Effect of angiotensin II on voltage-gated sodium currents in aortic baroreceptor neurons and arterial baroreflex sensitivity in heart failure rats

Zhang, Dongze; Liu, Jinxu; Zheng, Hong; Tu, Huiyin; Muelleman, Robert L.; Li, Yu Long

doi:10.1097/hjh.0000000000000563

Cited by 10 publications

(16 citation statements)

References 41 publications

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Section: Angiotensin II Signaling Pathway and Reduced Activation Of Tsupporting

confidence: 81%

“…Our recent study has also confirmed the involvement of Ang II in CHF-induced arterial baroreflex abnormality (Zhang et al, 2015 ). In our study, overexpression of the AT1R mRNA and protein and elevation of the local Ang II concentration in the NG from CHF rats were observed (Zhang et al, 2015 ). Additionally, local microinjection of losartan into the NG significantly improved CHF-attenuated arterial baroreflex sensitivity, whereas this drug did not change the arterial baroreflex sensitivity in sham rats.…”

Section: Angiotensin II Signaling Pathway and Reduced Activation Of Tsupporting

confidence: 81%

“…Therefore, it is possible that the Na v channel is a potential target associated with the regulatory effect of Ang II on the aortic baroreceptor function. In isolated aortic baroreceptor neurons of sham rats, application of exogenous Ang II acutely inhibits Na v currents, and pretreatment of losartan totally abolishes the inhibitory effect of Ang II on Na v currents (Zhang et al, 2015 ), which supports the view that the acute inhibitory effect of Ang II on Na v currents mediates Ang II-attenuated arterial baroreflex function. However, losartan alone did not change Na v currents in isolated aortic baroreceptor neurons of CHF rats although this drug markedly improved the arterial baroreflex function in anesthetized CHF rats (Zhang et al, 2015 ).…”

Section: Angiotensin II Signaling Pathway and Reduced Activation Of Tmentioning

confidence: 71%

“…Additionally, local microinjection of losartan into the NG significantly improved CHF-attenuated arterial baroreflex sensitivity, whereas this drug did not change the arterial baroreflex sensitivity in sham rats. Furthermore, local application of exogenous Ang II in the NG from sham rats mimicked CHF to depress the arterial baroreflex function (Zhang et al, 2015 ). These results suggest that elevation of endogenous Ang II with AT1R overexpression in the NG contributes to the aortic baroreceptor dysfunction and subsequent down-regulation of the arterial baroreflex sensitivity in CHF rats, although a physiological level of endogenous Ang II does not affect the baroreceptor function and arterial baroreflex sensitivity.…”

Section: Angiotensin II Signaling Pathway and Reduced Activation Of Tmentioning

confidence: 99%

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Angiotensin II-superoxide-NFκB signaling and aortic baroreceptor dysfunction in chronic heart failure

Zhang

Muelleman

2015

Front. Neurosci.

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Chronic heart failure (CHF) affects approximately 5.7 million people in the United States. Increasing evidence from both clinical and experimental studies indicates that the sensitivity of arterial baroreflex is blunted in the CHF state, which is a predictive risk factor for sudden cardiac death. Normally, the arterial baroreflex regulates blood pressure and heart rate through sensing mechanical alteration of arterial vascular walls by baroreceptor terminals in the aortic arch and carotid sinus. There are aortic baroreceptor neurons in the nodose ganglion (NG), which serve as the main afferent component of the arterial baroreflex. Functional changes of baroreceptor neurons are involved in the arterial baroreflex dysfunction in CHF. In the CHF state, circulating angiotensin II (Ang II) and local Ang II concentration in the NG are elevated, and AT1R mRNA and protein are overexpressed in the NG. Additionally, Ang II-superoxide-NFκB signaling pathway regulates the neuronal excitability of aortic baroreceptors through influencing the expression and activation of Nav channels in aortic baroreceptors, and subsequently causes the impairment of the arterial baroreflex in CHF. These new findings provide a basis for potential pharmacological interventions for the improvement of the arterial baroreflex sensitivity in the CHF state. This review summarizes the mechanisms responsible for the arterial baroreflex dysfunction in CHF.

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Section: Angiotensin II Signaling Pathway and Reduced Activation Of Tsupporting

confidence: 81%

Section: Angiotensin II Signaling Pathway and Reduced Activation Of Tsupporting

confidence: 81%

Section: Angiotensin II Signaling Pathway and Reduced Activation Of Tmentioning

confidence: 71%

Section: Angiotensin II Signaling Pathway and Reduced Activation Of Tmentioning

confidence: 99%

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Angiotensin II-superoxide-NFκB signaling and aortic baroreceptor dysfunction in chronic heart failure

Zhang

Muelleman

2015

Front. Neurosci.

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“…These signals are transmitted to the Nucleus Tractus Solitarius from which secondary projections arise for control of sympathetic and parasympathetic outflows 19 . Baroreceptor sensitivity is depressed in heart failure due to persistent enhancement of the sympathetic activity, possibly related to central angiotensin II levels 18, 77 . Impairment in baroreceptor sensitivity in heart failure is associated with increased mortality 30, 78, 79 .…”

Section: Introductionmentioning

confidence: 99%

Autonomic Regulation Therapy in Heart Failure

Buckley

Shivkumar

Ardell

2015

Curr Heart Fail Rep

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Autonomic Regulation Therapy (ART) is a rapidly emerging therapy in the management of congestive heart failure secondary to systolic dysfunction. Modulation of the cardiac neuronal hierarchy can be achieved with bioelectronics modulation of the spinal cord, cervical vagus, baroreceptor, or renal nerve ablation. This review will discuss relevant preclinical and clinical research in ART for systolic heart failure. Understanding mechanistically what is being stimulated within the autonomic nervous system by such device-based therapy and how the system reacts to such stimuli is essential for optimizing stimulation parameters and for the future development of effective ART.

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Prenatal High‐Sucrose Diet Induced Vascular Dysfunction in Thoracic Artery of Fetal Offspring

Feng

Zhang

et al. 2021

Molecular Nutrition Food Res

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Scope Maternal nutrition during pregnancy is related to intrauterine fetal development. The authors’ previous work reports that prenatal high sucrose (HS) diet impaired micro‐vascular functions in postnatal offspring. It is unclear whether/how prenatal HS causes vascular injury during fetal life. Methods and results Pregnant rats are fed with normal drinking water or 20% high‐sucrose solution during the whole gestational period. Pregnant HS increases maternal weight before delivery. Fetal thoracic aorta is separated for experiments. Angiotensin II (AII)‐stimulated vascular contraction of fetal thoracic arteries in HS group is greater, which mainly results from the enhanced AT1 receptor (AT1R) function and the downstream signaling. Nifedipine significantly increases vascular tension in HS group, indicating that the L‐type calcium channels (LTCCs) function is strengthened. 2‐Aminoethyl diphenylborinate (2‐APB), inositol 1,4,5‐trisphosphate receptors (IP3Rs) inhibitor, increases vascular tension induced by AII in HS group and ryanodine receptors‐sensitive vascular tone shows no difference in the two groups, which suggested that the activity of IP3Rs‐operated calcium channels is increased. Conclusion These findings suggest that prenatal HS induces vascular dysfunction of thoracic arteries in fetal offspring by enhancing AT1R, LTCCs function and IP3Rs‐associated calcium channels, providing new information regarding the impact of prenatal HS on the functional development of fetal vascular systems.

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Effect of angiotensin II on voltage-gated sodium currents in aortic baroreceptor neurons and arterial baroreflex sensitivity in heart failure rats

Cited by 10 publications

References 41 publications

Angiotensin II-superoxide-NFκB signaling and aortic baroreceptor dysfunction in chronic heart failure

Angiotensin II-superoxide-NFκB signaling and aortic baroreceptor dysfunction in chronic heart failure

Autonomic Regulation Therapy in Heart Failure

Prenatal High‐Sucrose Diet Induced Vascular Dysfunction in Thoracic Artery of Fetal Offspring

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