Key result
Inhibition of neuronal NO synthase within the brain stem of pigs potentiated the sympathoexcitatory effects of glutamate on blood pressure, cardiac output, and heart rate.
Why the study?
Does neuronal NO synthase inhibition modulate the sympathoexcitatory effects of central glutamate in vagotomized anesthetized pigs?
Population
Vagotomized anesthetized pigs
Comparison
Intracerebroventricular administration of… vs Responses to glutamate or somatosympathetic…
Design
Preclinical
Authors
Loading...
Supports nNOS modulation of central sympathetic drive; leaves open translation to human autonomic regulation.
Does neuronal NO synthase inhibition modulate the sympathoexcitatory effects of central glutamate in vagotomized anesthetized pigs?
Neuronal NO derived from nNOS reduces sympathetic excitability by modulating central glutamate effects in a porcine model.
Zanzinger et al. (1997) studied Vagotomized anesthetized pigs. nNOS inhibitors (7-nitroindazole or S-methyl-L-thiocitrulline) was evaluated on Renal sympathetic nerve activity, arterial blood pressure, and cardiac output. Inhibition of neuronal NO synthase within the brain stem of pigs potentiated the sympathoexcitatory effects of glutamate on blood pressure, cardiac output, and heart rate.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: