SYSTEMIC AND RENAL EFFECTS OF NIFEDIPINE IN CYCLOSPORINE-ASSOCIATED HYPERTENSION

Cyclosporine induces hypertension and widespread vasoconstriction afte r transplantation in addition to reducing kidney function. We studied hemodynamic, renal, and hormonal effects of monotherapy with nifedipin e XL (n=37) in liver transplant recipients within a year after transpl ant (median, 4.4 months). Systemic hemodynamics were determined with t horacic electrical bioimpedance. Blood pressure before therapy was 172 +/-4/108+/-2 mm Hg. Sixty-four percent of recipients achieved blood pr essures less than 140/90 mm Hg mediated by a fall in systemic vascular resistance index (2427+/-245 dyne.s.cm(-5) m(-2) in responders versus 2905+/-281 in nonrespenders, P<.01). Despite the fall in systemic vas cular resistance, glomerular filtration rates were not changed during nifedipine therapy, as measured by both creatinine and iothalamate cle arances. Urinary prostacyclin (6-ketoprostaglandin F-1 alpha) was supp ressed below normal from 2468+/-323 ng/d before transplant to 1103+/-9 9 ng/d (P<.01) after transplant and did not change during nifedipine t herapy. Urinary thromboxane B-2 and plasma renin activity also fell af ter transplant and remained low during nifedipine. These data demonstr ate that nifedipine can reverse systemic vasoconstriction associated w ith hypertension after transplantation. Systemic effects were not tran smitted to the kidney sufficiently to improve glomerular filtration ra te or reverse hormonal changes within the kidney. Hence, vascular and functional regulation of the kidney was dissociated from the systemic circulation