FLUID-REGULATING AND SYMPATHOADRENAL HORMONAL RESPONSES TO PEAK EXERCISE FOLLOWING CARDIAC TRANSPLANTATION

Citation
H. Perrault et al., FLUID-REGULATING AND SYMPATHOADRENAL HORMONAL RESPONSES TO PEAK EXERCISE FOLLOWING CARDIAC TRANSPLANTATION, Journal of applied physiology, 76(1), 1994, pp. 230-235
Citations number
34
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
76
Issue
1
Year of publication
1994
Pages
230 - 235
Database
ISI
SICI code
8750-7587(1994)76:1<230:FASHRT>2.0.ZU;2-I
Abstract
Orthotopic heart transplantation results in cardiac denervation that c an disrupt the normal regulation of hydromineral balance. This study c ompared the exercise-induced variations in plasma osmolality; atrial n atriuretic peptide (ANP), arginine vasopressin (AVP), norepinephrine ( NE), epinephrine (E), and dopamine (DA) concentrations; and plasma ren in activity (PRA) of six cardiac transplant recipients (HTX) and six h ealthy age-matched controls (C) submitted to graded upright maximal cy cling. Venous blood samples were obtained at rest, at submaximal (70% O-2, uptake) and peak exercise, and after 10 and 30 min of sitting re covery. Peak O-2 uptake was not different between groups despite lower maximal heart rate in HTX (136 +/- 6 vs. 183 +/- 9 beats/min). Baseli ne plasma ANP and PRA were higher in HTX (203 +/- 55 pg/ml and 29.9 +/ - 7.4 ng.ml(-1).h(-1)) than in C (71 +/- 17 pg/ml and 5.4 +/- 0.96 ng. ml(-1).h(-1)); AVP was lower in HTX than in C (1.1 +/- 0.3 vs. 3.2 +/- 0.8 pg/ml; P < 0.05); and circulating E, NE, and DA were not differen t between groups. Exercise resulted in more marked increases in HTX th an in C for ANP (300 vs. 100%), AVP (2,000 vs. 300%), NE (860 vs. 500% ), and DA (611 vs. 187%) but not for PRA and a higher E response in C than in HTX (455 vs. 1,258%). These observations confirm that the pote ntial for ANP release to central volume loading is independent of inta ct cardiac innervation. The exaggerated AVP response in HTX could, how ever, reflect the absence of inhibitory influences consecutive to dene rvation. The blunted rise in E could be related to a partial inhibitio n of PNMT as a result of the chronic glucocorticoid therapy in HTX.