Chronic angiotensin-converting enzyme inhibition may improve sodium excretion in cardiac transplant hypertension

• Published in: Transplantation Vol. 59; no. 7; p. 999
• Main Authors: Schwietzer, G K, Hartmann, A, Kober, G, Jungmann, E, Stratmann, D, Kaltenbach, M, Schoeppe, W
• Format: Journal Article
• Language: English
• Published: United States 15.04.1995
• Subjects: Angiotensin-Converting Enzyme Inhibitors - pharmacology; Blood Pressure; Body Weight; Creatinine - blood; Cross-Over Studies; Cyclosporine - adverse effects; Cyclosporine - blood; Dopamine - metabolism; Double-Blind Method; Glomerular Filtration Rate; Heart Transplantation - adverse effects; Humans; Hypertension - chemically induced; Hypertension - etiology; Hypertension - urine; Kidney - physiology; Lisinopril - pharmacology; Male; Middle Aged; Natriuresis - drug effects; Nitrendipine - pharmacology
• ISSN: 0041-1337
• DOI: 10.1097/00007890-199504150-00014

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 (insulin 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.