Hemodynamic responsiveness is caused by skeletal muscle mechanoreflex as it is in many evidence from multiple animal models of hypertension. There is very little evidence proving that peripheral mechanism triggers pathogens that cause mechanoreflex dysfunction. Past data indicates the likely culprit as a mechanism of central origin. Studies suggest that nitric oxide lane inside the NTS is abnormal hypertension. The research indicates that reduction in the activity of NOS in coincidence with increases in the manufacture of relative oxygen species. This results in a reduction in nitric oxide within the NTS.Nitric oxide restrains muscle reflex activity. Mechanoreflex is caused by a decrease in activity in the neuromodulator. There need of increased research on the cause of mechanoreflex dysfunction in hypertension. This can be achieved by experimentation on human patients .these can help to come up with a treatment that reduces associated with the disease. Safety of exercise could be the best prescription as it is in non-pharmacological therapy for hypertension.
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The sympathetically-mediated hemodynamic response to exercise is abnormally exaggerated in hypertension increasing the risk for occurrence of deleterious cardiovascular or cerebrovascular events. Accumulating evidence in multiple animal models of human hypertension suggests that the skeletal muscle mechanoreflex contributes significantly to this potentiated hemodynamic responsiveness. At present, very little evidence exists indicating that a peripheral mechanism underlies the pathogenesis of mechanoreflex dysfunction in this disease. Conversely, recent data implicates a mechanism of central origin as a likely culprit. Specifically, studies have demonstrated that the nitric oxide pathwaywithin the NTS (the primary center for initial processing of mechanoreflex somatosensory inputwithin the brain stem) is abnormal in hypertension. The data suggest that decreases in the expression/ activity of NOS, independent from or in conjunction with increases in the production of reactive oxygen species, reduce the availability of nitric oxide within the NTS. Given that nitric oxide normally acts to restrain or buffer muscle reflex activity, a decrease in the availability of this neuromodulator may underlie the mechanoreflex overactivity manifest in this disease. Although this initial evidence increases our understanding of the derivation of mechanoreflex dysfunction in hypertension, there is a clear need for additional experimentation; particularly in human patients. Continued research in this areamay identify novel treatments that, when implemented, reduce the risks associated with exercise in this disease. This could enhance the safety of exercise prescription as a non-pharmacological treatment for hypertension.