Role of sympathetic nervous system in cyclosporine-induced rise in blood pressure

To clarify the role of the sympathetic nervous system in, the development o f cyclosporine A (CsA)-induced rise in blood pressure (BP), the effects of CsA on 24-hour ambulatory BP (ABP) were studied in patients with familial a myloid polyneuropathy (FAP) who underwent a liver transplantation. On the b asis of autonomic function tests, patients with absent or mild-to-moderate sympathetic damage (Group A, n=11; age 29 to 43 years, disease duration 2 t o 6 years) and patients with severe sympathetic damage (Group B, n=9, age 2 7 to 38 years, disease-duration 3 to 9 years) were identified. Both groups were followed for 1 year. The daily doses of CsA and the CsA whole blood tr ough levels between the groups did not differ. Pretransplantation values of daytime and nighttime ABP were, respectively, 117+/-8/76+/-7 mm Hg and 108 +/-12/68+/-9 mm Hg in group A and 107+/-6/66+/-4 mm Hg (P<0.05 group A vers us group B) and 102+/-6/62+/-4 mm Hg in group B. In response to CsA, BP inc reased in all patients, but more so in patients of group B than in patients of group A. One year after transplantation, daytime and nighttime ABP had increased by 6+/-9/3+/-11% and 12+/-10/14+/-14% in group A and by 12+/-6/13 +/-10% (P<0.05) and 21+/-11/27+/-21% (P<0.01) in group B. In both groups, t he increase in nighttime ABP was greater than the increase in daytime ABP, which resulted in an attenuation or, even, a reversal of the diurnal BP rhy thm. Because the rise in BP was greater in patients with more advanced symp athetic dysfunction, the sympathetic nervous system appears to counteract t he CsA-induced rise in BP rather than causing it. This implies involvement of factors other than sympathetic activation in the pathogenesis of CsA-ind uced rise in BP in patients with familial amyloid polyneuropathy.