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 V(1)-receptor antagonist d(CH(3))(5) Tyr(Me)-AVP (AVP-X). AP and HR were significantly decreased below preexercise values with central administration of vehicle [P < 0.05, change (Delta)-21 +/- 4 mmHg and Delta-20 +/- 6 beats/min, respectively]. In sharp contrast, after exercise with central administration of AVP-X, both AP (Delta+8 +/- 5 mmHg) and HR (Delta+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 V(1) 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.

Postexercise α-adrenergic receptor hyporesponsiveness in hypertensive rats is due to nitric oxide

“…These results are consistent with several previous reports (4,5,7,11,20,31,35). In addition, postexercise vasoconstrictor responses to PE were significantly attenuated (15 Ϯ 3%) in male but not female SHR.…”

“…It is well documented that a single bout of dynamic exercise reduces postexercise AP for several hours (11,20,31). Thus acute exercise may be a safe therapeutic approach for lowering AP in hypertensive individuals.The mechanisms mediating postexercise hypotension (PEH) remain the focus of numerous investigative efforts (7,22,35,55). It is generally accepted that PEH is most often associated with elevations in cardiac output (CO) as well as reductions in peripheral vascular resistance (22,24,35) and sympathetic nerve activity (SNA) (16,22,24,35).…”

A comparison of two treatment protocols in the management of exercise-associated postural hypotension: a randomised clinical trial

“…The arterial baroreflex also establishes the prevailing systemic arterial pressure by setting the operating point 28. On this basis arginine vasopressin (AVP), by its action on V1 receptors,29 may contribute to the development of post-exercise hypotension. AVP enhances both cardiopulmonary and arterial baroreflex function, and lowers the operation point of the arterial baroreflex 28.…”

Neural mechanismsand post-exercise hypotension: The importance of experimental studies

“…Boone and Jr. Corry 62 demonstrated that the expression of the gene preproenkephalin (PPK) increases in the CNS after treadmill exercise in SHRs, suggesting that increase in PPK synthesis and release in the NTS, CVLM, and RVLM may be involved in regulating PEH. Previous studies on both humans and SHRs indicate that endorphin systems (opioid receptor antagonist, naloxone) attenuate PEH, and they trigger the transient depression of blood pressure immediately after running period in the SHR 63 . In addition, injections of vasopressin V1 receptor antagonist into the lateral cerebral ventricle impedes the manifestation of PEH 64 .…”