[Nitric oxide and reflectory regulation of blood circulation in rats].
In acute experiments on anaesthetized with urethane normotensive rats we studied the ways of participation of nitric oxide (NO) in reflector control of the cardiovascular system by the medullary neurons within n.tractus solitarii (NTS), dorsal nucleus of the vagus nerve (DNV), n. ambiguus (AMB), and the lateral reticular nucleus (LRN). Modulations of the activities of neuronal NO-synthase (nNOS) in the populations of the cardiovascular neurons within the medullary nuclei which are involved in the reflector cardiovascular control were induced by intramedullary injections of sodium nitroprusside as NO donor, L-arginine as NO precursor, L-NNA as an inhibitor of NOS, as well as by intraperetoneal injections of 7-nitroindazol (nNOS inhibitor). We have determined that stimulation of nNOS activity in the populations of the medullary neurons resulted in both remarkable shifts in the SAP level and in inhibiting the chemoreceptor reflector responses. After preliminary inhibiting nNOS chemoreceptor reflexes induced by epinephrine were found to be enhanced in most experiments.
D000818:Animals; D001775:Blood Circulation / Q000502:physiology*; D002628:Chemoreceptor Cells / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D009474:Neurons / Q000201:enzymology* / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D052248:Nitric Oxide Synthase Type I; D051381:Rats; D012154:Reticular Formation / Q000166:cytology / Q000201:enzymology / Q000502:physiology; D017552:Solitary Nucleus / Q000166:cytology / Q000201:enzymology / Q000502:physiology; D014630:Vagus Nerve / Q000166:cytology / Q000201:enzymology / Q000502:physiology
D004791:Enzyme Inhibitors; D020030:Nitric Oxide Donors; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496322:Nos1 protein, rat