Neurohumoral mechanisms of the rat heart adaptation to overload

Федоров, В. Н.; Фатеев, М. М.; Сальников, Е. В.; Сидоров, А. В.

doi:10.1134/s0022093009040069

Cited by 2 publications

(2 citation statements)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is well established that neurohumoral factors play important roles in both physiological and pathophysiological conditions of the heart [1][2][3]. Among numerous neurohumoral factors, angiotensin II (Ang II) has drawn a lot of attention because of its involvement in the development of cardiovascular diseases (CVD) [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Acetylcholine prevents angiotensin II-induced oxidative stress and apoptosis in H9c2 cells

Liu

Zhou

et al. 2010

Apoptosis

View full text Add to dashboard Cite

Apoptosis of cardiomyocytes plays an important role in the development of cardiovascular diseases (CVD). Numerous studies have shown that generation of reactive oxygen species (ROS) induced by the renin-angiotensin system (RAS) is involved in this pathological process. Recent studies also suggested that acetylcholine (ACh) prevented the hypoxia-induced apoptosis of mouse ES cells by inhibiting the ROS production. However, whether ACh can inhibit the action of angiotensin II (Ang II) and subsequently prevent CVD development remains unclear. In this study, H9c2 cells were stimulated by 10(-6) M Ang II for 24 h with or without 10(-5) M ACh, 10(-5) M ACh + 10(-4) M atropine respectively. The results demonstrated that Ang II increased apoptosis index by fourfold (vs. the control group, P < 0.01), which were significantly diminished by ACh. However, the atropine (ACh receptor [AChR] inhibitor) treatment blocked the protective effect of ACh. Subsequently, Ang II significantly increases the expression and activity of NADPH oxidase so that ROS production is increased by sevenfold (vs. control group, P < 0.01). The activity and expression of caspase-3 along with the Bax/Bcl2 ratio and the levels of p38 mitogen activated protein kinase (MAPK) phosphorylation also appeared to follow a similar trend. Furthermore, we observed that ACh could reduce up-regulation of AT1 receptor expression induced by Ang II. However, all these effects of ACh were inhibited by atropine. In conclusion, ACh prevents Ang II-induced H9c2 cells apoptosis through down-regulation of the AT1 receptor and inhibition of ROS-mediated p38 MAPK activation as well as regulation of Bcl-2, Bax and caspase-3.

show abstract

Section: Introductionmentioning

confidence: 99%

Acetylcholine prevents angiotensin II-induced oxidative stress and apoptosis in H9c2 cells

Liu

Zhou

et al. 2010

Apoptosis

View full text Add to dashboard Cite

show abstract

“…Initially, 1.5 ml silicon oil per 100 g of body mass was introduced in each pleural cavity of the rat; after 30 days the repeated injection into both pleural cavities was performed at a dose of 1.0 ml/100 g of body mass. This repeated oil injection completed development of the CHF model of the right-and left-ventricular type, which was confirmed by physiological, biochemical, and pathomorphological investigations [8][9][10]. The subsequent injections of silicon oil were performed each two months at a dose of 1.0 ml/100 g of body mass.…”

Section: Methodsmentioning

confidence: 71%

Effect of angiotensin-converting enzyme inhibitors, beta-adrenoblockers and their combinations on survival and blood plasma catecholamine levels in rats with chronic heart failure with induced exacerbations

Сидоров

Фатеев

2013

J Evol Biochem Phys

Self Cite

View full text Add to dashboard Cite

It has been shown, using the model of the chronic heart failure proceeded with induced decompensations, that the ACE inhibitors and β-adrenoblockers promoted at different degree the correction of hypercatecholaminemia and an increase of the rat survival. The β-adrenoblockers Atenolol, Propranolol and Carvedilol had the most effect. The remaining β-adrenoblockers, not possessing the inner sympathetic-mimetic activity, as well as Captopril, demonstrated the less activity. However the positive effect of these preparations occurred on the rat survival independent on the expression of their modulating effect on the sympathetic -adrenal system. The ACE inhibitors, especially the hydrophilic Lisinopril, prevent at less degree, than the β-adrenoblockers, the death of animals at the period of CHF exacerbation. A combine using of β-adrenoblockers with the ACE inhibitors , especially with the Carvedilol, promotes a maximally expressed decrease of the sympathetic-adrenal activity and an increase of the rat survival, especially at the period of CHF exacerbation.

show abstract

Neurohumoral mechanisms of the rat heart adaptation to overload

Cited by 2 publications

References 3 publications

Acetylcholine prevents angiotensin II-induced oxidative stress and apoptosis in H9c2 cells

Acetylcholine prevents angiotensin II-induced oxidative stress and apoptosis in H9c2 cells

Effect of angiotensin-converting enzyme inhibitors, beta-adrenoblockers and their combinations on survival and blood plasma catecholamine levels in rats with chronic heart failure with induced exacerbations

Contact Info

Product

Resources

About