Modulation of cardiovascular responses and neurotransmission during peripheral nociception following nNOS antagonism within the periaqueductal gray

Karlsson, Gudbjorn A.; Chaitoff, Kevin A.; Hossain, Shamma; Böhlke, Mark; Maher, Timothy J.; Ally, Ahmmed

doi:10.1016/j.brainres.2007.01.101

Cited by 13 publications

(9 citation statements)

References 54 publications

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“…First, nNOS-generated NO reduces GABA release in the dorsal periaqueductal gray matter and RVLM along with a pressor response (Chan et al, 2003;Karlsson et al, 2007;Martins-Pinge et al, 2007). Second, ERK1/2-dependent phosphorylation of nNOS in the RVLM mediates sympathoexcitation (Chan et al, 2004(Chan et al, , 2005(Chan et al, , 2010.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of Rostral Ventrolateral Medulla Neuronal Nitric-Oxide Synthase–Nitric-Oxide Signaling Mediates the Central Cannabinoid Receptor 1-Evoked Pressor Response in Conscious Rats

Ibrahim

Abdel‐Rahman²

2012

The Journal of Pharmacology and Experimental Therapeutics

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Our recent studies implicated brainstem GABAergic signaling in the central cannabinoid receptor 1 (CB 1 R)-mediated pressor response in conscious rats. Given the well established link between neuronal nitric-oxide synthase (nNOS)/nitric oxide (NO) signaling and GABAergic transmission in brainstem cardiovascular regulating areas, we elucidated the role of nNOSgenerated NO in the central CB 1 R-elicited pressor response. Compared with vehicle, intracisternal (i.c.) microinjection of themethanone mesylate (WIN55212-2) (15 g/rat) significantly enhanced nNOS phosphorylation as well as the total nitrate and nitrite content in the rostral ventrolateral medulla (RVLM) at 5, 10, and 30 min, which paralleled the elicited pressor response. These findings were corroborated by: 1) the parallel dose-related increases in blood pressure and RVLM-NO levels, measured in real time by in vivo electrochemistry, elicited by intra-RVLM WIN55212-2 (100, 200, or 300 pmol /80 nl; n ϭ 5) in conscious rats; and 2) the significantly higher phosphorylated nNOS (pnNOS) levels in the WIN55212-2-injected RVLM compared with the contralateral RVLM. Subsequent neurochemical studies showed that WIN55212-2 (15 g/rat i.c.) significantly increased the number and percentage of neurons immunostained for nNOS (nitroxidergic neurons) and c-Fos (marker of neuronal activity) within the RVLM. The increases in blood pressure and the neurochemical responses elicited by intracisternal WIN55212-2 were attenuated by prior central CB 1 R blockade by N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM251; 30 g/rat i.c.) or selective nNOS inhibition by N -propyl-L -arginine (1 g/rat i.c.). These findings implicate RVLM p-nNOS/NO signaling as a molecular mechanism in the central CB 1 R-evoked pressor effect in conscious rats.

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Section: Discussionmentioning

confidence: 99%

Enhancement of Rostral Ventrolateral Medulla Neuronal Nitric-Oxide Synthase–Nitric-Oxide Signaling Mediates the Central Cannabinoid Receptor 1-Evoked Pressor Response in Conscious Rats

Ibrahim

Abdel‐Rahman²

2012

The Journal of Pharmacology and Experimental Therapeutics

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“…Moreover, functional results have supported a role of these structures in cardiovascular adjustments to (Li, 2004;Crestani et al, 2010;Alves et al, 2011;Mastelari et al, 2011). NMDA glutamate receptor and nNOS interaction is an important signaling mechanism involved in control of autonomic and cardiovascular function in several CNS regions (Wu et al, 2000;Li et al, 2001;Ryu et al, 2001;Resstel and Correa, 2006;Karlsson et al, 2007;Tavares et al, 2007;Alves et al, 2009;Busnardo et al, 2010). Furthermore, acute exercise by contractions of the tibialis anterior muscle increased nitrite, a stable metabolite of NO, in the brain (Paula et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Involvement of N-methyl-d-aspartate glutamate receptor and nitric oxide in cardiovascular responses to dynamic exercise in rats

Camargo

Alves

Biojone

et al. 2013

European Journal of Pharmacology

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Dynamic exercise evokes sustained cardiovascular responses, which are characterized by arterial pressure and heart rate increases. Although it is well accepted that there is central nervous system mediation of cardiovascular adjustments during exercise, information on the role of neural pathways and signaling mechanisms is limited. It has been reported that glutamate, by acting on NMDA receptors, evokes the release of nitric oxide through activation of neuronal nitric oxide synthase (nNOS) in the brain. In the present study, we tested the hypothesis that NMDA receptors and nNOS are involved in cardiovascular responses evoked by an acute bout of exercise on a rodent treadmill. Moreover, we investigated possible central sites mediating control of responses to exercise through the NMDA receptor-nitric oxide pathway. Intraperitoneal administration of the selective NMDA glutamate receptor antagonist dizocilpine maleate (MK-801) reduced both the arterial pressure and heart rate increase evoked by dynamic exercise. Intraperitoneal treatment with the preferential nNOS inhibitor 7-nitroindazole reduced exercise-evoked tachycardiac response without affecting the pressor response. Moreover, treadmill running increased NO formation in the medial prefrontal cortex (MPFC), bed nucleus of the stria teminalis (BNST) and periaqueductal gray (PAG), and this effect was inhibited by systemic pretreatment with MK-801. Our findings demonstrate that NMDA receptors and nNOS mediate the tachycardiac response to dynamic exercise, possibly through an NMDA receptor-NO signaling mechanism. However, NMDA receptors, but not nNOS, mediate the exercise-evoked pressor response. The present results also provide evidence that MPFC, BNST and PAG may modulate physiological adjustments during dynamic exercise through NMDA receptor-NO signaling.

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“…36,37 In addition, NO-dependent pathways can be activated by neurotransmitters such as noradrenalin and glutamate. [38][39][40] Therefore, it is likely that the NO generated by restraint stress activates these pathways.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide levels in rat hypothalamus are increased by restraint stress and decreased by biting

et al. 2008

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Mastication, which includes biting, is of great importance not only for the intake of food but also for the mental, physical and physiological functioning of the body. For example, biting suppresses the stress response. Although biting and nitric oxide (NO) appear to modulate brain dynamics during stress, the underlying mechanisms have not been elucidated. In this study, we examined the effect of biting during restraint stress on NO levels in the rat hypothalamus. To this end, we used NO-selective electrodes that were calibrated by electron spin resonance (ESR) spectroscopy. We implanted the electrodes and probes for perfusion of solutions into the brain of rats, near the hypothalamus. Saline containing 10 mM N-nitro-L-arginine methyl ester (L-NAME), which is one of the most commonly used inhibitors of nitric oxide synthase (NOS), was employed as the perfusate. L-NAME prevented increases in NO levels in the rat hypothalamus that were induced by restraint stress and biting. Hypothalamic NO levels in rats under restraint stress for 180 min were increased above levels observed in unrestrained control rats. The increase in hypothalamic NO (from 2.123 muM to 4.760 muM) during restraint stress was reduced after biting for 30 min. The decay rate of NO levels after biting was -0.584 pA/min (-0.071 muM/min). We conclude that: (i) it is possible to evaluate NO levels in vivo in rat brain; (ii) NO levels are increased by restraint stress; and (iii) this increase is prevented by biting behavior.

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Modulation of cardiovascular responses and neurotransmission during peripheral nociception following nNOS antagonism within the periaqueductal gray

Cited by 13 publications

References 54 publications

Enhancement of Rostral Ventrolateral Medulla Neuronal Nitric-Oxide Synthase–Nitric-Oxide Signaling Mediates the Central Cannabinoid Receptor 1-Evoked Pressor Response in Conscious Rats

Enhancement of Rostral Ventrolateral Medulla Neuronal Nitric-Oxide Synthase–Nitric-Oxide Signaling Mediates the Central Cannabinoid Receptor 1-Evoked Pressor Response in Conscious Rats

Involvement of N-methyl-d-aspartate glutamate receptor and nitric oxide in cardiovascular responses to dynamic exercise in rats

Nitric oxide levels in rat hypothalamus are increased by restraint stress and decreased by biting

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