The nucleus tractus solitarius (NTS), a major hindbrain area involved in cardiovascular regulation, receives primary afferent fibers from peripheral baroreceptors and chemoreceptors.
Hydrogen peroxide (H(2)O(2)) is a relatively stable and diffusible
reactive oxygen species (ROS), which acting centrally, may affect neural mechanisms. In the present study, we investigated effects of H(2)O(2) alone or combined with the glutamatergic antagonist
kynurenate into the NTS on mean arterial pressure (MAP) and heart rate (HR). Conscious or anesthetized (
urethane and
alpha-chloralose) male Holtzman rats (280-320 g) were used.
Injections of H(2)O(2) (125 to 1500 pmol/40 nl) into the intermediate NTS of anesthetized rats evoked dose-dependent and transient
hypotension (-18 +/- 3 to -55 +/- 11 mmHg) and
bradycardia (-16 +/- 5 to -116 +/- 40 bpm). Injection of the
catalase inhibitor
3-amino-1,2,4-triazole (100 nmol/40 nl) into the NTS also produced
hypotension and
bradycardia. Previous injection of the ionotropic
L-glutamate receptor antagonist
kynurenate (7 nmol/40 nl) attenuated by 48% the bradycardic response, without changing the
hypotension evoked by H(2)O(2) (500 pmol/40 nl) in anesthetized rats. The
antioxidant L-ascorbate (600 pmol/80 nl) injected into the NTS attenuated the bradycardic (42%) and hypotensive (67%) responses to H(2)O(2) (500 pmol/40 nl) into the NTS. In conscious rats, injection of H(2)O(2) (50 nmol/100 nl) into the NTS also evoked intense
bradycardia (-207 +/- 8 bpm) and
hypotension (-54 +/- 6 mmHg) that were abolished by prior injection of
kynurenate (7 nmol/100 nl). The results show that H(2)O(2) into the NTS induces
hypotension and
bradycardia probably due to activation of glutamatergic mechanisms.