Estudo da participação da enzima óxido nítrico sintase Neuronial sobre as respostas cardiovasculares, autonômicas e neuroendócrinas durante o choque hemorrágico em ratos

Abstract

Nitric oxide (NO), synthesized by the neuronal isoform of nitric oxide synthase (nNOS), is a neuromodulator widely distributed in the central nervous system, involved in the regulation of autonomic and cardiovascular functions. This study aimed to investigate the role of neuronal nitric oxide synthase (nNOS) in cardiovascular, autonomic, and neuroendocrine responses to hemorrhagic shock in rats. For this purpose, 7-Nitroindazole (7-NI), a selective nNOS inhibitor, was administered intraperitoneally. The effects of the treatment were evaluated on mean arterial pressure (MAP), heart rate (HR), tail skin temperature (TST), and plasma concentrations of vasopressin (AVP), in an experimental model of acute hemorrhage. The results showed that nNOS inhibition increased the latency to the onset of hypotension and attenuated the drop in MAP during hemorrhage, without affecting tail skin temperature. In addition, 7-NI treatment induced a more pronounced tachycardic response during and after hemorrhage, suggesting a possible enhancement of sympathetic activity. It was observed that nNOS inhibition attenuated the increase in plasma AVP release in response to hemorrhage, suggesting that neuronally- derived NO contributes to the stimulation of this hormone's secretion under hypovolemic conditions. These findings indicate that nNOS-derived NO actively participates in the modulation of physiological responses to hemorrhagic shock and that its inhibition may represent a potential therapeutic target to improve hemodynamic stability in situations of severe hypovolemia.