Neurokinin‐1 receptor expressing neurons in the nucleus of the solitary tract are required for full expression of post‐exercise hypotension in spontaneously hypertensive rats

Abstract

A single bout of exercise decreases blood pressure (post‐exercise hypotension; PEH) in both hypertensive humans and spontaneously hypertensive rats (SHR). Our recent studies suggest that in SHR, PEH may be dependent in part on activation of neurokinin‐1 receptors (NK1‐R) in the nucleus of the solitary tract (NTS). The current experiments were performed to test the hypothesis that selective elimination of NK1‐R expressing neurons in the NTS would attenuate PEH in SHR. The NK1‐R targeted neurotoxin, stable substance‐P saporin (SSP‐SAP) was microinjected into the NTS to ablate NK1‐R neurons in adult male SHR implanted with telemetry transmitters to measure blood pressure (BP) and heart rate. SSP‐SAP induced a transient (5 day) increase in BP after ablation relative to control (blank saporin; p<0.01) rats. Blood pressure variability, assessed as the standard deviation of daily systolic BP, increased by the second week after NK1‐R neuron ablation (p<0.05). Two weeks after NK1‐R neuron ablation, rats were subjected to a single bout of dynamic exercise or sham exercise. SSP‐SAP significantly blunted PEH (p<0.005, 2‐way RM ANOVA). For example, by 120 min post‐exercise blood pressure was decreased by −15.2 ± 2 mmHg in control (n=4) versus 0.5 ± 2.7 mmHg in SSP‐SAP (n=6) treated rats. We conclude that ablation of NTS NK1‐R expressing neurons increases blood pressure variability and attenuates PEH in SHR. (Support: HL‐67183)