Are We on the Path to Solve the Enigma of Resistant Hypertension: Renal Sympathetic Denervation

Gerc, Vjekoslav; Buksa, M

doi:10.5455/medarh.2013.67.454-459

Cited by 2 publications

(2 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A limited number of inpatients have been treated with RSD and followed up for long term. Grec et al pointed out that RSD treatment not only provides an insight on the treatment of resistant hypertension, but also brings new hope for patients with cardiovascular metabolic diseases ( 25 ). Since norepinephrine and Ang II are two important factors for myocardial apoptosis, RSD is likely to achieve its role of inhibiting myocardial apoptosis by suppressing the release of norepinephrine and Ang II.…”

Section: Discussionmentioning

confidence: 99%

Renal sympathetic denervation improves myocardial apoptosis in rats with isoproterenol‑induced heart failure by downregulation of tumor necrosis factor‑α and nuclear factor‑κB

et al. 2017

View full text Add to dashboard Cite

Chronic congestive heart failure (CHF) is the end outcome of organic heart diseases and one of the major diseases harmful to human health. Renal sympathetic denervation (RSD) is the anatomical basis of transcatheter renal sympathetic nerve ablation within the renal artery. To date, the roles of norepinephrine and angiotensin II (Ang II) in myocardial apoptosis and their underlying mechanisms have not been well explored. The aim of the present study was to verify the hypothesis that RSD is likely to inhibit myocardial apoptosis by inhibiting the release of norepinephrine and Ang II. An isoproterenol-induced CHF rat model was established, and the effects of RSD on myocardial apoptosis were examined using flow cytometry and TUNEL staining. The expression of factors associated with myocardial apoptosis, including p53, tumor necrosis factor-α (TNF-α), nuclear factor-κB (NF-κB), caspase-2 and −3, were measured using quantitative polymerase chain reaction and western blot analysis. The results indicated that the mRNA levels of p53, TNF-α, NF-κB, caspase-2 and −3 were significantly reduced in the myocardial tissues of rats in the CHF+RSD group when compared with the levels in the CHF+sham group (P<0.01 for all). In addition, the protein levels of p53, TNF-α, NF-κB and caspases-2 and −3 were decreased by 42.6, 41.3, 46.7, 30.0 and 35.8%, respectively, in myocardial tissues of rats in the CHF+RSD group in comparison with the CHF+sham group (P<0.01 for all). Furthermore, myocardial apoptosis was improved in rats in the CHF+RSD group compared with that in the CHF+sham group (P<0.01). In conclusion, the present study provides a theoretical basis for application of RSD in the treatment of CHF.

show abstract

Section: Discussionmentioning

confidence: 99%

Renal sympathetic denervation improves myocardial apoptosis in rats with isoproterenol‑induced heart failure by downregulation of tumor necrosis factor‑α and nuclear factor‑κB

et al. 2017

View full text Add to dashboard Cite

show abstract

“…The blood pressure has been reported to be regulated by the renin angiotensin aldosterone system (RAAS) (1). The RAAS has been reported to develop and progress hypertensive heart disease (2). Therefore, the RAAS has been considered as a major pharmacological target of cardiovascular medicine (3,4).…”

Section: Introductionmentioning

confidence: 99%

Azilsartan attenuates cardiac damage caused by high salt intake through the downregulation of the cardiac (pro)renin receptor and its downstream signals in spontaneously hypertensive rats

et al. 2018

View full text Add to dashboard Cite

We examined whether the stimulation of the angiotensin II AT1 receptor increases the expression of the cardiac (pro)renin receptor ((P)RR) and its downstream signals and whether the blockade of the angiotensin II AT1 receptor by azilsartan decreases the expression of the cardiac (P)RR and its signaling in spontaneously hypertensive rats (SHRs) with a high-salt intake. Rats received normal-salt (0.9%) chow, high-salt (8.9%) chow, normal-salt chow with 1 mg/day of azilsartan, and high-salt chow with 1 mg/day of azilsartan from 6 to 12 weeks of age. Rats with normal-salt chow were administered 100 ng/kg/min of angiotensin II by osmotic minipump from 6 to 12 weeks of age. A high-salt diet and angiotensin II significantly increased the systolic blood pressure; overexpressed cardiac (P)RR, phosphorylated (p)-ERK1/2, p-p38MAPK, p-HSP27, and TGF-ß1; enhanced cardiac interstitial and perivascular fibrosis, cardiomyocyte size, interventricular septum (IVS) thickness, and left ventricular (LV) end-diastolic dimension; and decreased LV fractional shortening. Azilsartan decreased systolic blood pressure, cardiac expressions of (P)RR, p-ERK1/2, p-p38MAPK, p-HSP27, and TGF-ß1, cardiac interstitial and perivascular fibrosis, cardiomyocyte size, and LV diastolic dimension, and improved LV fractional shortening. In conclusion, azilsartan attenuates cardiac damage caused by high salt intake through the downregulation of the cardiac (pro)renin receptor and its downstream signals in SHRs.

show abstract

Are We on the Path to Solve the Enigma of Resistant Hypertension: Renal Sympathetic Denervation

Cited by 2 publications

References 39 publications

Renal sympathetic denervation improves myocardial apoptosis in rats with isoproterenol‑induced heart failure by downregulation of tumor necrosis factor‑α and nuclear factor‑κB

Renal sympathetic denervation improves myocardial apoptosis in rats with isoproterenol‑induced heart failure by downregulation of tumor necrosis factor‑α and nuclear factor‑κB

Azilsartan attenuates cardiac damage caused by high salt intake through the downregulation of the cardiac (pro)renin receptor and its downstream signals in spontaneously hypertensive rats

Contact Info

Product

Resources

About