internal Medicine, Sapporo Medical University School of Medicine
  • Iimura Osamu
    the Second Department of Internal Medicine, Sapporo Medical University School of Medicine

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Abstract

To clarify the role of renal dopaminergic activity in patients with primary aldosteronism (PA), urinary excretion of free dopamine (DA) and the conversion ratio of DA from 1-dopa in the kidney were investigated in 8 patients with PA and 10 normotensive subjects (NT). All subjects were hospitalized and received a standard diet (Na 120mEq, K 75mEq/day) and 2h renal clearance test was performed. Plasma l-dopa concentration (p-DOPA), creatinine clearance (Ccr), urinary excretion of sodium (UNaV) and DA (uDA) as well as fractional excretion of sodium (FENa) were measured. No significant difference was found in UNaV or FENa between NT and PA, or between before and after adrenalectomy (Adx) in PA. UDA was significantly higher in PA than NT, and decreased significantly after Adx. There was no difference in the product of Ccr×p-DOPA between NT and PA, or between before and after Adx in PA. The ratio of uDA/(Ccr×p-DOPA) was significantly higher in PA than NT. After Adx this ratio decreased significantly to the normal range. These results suggest that (1) renal dopaminergic activity is augmented and contributes to the escape phenomenon in PA, and (2) augmented renal DA production in PA might be caused by an increase of conversion to DA from l-dopa at the renal proximal tubules. Hypertens Res 1995; 18 Suppl. I: S193-S195)

Journal

  • Hypertension Research

    Hypertension Research 18 (SupplementI), S193-S195, 1995

    The Japanese Society of Hypertension

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