Mechanisms of postexercise hypotension: Contribution of histamine-1 and -2 receptors

Abstract

After a single bout of dynamic exercise, there are profound changes in the mechanisms that regulate and determine arterial pressure, resulting in postexercise hypotension. The basic postexercise hypotensive response results from a persistent decrease in systemic vascular resistance that is not completely offset by increases in cardiac output. In addition, calf and forearm vascular resistances are decreased in parallel with systemic vascular resistance, suggesting a postexercise skeletal muscle hyperemia. While the response has been well documented, the mechanisms responsible have been elusive. The experiments described in this dissertation were designed to examine if there was a mechanistic role for histamine-1 (H₁) and histamine-2 (H₂) receptors in postexercise hyperemia leading to a reduction in arterial pressure. The studies described in Chapters III and IV were designed to investigate the individual contributions of H₁- and H₂-receptors to postexercise hyperemia. Results showed that H₁-receptors mediate the early (∼30 minutes) postexercise hypotension, while H₂-receptors control the later stages (∼60-90 minutes) of postexercise hypotension. Chapter V studied the combined contribution of H₁- and H₂ -receptors to postexercise hyperemia, as well as the mechanisms of postexercise hypotension in endurance-exercise trained population. The results indicated that the entire 90 minute period of postexercise hyperemia was abolished by the histamine receptor antagonists in the sedentary and endurance exercise-trained men and women. Importantly, the results suggest that postexercise hyperemia is present and mediated by H₁- and H₂-receptors in endurance trained men and women. The study described in Chapter VI sought to determine whether histamine concentrations increased in inactive muscle interstitium during exercise and postexercise. The results demonstrated that histamine concentrations were not increased in the inactive skeletal muscle interstitium suggesting that either histamine is not present in the inactive muscle or that activation could occur through another means. Finally, the study in Chapter VII was designed to determine if the reduction in postexercise hypotension, provided by the blockade of H₁-receptors, could alleviate postexercise syncope. The results indicate that postexercise syncope is not dependent on activation of H₁-receptors. This dissertation includes both my previously published and co-authored materials.