Contribution of the renin–angiotensin system in chronic foot-shock induced hypertension in rats

Wang, Linhui; Dong, Tao; Liu, Beibei; Zhao, Xiaodong; Chen, Jingwei; Murao, Koji; Zhu, Wei; Zhang, Guoxing

doi:10.1016/j.lfs.2014.12.004

Cited by 15 publications

(23 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous reports have shown that an augmentation of ROS dependent on NADPH oxidase activation in the brain leads to a long-term pressor response to angiotensin II via transcriptional up-regulation of angiotensin II type-1 (AT1) receptor mRNA expression, indicating that the brain renin-angiotensin system is important for the regulation of AP and sympathetic activity. 73,74 It has also been shown that a maternal low-protein diet during the second half of the pregnancy promotes an increase in mRNA expression of angiotensinogen and the angiotensin converting enzyme-1 (ACE-1) associated with a decrease in mRNA levels of angiotensin II type-2 (AT2) receptors in the fetal brain. 21 This alteration has been linked to hypomethylation of the CpG islands in the promoter regions of ACE-1 gene, 21 suggesting that epigenetic mechanisms could be involved in development of sympathetic overactivity and hypertension in protein-restricted rats.…”

Section: Maternal Protein Restriction and The Development Of Hypertmentioning

confidence: 99%

Maternal protein malnutrition induced‐hypertension: New evidence about the autonomic and respiratory dysfunctions and epigenetic mechanisms

Alves

Costa‐Silva

2017

Clin Exp Pharma Physio

View full text Add to dashboard Cite

SummaryMaternal protein malnutrition during the critical stages of development (pregnancy, lactation and first infancy) can lead to adult hypertension. Studies have shown that renal and cardiovascular dysfunctions can be associated to the development of hypertension in humans and rats exposed to maternal protein malnutrition. The etiology of hypertension, however, includes a complex network involved in central and peripheral blood pressure control. Recently, the hyperactivity of the sympathetic nervous system in protein-restricted rats has been reported. Studies have shown that protein malnutrition during pregnancy and/or lactation alters blood pressure control through mechanisms that include central sympathetic-respiratory dysfunctions and epigenetic modifications, which may contribute to adult hypertension. Thus, this review will discuss the historical context, new evidences of neurogenic disruption in respiratorysympathetic activities and possible epigenetic mechanisms involved in maternal protein malnutrition induced-hypertension. K E Y W O R D Shypertension, malnutrition, phenotypic plasticity, sympathetic activity, ventilation | INTRODUCTIONArterial hypertension (AH) affects more than 1 billion people around the world and is a major risk factor for cardiovascular dysfunction, recognized as the main cause of morbidity and mortality. Because of the interaction between the sympathetic and respiratory nervous systems, growing evidence supports the notion that an increase in sympathetic and respiratory activities plays an important role in the development of hypertension. [8][9][10] This observation has prompted the development of several studies evaluating sympathetic and respiratory activities and sensitivity of peripheral and central chemoreceptors in various hypertension models. For example, in chronic intermittent hypoxia 8,11 in spontaneously hypertensive rats (SHR) 4 and in renovascular hypertension, 12 augmented sympathetic-respiratory activities and higher peripheral chemosensitivity were seen to be associated to hypertension.

show abstract

Section: Maternal Protein Restriction and The Development Of Hypertmentioning

confidence: 99%

Maternal protein malnutrition induced‐hypertension: New evidence about the autonomic and respiratory dysfunctions and epigenetic mechanisms

Alves

Costa‐Silva

2017

Clin Exp Pharma Physio

View full text Add to dashboard Cite

show abstract

“…Its action takes place through activation of its receptors AT 1 and AT 2 [51,52], where vasoconstriction is promoted by AT 1 receptors, present in vascular smooth muscles [54]. The AT 2 receptors counterbalance the action of AT 1 receptors; however, its expression is considered mild compared to its counterpart [51,55].…”

Section: Angiotensin IImentioning

confidence: 99%

“…Angiotensin II also releases aldosterone, which promotes secretion of K + and consequent retention of Na + and water [52]. Hyperactivation of RAAS is linked to high blood pressure, highlighting the RAAS products as the main target for the antihypertensive therapies [52,54,57].…”

Section: Angiotensin IImentioning

confidence: 99%

History of vascular reactivity models and their involvement in hypertension pathogenesis

Conceição-Vertamatti

Borghi

Canova

et al. 2017

Vasa

View full text Add to dashboard Cite

Summary:Hypertension is a silent and multifactorial disease. Over two centuries ago, the fi rst device to record blood pressure was developed, making it possible to determine normotension and to establish criteria for hypertension. Since then, several studies have contributed to advance knowledge in this area, promoting signifi cant advances in pharmacological treatments and, as a result, increasing survival of hypertensive people. The main models developed for the study of hypertension and the main fi ndings in the vascular area are included in this review. We considered aspects related to vascular reactivity, changes in the population, and action of beta adrenergic receptors in the pathogenesis of hypertension.

show abstract

“…Evidence shows that chronic psychosocial stress is directly linked to the development of hypertension, cardiovascular disease, and stroke [1]. The activation of various neurogenic pathways, such as stimulation of the sympathetic nervous system (SNS), mediates not only short-term increases in blood pressure (BP), but also the elevation of chronic BP in response to specific stresses [2].…”

Section: Introductionmentioning

confidence: 99%

Microglia-Derived NLRP3 Activation Mediates the Pressor Effect of Prorenin in the Rostral Ventrolateral Medulla of Stress-Induced Hypertensive Rats

Zhang

Ooi

et al. 2020

Neurosci. Bull.

View full text Add to dashboard Cite

Increased microglial activation and neuroinflammation within autonomic brain regions such as the rostral ventrolateral medulla (RVLM) have been implicated in stress-induced hypertension (SIH). Prorenin, a member of the brain renin-angiotensin system (RAS), can directly activate microglia. The present study aimed to investigate the effects of prorenin on microglial activation in the RVLM of SIH rats. Rats were subjected to intermittent electric foot-shocks plus noise, this stress was administered for 2 h twice daily for 15 consecutive days, and mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were monitored. The results showed that MAP and RSNA were augmented, and this paralleled increased pro-inflammatory phenotype (M1) switching. Prorenin and its receptor (PRR) expression and the NLR family pyrin domain containing 3 (NLRP3) activation were increased in RVLM of SIH rats. In addition, PLX5622 (a microglial depletion agent), MCC950 (a NLRP3 inhibitor), and/or PRO20 (a (Pro)renin receptor antagonist) had antihypertensive effects in the rats. The NLRP3 expression in the RVLM was decreased in SIH rats treated with PLX5622. Mito-tracker staining showed translocation of NLRP3 from mitochondria to the cytoplasm in proreninstimulated microglia. Prorenin increased the ROS-triggering M1 phenotype-switching and NLRP3 activation, while MCC950 decreased the M1 polarization. In conclusion, upregulated prorenin in the RVLM may be involved in the pathogenesis of SIH, mediated by activation of the microglia-derived NLRP3 inflammasome. The link between prorenin and NLRP3 in microglia provides insights for the treatment of stress-related hypertension.

show abstract

Contribution of the renin–angiotensin system in chronic foot-shock induced hypertension in rats

Cited by 15 publications

References 42 publications

Maternal protein malnutrition induced‐hypertension: New evidence about the autonomic and respiratory dysfunctions and epigenetic mechanisms

Maternal protein malnutrition induced‐hypertension: New evidence about the autonomic and respiratory dysfunctions and epigenetic mechanisms

History of vascular reactivity models and their involvement in hypertension pathogenesis

Microglia-Derived NLRP3 Activation Mediates the Pressor Effect of Prorenin in the Rostral Ventrolateral Medulla of Stress-Induced Hypertensive Rats

Contact Info

Product

Resources

About