• Conn's syndrome
• aldosterone
• calcium blockade

Since its first recognition, the prevalence of primary hyperaldosteronism, or Conn's syndrome, as a cause of hypertension has been disputed. Initial optimism that 20% of hypertensives may have a curable cause gave way to a realisation that many patients with essential hypertension have low renin hypertension, and nowadays less than 1% of patients started on treatment for hypertension are considered to have the diagnosis. Recently, systematic surveys using a ratio of aldosterone to renin above 800 as an upper limit of normal have suggested prevalence figures greater than 10% (of hypertensives).1 Ironically, changes in modern pharmacological treatment of hypertension have probably reduced the sensitivity of plasma electrolyte measurements for detection of Conn's syndrome, since the 4–8-fold lower doses of diuretics − and lower overall use of this class − than in Conn's time means that plasma K⁺ values <3 mmol/l are seen infrequently; it is also likely that reductions in average salt intake limit the degree of hypokalaemia in Conn's syndrome. Both sodium and diuretic intake influence how much K⁺ is lost through K⁺/Na⁺ exchange in the renal distal tubule. Angiotensin-converting enzyme (ACE) inhibitors suppress angiotensin-II-mediated aldosterone secretion. Suppression of aldosterone release from adrenal zona glomerulosa cells by Ca⁺⁺ entry blockers is well described,2 3 but their effect in Conn's syndrome has been controversial.4 5 While the specific antagonist for aldosterone, spironolactone, is known sometimes to confuse diagnosis of an adenoma by masking suppression of the contralateral adrenal, there is no generally recognised recommendation to withdraw Ca⁺⁺blockers during investigation of possible Conn's syndrome; there is also no published experience with amlodipine, arguably the most powerful and now most widely used member of the class in hypertension. We therefore report here a patient with a Conn's adenoma in whom serial K⁺ and aldosterone measurements demonstrated how treatment with amlodipine can completely mask the diagnosis.

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Figure Effects of treatment on plasma K⁺ and aldosterone levels in a patient with Conn's syndrome. Plasma K⁺ (o–––o, left axis) and aldosterone ( - - - - , right axis) were measured before any treatment, and 4 weeks after the drug or surgical interventions shown on the x-axis.

A previously asymptomatic 30-year-old doctor's wife was found to have a blood pressure of 160/110 mmHg at her general practice new patient medical. Plasma electrolytes showed a Na⁺ of 144 and K⁺ of 2.8 mmol/l, and the patient was referred untreated for further investigation. A low plasma renin (<0.2 pmol/ml/h) and elevated plasma aldosterone (730 pmol/l) suggested a diagnosis of Conn's syndrome. Onset of early morning headaches necessitated some antihypertensive treatment, and the patient was started on amlodipine 5 mg daily since premature use of spironolactone can confuse tests to distinguish adenomas from bilateral hyperplasia. Two weeks later, blood pressure had fallen to 110/70 mmHg, and the diagnosis of a right adrenal adenoma was made by computed tomography (CT) scan, and unilateral increased uptake of selenium cholestenol by the right adrenal on scintiscan. At this stage, treatment was changed from amlodipine to spironolactone, with continued excellent blood pressure control. A 2 × 1 cm adrenal adenoma was removed one month later.

The figure shows the changes in plasma K⁺ and aldosterone in response to each change in treatment. At least two K⁺measurements were made during each phase, with all the pairs being similar except for the spontaneous variation in K⁺ before treatment was started. Unexpectedly, plasma K⁺ was > 4.0 mmol/l on each occasion after introduction of amlodipine, almost certainly due to a suppression of aldosterone secretion. Indeed the fall in plasma aldosterone is all the more impressive in that a rise in plasma K⁺ usually stimulates aldosterone secretion.