Central blockade of vasopressin V1receptors attenuates postexercise hypotension

Abstract

We tested the hypothesis that central arginine vasopressin (AVP) mediates postexercise reductions in arterial pressure (AP) and heart rate (HR). To test this hypothesis, nine spontaneously hypertensive rats (SHR) were instrumented with a 22-gauge stainless steel guide cannula in the right lateral cerebral ventricle and with a carotid arterial catheter. After the rats recovered, AP and HR were assessed before and after a single bout of dynamic exercise with the central administration of vehicle or the selective AVP V1-receptor antagonist d(CH3)5Tyr(Me)-AVP (AVP-X). AP and HR were significantly decreased below preexercise values with central administration of vehicle [ P < 0.05, change (Δ)−21 ± 4 mmHg and Δ−20 ± 6 beats/min, respectively]. In sharp contrast, after exercise with central administration of AVP-X, both AP (Δ+8 ± 5 mmHg) and HR (Δ+24 ± 9 beats/min) were not significantly different from preexercise values ( P > 0.05). Furthermore, AVP-X at rest did not significantly alter AP (181 ± 11 vs. 178 ± 11 mmHg, P > 0.05) or HR (328 ± 24 vs. 331 ± 22 beats/min, P > 0.05). Thus central blockade of AVP V1 receptors prevented postexercise reductions in AP and HR. These data suggest that AVP, acting within the central nervous system, mediates postexercise reductions in AP and HR in the SHR.