CHRONIC ANGIOTENSIN-CONVERTING ENZYME INHIBITION MAY IMPROVE SODIUM EXCRETION IN CARDIAC TRANSPLANT HYPERTENSION

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Abstract
Cyclosporine-associated hypertension (CAH) may be mediated in part by sodium and volume retention. To investigate this issue, we studied the effects of a calcium antagonist, nitrendipine (NIT, 10–20 mg b.i.d.), and a converting enzyme inhibitor, lisinopril (LIS, 10–20 mg o.d.), on blood pressure (office BP, 24 hr ambulatory BP), excretion of an acute sodium load (200 mmol/2 hr i.v.), glomerular filtration rate (inulin clearance), cumulative dopamine excretion, plasma atrial natriuretic peptide (ANP), and endothelin excretion in 8 patients with CAH after cardiac transplantation in a double-blind, randomized, crossover trial for 6 weeks. Five patients received a diuretic during the trial at a constant dose. Office diastolic BP (DBP) decreased significantly with LIS from 97±6 to 87±9 mmHg and with NIT from 96±7 to 92±12 mmHg. Ambulatory 24 hr DBP decreased significantly from 96±7 mmHg to 86±10 mmHg (LIS) and to 84±11 mmHg (NIT). Ambulatory DBP during the day was lowered significantly from 98±11 mmHg to 87±10 mmHg (LIS) and to 88 ±9 mmHg (NIT) and during the night from 95±9 mmHg to 86 ±8 mmHg (LIS) and to 79±7 mmHg (NIT). Cumulative sodium excretion 6 hr after an acute sodium load increased to 52±39 mmol (placebo), 96±44 mmol (LIS, P<0.05 vs. placebo), and 71 ±34 mmol (NIT). Glomerular filtration rate, cumulative dopamine excretion, ANP, and endothelin excretion did not differ between either treatment group. We conclude, that: (1) both drugs were similar in lowering office BP and during the day, but NIT tended to be more effective during the night; and (2) cumulative sodium excretion during LIS was significantly increased compared with placebo. There was a similar trend during NIT also. Therefore, it is possible that chronic angiotensin-converting enzyme inhibition and possibly calcium antagonists might improve the sodium-retaining state in CAH independent of differences in blood pressure, ANP, dopamine, or renal function.

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