Neural control of blood pressure and cardiovascular reactivity to stress in a spontaneously hypertensive mouse

Abstract

We investigated the contribution of the sympathetic nervous system (SNS) to spontaneous hypertension in the BPH/2J Schlager mouse. Male hypertensive (n = 6) and normotensive (BPN/3J; n = 8) mice were implanted with telemetry probes and recordings of cardiovascular and activity parameters made before and during aversive stress (shaker, restraint, cage‐swap) and non‐aversive stress (feeding). MAP was higher in BPH/2J than BPN/3J mice (128±1 vs 111±1 mmHg; P<0.001) as was the day‐night difference in MAP in BPH/2J animals (17±2 vs 6±1 mm Hg; P<0.001). Heart rate and activity were also greater in BPH/2J compared to BPN/3J (+19% and +88%, P<0.001). BPH/2J showed greater pressor responses to aversive stress (+70–100%) but a slightly greater pressor responses to feeding (+21%) compared with BPN/3J. Sympathetic blockade by pentolinium reduced blood pressure to comparable levels in both strains. The greater pressor response to aversive stimuli in BPH/2J mice but not feeding also suggests that the greater stress response observed in these animals is not due to a vascular amplifying effect which would likely affect all behavioural responses. Our findings of an exaggerated day‐night rhythms, responses to pentolinium as well as the hyper‐responsiveness to aversive stimuli suggests a major contribution from the SNS in the hypertension observed in this animal model.