Opposite effects of hypertension and exercise training (ET) on central vasopressinergic system

We have shown that ET augments intrinsic excitability of vasopressinergic (VPergic) and oxytocinergic (OTergic) hypothalamic pre‐autonomic neurons and improves the depressed OTergic modulation of cardiovascular control in hypertension. We sought now to study ET effects on VPergic control of cardiovascular parameters in normotension and hypertension. WKY and SHR submitted to ET (55% VO2 max, 1h/day, 3 mo) or kept sedentary (S) were instrumented with brainstem (BS) cannula, arterial catheter and iliac probe for nucleus tractus solitary (NTS) injection, AP, HR and skeletal muscle blood flow (SMF) recordings, respectively. SHRs showed higher AP, HR and SMF with elevated AP and SMF variabilities, as measured by power spectral analysis: 3.6‐ and 8.6‐fold with marked increase on low frequency component (LF ~12‐fold, p<0.05 vs WKYs). ET reduced basal AP, HR and SMF only in SHRt (−5%, −12% and −20%) with 52% reduction on SMF LF variability. V1 blocker NTS‐treated SHRs showed similar LF reduction. Brains from other groups were prepared for in situ hybridization (autoradiography on sequential BS slices hybridized with 35S‐oligonucleotides) and RT‐PCR studies (BS/hypothalamus punches). In SHRs high LF variability was correlated with both increased VP mRNA expression in BS target areas and V1a mRNA within the NTS (+4.7‐fold and +25%, p<0.05). SHRt vs SHRs showed reductions on hypothalamic VP and NTS V1a mRNA densities (p<0.05). Data suggest: 1) high sympathetic outflow and elevated AP and SMF variabilities (main features of SHR) are caused by overactivation of central VPergic system; 2) ET reduces sympathetic activity by blunting central VPergic system. Supported by FAPESP, CNPq, CAPES.