The PI3K signaling-mediated nitric oxide contributes to cardiovascular effects of angiotensin-(1-7) in the nucleus tractus solitarii of rats

Wu, Zhao-Tang; Ren, Changzhen; Yang, Yi; Zhang, Ruwen; Sun, Jia-Cen; Wang, Yang-Kai; Su, Ding‐Feng; Wang, Weizhong

doi:10.1016/j.niox.2015.12.002

Cited by 25 publications

(17 citation statements)

References 51 publications

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“…More importantly, gene transfer of PI3K p110δ shRNA in the RVLM reduced levels of cardiovascular activity, but also inhibits neuroinflammation in Ang II‐induced hypertensive rats and SHR. The subunit p110δ belongs to the catalytic subunit of PI3K, and its blockade effectively prevents activity of PI3K in the RVLM . In this study, there is a limitation that we did not directly observe the effect of PI3K knockdown on the LPS‐induced neuroinflammation.…”

Section: Discussionmentioning

confidence: 91%

The phosphoinositide‐3 kinase signaling is involved in neuroinflammation in hypertensive rats

et al. 2017

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Section: Discussionmentioning

confidence: 91%

The phosphoinositide‐3 kinase signaling is involved in neuroinflammation in hypertensive rats

et al. 2017

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“…; Wu et al . ). Similarly, an increase in circulating Ang II, in hypertension, has been linked to the up‐regulation of downstream molecules and receptors implicated in HMGB1‐driven inflammation and synaptic dysfunction (de Kloet et al .…”

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confidence: 97%

“…Synergistically, Ang II and HMGB1 facilitate the depletion of nNOS and adversely alter synaptic activity (Reis et al 2016). Owing to its effect on nNOS, Ang II can reduce the bioavailability of NO and inhibitory ϒ-aminobutyric acid (GABA) neurotransmission while increasing paraventricular sympathoexcitation in hypertension (Zhang et al 1998;Campese et al 2002;DiCarlo et al 2002;Li and Pan 2005;Jang et al 2015;Yuan et al 2015;Wu et al 2016). Similarly, an increase in circulating Ang II, in hypertension, has been linked to the up-regulation of downstream molecules and receptors implicated in HMGB1-driven inflammation and synaptic dysfunction (de Kloet et al 2013;Song et al 2014;Dange et al 2015;Lin et al, 2015).…”

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confidence: 99%

Age‐dependent alterations to paraventricular nucleus insulin‐like growth factor 1 receptor as a possible link between sympathoexcitation and inflammation

Ogundele

Lee

Francis

2016

Journal of Neurochemistry

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Modifications to neural circuits of the paraventricular hypothalamic nucleus (PVN) have been implicated in sympathoexcitation and systemic cardiovascular dysfunction. However, to date, the role of insulin-like growth factor 1 receptor (IGF-1R) expression on PVN pathophysiology is unknown. Using confocal immunofluorescence quantification and electrophysiological recordings from acute PVN slices, we investigated the mechanism through which age-dependent IGF-1R depletion contributes to the progression of inflammation and sympathoexcitation in the PVN of spontaneously hypertensive rats (SHR). Four and twenty weeks old SHR and Wistar Kyoto (WKY) rats were used for this study. Our data showed that Angiotensin I/II and pro-inflammatory high mobility box group protein 1 (HMGB1) exhibited increased expression in the PVN of SHR versus WKY at 4 weeks (p<0.01), and were even more highly expressed with age in SHR (p<0.001). This correlated with a significant decrease in IGF-1R expression, with age, in the PVN of SHR when compared with WKY (p<0.001) and were accompanied by related changes in astrocytes and microglia. In subsequent analyses, we found an age-dependent change in the expression of proteins associated with IGF-1R signaling pathways involved in inflammatory responses and synaptic function in the PVN. MAPK/ErK was more highly expressed in the PVN of SHR by the 4th week (p<0.001; vs WKY), while expression of neuronal nitric oxide synthase (nNOS; p<0.001) and calcium-calmodulin dependent kinase II alpha (CamKIIα; p<0.001) were significantly decreased by the 4th and 20th week respectively. Age-dependent changes in MAPK/ErK expression in the PVN correlated with an increase in the expression of vesicular glutamate transporter (VGLUT2) (p<0.001 vs WKY), while decreased levels of CamKIIα was associated with a decreased expression of tyrosine hydroxylase (p<0.001) by the 20th week. In addition, reduced labeling for GABA in the PVN of SHR (p<0.001) correlated with a decrease in nNOS labeling (p<0.001) when compared with the WKY by the 20th week. Electrophysiological recordings from neurons in acute slice preparations of the PVN of 4 weeks old SHR revealed spontaneous post-synaptic currents of higher frequency when compared with neurons from WKY PNV slices of the same age (p<0.001; n=14 cells). This also correlated with an increase in post-synaptic densities (PSD-95) in the PVN of SHR when compared with the WKY (p<0.001). Overall, we found an age-dependent reduction of IGF-1R, and related altered expression of associated downstream signaling molecules that may represent a link between the concurrent progression of synaptic dysfunction and inflammation in the PVN of SHR.

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“…Data were acquired by a PowerLab system. The maximum of RSNA was measured when the rat was euthanized with an overdose of pentobarbital sodium (200 mg/kg), as reported previously (Wu et al, 2016). Baseline and constant lightexposed RSNA was analyzed as a percentage of maximal RSNA.…”

Section: Measurements Of Bp Hr and Sympathetic Nerve Activitymentioning

confidence: 99%

Constant Light Exerted Detrimental Cardiovascular Effects Through Sympathetic Hyperactivity in Normal and Heart Failure Rats

Jing¹,

Wu²,

et al. 2020

Front. Neurosci.

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It has been documented that constant light exposure exerts complicated cardiovascular effects. However, a mounting collection of conflicting results did not make it any easier for researchers and physicians to consider the role of light on cardiovascular function. This study was designed to investigate how constant light exposure (24 h light/day) influences the cardiac function in normal and heart-failure (HF) rats. In normal rats, two groups of SD rats were accustomed in 12 h light/12 h dark (LD) or 24 h light (constant light, CL) for 4 weeks. In HF rats which was induced by myocardial infarction (MI) was let recover in LD for 4 weeks. Interestingly, compared with rats in LD environment (ejection fraction, EF%: 93.64 ± 2.02 in LD, 14.62 ± 1.53 in HF-LD), constant light (2 weeks) weakened the cardiac function in normal and HF rats (EF%: 79.42 ± 2.91 in CL, 11.50 ± 1.08 in HF-CL). The levels of renal sympathetic nerve activity and c-fos expression in the rostral ventrolateral medulla (RVLM), a key region controlling sympathetic outflow, were significantly increased in normal and HF rats after

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The PI3K signaling-mediated nitric oxide contributes to cardiovascular effects of angiotensin-(1-7) in the nucleus tractus solitarii of rats

Cited by 25 publications

References 51 publications

The phosphoinositide‐3 kinase signaling is involved in neuroinflammation in hypertensive rats

The phosphoinositide‐3 kinase signaling is involved in neuroinflammation in hypertensive rats

Age‐dependent alterations to paraventricular nucleus insulin‐like growth factor 1 receptor as a possible link between sympathoexcitation and inflammation

Constant Light Exerted Detrimental Cardiovascular Effects Through Sympathetic Hyperactivity in Normal and Heart Failure Rats

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