Neuronal Nitric Oxide Synthase (nNOS) blockade within the ventrolateral medulla differentially modulates cardiovascular responses and nNOS expression during static skeletal muscle contraction

Ally, Ahmmed; Kabadi, Shruti V.; Phattanarudee, Siripan; Patel, Maitreyee; Maher, Timothy J.

doi:10.1016/j.brainres.2007.02.064

Cited by 6 publications

(3 citation statements)

References 47 publications

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“…However, it should be remembered that nNOS-derived NO in the RVLM is implicated in pressor responses (Kishi et al, 2001;Chan et al, 2003;Ally et al, 2007;Martins-Pinge et al, 2007). Therefore, we used a selective nNOS inhibitor (NPLA) to further confirm this point in our model system.…”

Section: Discussionmentioning

confidence: 73%

“…‫,ء‬ P Ͻ 0.05 versus vehicle. , 2007Chan et al, 2003Chan et al, , 2004Ally et al, 2007;Mayorov, 2007;Guo et al, 2009)]; and 2) many of the CB 1 R-mediated neurobiological responses depend on nNOS/NO signaling (Makara et al, 2007;Jones et al, 2008;Carney et al, 2009). Here, we present the first evidence that early (5 min) activation (phosphorylation) of RVLM nNOS (Fig.…”

Section: Discussionmentioning

confidence: 99%

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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

J Pharmacol Exp Ther

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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: 73%

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

J Pharmacol Exp Ther

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“…The nNOS isoform within the RVLM and the CVLM differentially modulates cardiovascular responses during static exercise [139,152]. Moreover, the modulation of the exercise pressor reflex by nNOS is attributed to differential alterations in glutamate and GABA neurotransmission within the RVLM and CVLM, and that blockade of nNOS can also modify the expression of the nNOS isoform within the RVLM and CVLM [181]. A similar modulation of the exercise pressor reflex by the iNOS isoform via glutamate, GABA, and expression of the iNOS protein is regulated within the RVLM and CVLM1.…”

Section: Enos and The Exercise Pressor Reflexmentioning

confidence: 99%

Endothelial Nitric Oxide Synthase (eNOS) and the Cardiovascular System: in Physiology and in Disease States

Nauli

2022

AJBSR

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erectile dysfunction [7]; the role of the eNOS enzyme, including its modulation, regulation, and relevance within the cardiovascular system (CVS) in both normal physiological state and in several important cardiovascular diseases is elaborated. In addition, because the amount of NO generated by the vascular endothelial cells plays critical roles in the regulation and maintenance of the vascular tone, migration, production, proliferation, and maturation of cells, leukocyte adhesion, and platelet aggregation, it can be implied that eNOS is indeed an essential molecule for a properly functioning and healthy CVS, thus emphasizing the protective action of eNOS on the CVS.

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Modulation of inducible nitric oxide synthase (iNOS) expression and cardiovascular responses during static exercise following iNOS antagonism within the ventrolateral medulla

et al. 2014

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Previous reports indicate that inducible nitric oxide synthase (iNOS) blockade within the rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla (CVLM) differentially modulated cardiovascular responses, medullary glutamate, and GABA concentrations during static skeletal muscle contraction. In the current study, we determined the role of iNOS antagonism within the RVLM and CVLM on cardiovascular responses and iNOS protein expression during the exercise pressor reflex in anesthetized rats. Following 120 min of bilateral microdialysis of a selective iNOS antagonist, aminoguanidine (AGN; 10 µM), into the RVLM, the pressor responses were attenuated by 72 % and changes in heart rate were reduced by 38 % during a static muscle contraction. Furthermore, western blot analysis of iNOS protein abundance within the RVLM revealed a significant attenuation when compared to control animals. In contrast, bilateral administration of AGN (10 µM) into the CVLM augmented the increases in mean arterial pressure by 60 % and potentiated changes in heart rate by 61 % during muscle contractions, but did not alter expression of the iNOS protein within the CVLM. These results demonstrate that iNOS protein expression within the ventrolateral medulla is differentially regulated by iNOS blockade that may, in part, contribute to the modulation of cardiovascular responses during static exercise.

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Neuronal Nitric Oxide Synthase (nNOS) blockade within the ventrolateral medulla differentially modulates cardiovascular responses and nNOS expression during static skeletal muscle contraction

Cited by 6 publications

References 47 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

Endothelial Nitric Oxide Synthase (eNOS) and the Cardiovascular System: in Physiology and in Disease States

Modulation of inducible nitric oxide synthase (iNOS) expression and cardiovascular responses during static exercise following iNOS antagonism within the ventrolateral medulla

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