The asymmetric dimethylarginine-mediated inhibition of nitric oxide in the rostral ventrolateral medulla contributes to regulation of blood pressure in hypertensive rats

Tan, Xing; Li, Ji-Kui; Sun, Jia-Cen; Jiao, Pei-Lei; Wang, Yang-Kai; Wu, Zhao-Tang; Liu, Bing; Wang, Weizhong

doi:10.1016/j.niox.2017.04.002

Cited by 12 publications

(9 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…NO, a key modulator of intracellular signaling, exerts its central control of arterial pressure and HR via various mechanisms including interaction with several neurotransmitter systems, receptors, and effectors, and the effects may be different depending on specific type of NO synthase (Chen et al., ; Mayorov, ; Shinohara et al., ; Tan et al., ). Studies showed that NO generated by neuronal NOS (nNOS) induced sympathoexcitation via glutamate receptors, while NO derived from inducible iNOS elicited sympathoinhibition via GABA receptors in RVLM (Chan et al., ).…”

Section: Discussionmentioning

confidence: 99%

Involvement of NMDA Receptors, Nitric Oxide, and GABA in Rostral Ventrolateral Medulla in Acute Ethanol‐Induced Cardiovascular Responses in Rats

Lin

Chen

et al. 2018

Alcoholism Clin & Exp Res

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Involvement of NMDA Receptors, Nitric Oxide, and GABA in Rostral Ventrolateral Medulla in Acute Ethanol‐Induced Cardiovascular Responses in Rats

Lin

Chen

et al. 2018

Alcoholism Clin & Exp Res

View full text Add to dashboard Cite

show abstract

“…After ICH, elevated ADMA levels might also affect systemic blood pressure. Experimental data in rats showed that microinjection of ADMA in the rostral ventrolateral medulla reduced NO synthesis and increased blood pressure [ 26 ]. Importantly, high blood pressure after ICH has been associated with poor clinical outcome and secondary complications such as hematoma enlargement [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Dimethylarginines in patients with intracerebral hemorrhage: association with outcome, hematoma enlargement, and edema

Worthmann

Martens‐Lobenhoffer

et al. 2017

J Neuroinflammation

View full text Add to dashboard Cite

BackgroundAsymmetric dimethylarginine (ADMA)––the most potent endogenous NO-synthase inhibitor, has been regarded as mediator of endothelial dysfunction and oxidative stress. Considering experimental data, levels of ADMA and its structural isomer symmetric dimethylarginine (SDMA) might be elevated after intracerebral hemorrhage (ICH) and associated with clinical outcome and secondary brain injury.MethodsBlood samples from 20 patients with acute ICH were taken at ≤ 24 h and 3 and 7 days after the event. Nine patients had favorable (modified Rankin Scale (mRS) at 90 days 0–2) outcome, and 11 patients unfavorable outcome (mRS 3–6). Patients’ serum ADMA, SDMA, and L-arginine levels were determined by high-performance liquid chromatography–tandem mass spectrometry. Levels were compared to those of 30 control subjects without ICH. For further analysis, patients were grouped according to outcome, hematoma and perihematomal edema volumes, occurrence of hematoma enlargement, and cytotoxic edema as measured by computed tomography and serial magnetic resonance imaging.ResultsLevels of ADMA––but not SDMA and L-arginine––were elevated in ICH patients compared to controls (binary logistic regression analysis: ADMA ≤ 24 h, p = 0.003; 3 days p = 0.005; 7 days p = 0.004). If patients were grouped according to outcome, dimethylarginines were increased in patients with unfavorable outcome. The binary logistic regression analysis confirmed an association of SDMA levels ≤ 24 h (p = 0.048) and at 3 days (p = 0.028) with unfavorable outcome. ADMA ≤ 24 h was increased in patients with hematoma enlargement (p = 0.003), while SDMA ≤ 24 h was increased in patients with large hematoma (p = 0.029) and perihematomal edema volume (p = 0.023).ConclusionsOur data demonstrate an association between dimethylarginines and outcome of ICH. However, further studies are needed to confirm this relationship and elucidate the mechanisms behind.

show abstract

“…Measurement of the total NO production in the RVLM was based on our previous study (Tan et al, 2017b). Briefly, the RVLM tissues were punched and lysed in lysis buffer (tissue specific, purchased from Beyotime Biotechnology, no.…”

Section: Total Nitric Oxide Production and Nitric Oxide Synthase Activity Detectionmentioning

confidence: 99%

“…As previously described (Tan et al, 2017b), rats were killed, and the brains were quickly extracted and stored at −80 • C. The RVLM tissues were punched in a freezing microtome (−20 • C) and thoroughly lysed in cell lysate for 30 min at 4 • C. After centrifugation for 20 min, the supernatant was left to measure the protein concentration by bicinchoninic acid (BCA) kit. Then, the protein samples (35 µg) were denaturalized and run on a 10% sodium dodecyl sulfatepolyacrylamide gel electrophoresis (SDS-PAGE) gel followed by transfer to polyvinylidene difluoride (PVDF) membrane (Millipore, Burlington, MA, United States).…”

Section: Western Blotting Analysismentioning

confidence: 99%

The Release of Nitric Oxide Is Involved in the β-Arrestin1-Induced Antihypertensive Effect in the Rostral Ventrolateral Medulla

Sun

Tan

et al. 2021

Front. Physiol.

Self Cite

View full text Add to dashboard Cite

β-Arrestin1 is a multifunctional scaffold protein with the ability to interact with diverse signaling molecules independent of G protein-coupled receptors. We previously reported that overexpression of β-arrestin1 in the rostral ventrolateral medulla (RVLM) decreased blood pressure (BP) and renal sympathetic nerve activity (RSNA) in spontaneously hypertensive rats (SHRs). Nitric oxide (NO) is widely reported to be involved in central cardiovascular regulation. The goal of this study was to investigate whether NO signaling contributes to the β-arrestin1-mediated antihypertensive effect in the RVLM. It was found that bilateral injection of adeno-associated virus containing Arrb1 gene (AAV-Arrb1) into the RVLM of SHRs significantly increased NO production and NO synthase (NOS) activity. Microinjection of the non-selective NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME; 10 nmol) into the RVLM prevented the β-arrestin1-induced cardiovascular inhibitory effect. Furthermore, β-arrestin1 overexpression in the RVLM significantly upregulated the expression of phosphorylated neuronal NOS (nNOS) by 3.8-fold and extracellular regulated kinase 1/2 (ERK1/2) by 5.6-fold in SHRs. The β-arrestin1-induced decrease in BP and RSNA was significantly abolished by treatment with ERK1/2 small interfering RNA (ERK1/2 siRNA). Moreover, ERK1/2 siRNA attenuated the β-arrestin1-induced NO production, NOS activity, and nNOS phosphorylation in the RVLM. Taken together, these data demonstrate that the antihypertensive effect of β-arrestin1 in the RVLM is mediated by nNOS-derived NO release, which is associated with ERK1/2 activation.

show abstract

The asymmetric dimethylarginine-mediated inhibition of nitric oxide in the rostral ventrolateral medulla contributes to regulation of blood pressure in hypertensive rats

Cited by 12 publications

References 57 publications

Involvement of NMDA Receptors, Nitric Oxide, and GABA in Rostral Ventrolateral Medulla in Acute Ethanol‐Induced Cardiovascular Responses in Rats

Involvement of NMDA Receptors, Nitric Oxide, and GABA in Rostral Ventrolateral Medulla in Acute Ethanol‐Induced Cardiovascular Responses in Rats

Dimethylarginines in patients with intracerebral hemorrhage: association with outcome, hematoma enlargement, and edema

The Release of Nitric Oxide Is Involved in the β-Arrestin1-Induced Antihypertensive Effect in the Rostral Ventrolateral Medulla

Contact Info

Product

Resources

About