Purinergic receptor antagonism does not attenuate the exercise pressor reflex in hypertensive adults

Abstract

A previous study reported that purinergic (P2) receptor antagonism attenuated the blood pressure (BP) response to static handgrip (HG) in healthy adults. The aim of this study was to determine if pyridoxine HCl is an effective in vitro P2 receptor antagonist and if localized P2 receptor antagonism with pyridoxine in vivo blunts the exaggerated exercise pressor reflex (EPR) in older hypertensive (HTN) adults. For in vitro studies, dorsal root ganglion (DRG) cells isolated from mice were loaded with fura 2‐AM and incubated in control buffer (HBSS) or 100μM pyridoxine. Following incubation, the effect of 10μM ATP on intracellular Ca2+ was measured. The Ca2+ response was attenuated in DRG cells incubated with pyridoxine (HBSS: Δ130±10 nM v pyridoxine: Δ13±2 nM; P<0.05). For in vivo studies, 8 HTN adults (6M; 67±1 yrs; BP 141±5/81±4 mmHg) completed a control (0.9% saline; NS) and P2 receptor blockade (730mM pyridoxine) trial (randomized; 1 month apart). BP (Finometer) was measured at baseline and during static HG at 40% maximal voluntary contraction followed by post‐exercise ischemia (PEI). P2 receptor blockade did not blunt the increases in mean BP during HG (NS: Δ21±4 v P2: Δ23±5 mmHg; P>;0.05) or PEI (NS: Δ15±3 v P2: Δ17±3 mmHg; P>;0.05). These preliminary data suggest that pyridoxine is an effective in vitro P2 receptor antagonist but indicate that in vivo P2 receptor antagonism does not attenuate the EPR in older HTN adults.Supported by AHA 11PRE7580029 and ACSM Foundation.