Endothelial dysfunction: a strategic target in the treatment of hypertension?

Tang, E.; Vanhoutte, Paul M.

doi:10.1007/s00424-010-0786-4

Cited by 150 publications

(132 citation statements)

References 91 publications

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“…Particularly, dihydropyridine, can reverse the impaired endothelium-dependent vasodilation impaired in different places, including subcutaneous, epicardial, renal circulation and forearm. On forearm circulation, Nifedipine and Lacidipine can improve endothelial dysfunction, restoring the NO availability through a mechanism that is likely related to an antioxidant effect (25) .…”

Section: Discussionmentioning

confidence: 99%

Pharmacotherapy and analysis of gaseous mediators in hypertensive patients

Eid

Soriano

Batalhão

et al. 2015

Rev. esc. enferm. USP

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Objective:To evaluate the effect of using antihypertensive classes of drugs of the calcium channel antagonists and inhibitors of angiotensin-converting enzyme in plasma concentrations of hydrogen sulfide and nitric oxide in patients with hypertension. Methods: Cross-sectional study with quantitative approach conducted with hypertensive patients in use of antihypertensive classes of drugs: angiotensin-converting enzyme inhibitors or calcium channel antagonists. Results: It was found that the concentration of plasma nitric oxide was significantly higher in hypertensive patients that were in use of angiotensin-converting enzyme inhibitors (p<0.03) and the hydrogen sulphide concentration was significantly higher in hypertensive plasma in use of calcium channel antagonists (p<0.002). Conclusion: The findings suggest that these medications have as additional action mechanism the improvement of endothelial dysfunction by elevate plasma levels of vasodilatory substances.

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Section: Discussionmentioning

confidence: 99%

Pharmacotherapy and analysis of gaseous mediators in hypertensive patients

Eid

Soriano

Batalhão

et al. 2015

Rev. esc. enferm. USP

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“…In many forms of human and experimental hypertension, endothelial dysfunction and arterial remodeling are considered key players in the development and maintenance of high blood pressure. [3][4][5] In spontaneously hypertensive rats (SHR) a well-described manifestation of endothelial dysfunction is an increased production of endotheliumderived contractile factors (EDCF). 6 Drug-intervention studies have shown that some anti-hypertensive treatments, for instance with angiotensin AT 1 receptor antagonists, not only lower blood pressure but also cause an improvement of endothelial function and regression of structural changes in resistance arteries.…”

Section: Introductionmentioning

confidence: 99%

Dual NEP/ECE inhibition improves endothelial function in mesenteric resistance arteries of 32-week-old SHR

et al. 2017

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Endothelin 1 (ET-1), a potent vasoconstrictor, pro-mitogenic and pro-inflammatory peptide, may promote development of endothelial dysfunction and arterial remodeling. ET-1 can be formed through cleavage of big-ET-1 by endothelin-converting enzyme (ECE) or neutral endopeptidase (NEP). We investigated whether chronic treatment with the novel dual NEP/ECE inhibitor SOL1 improves functional and structural properties of resistance-sized arteries of 32-week-old male spontaneously hypertensive rats (SHR). SHR received a chronic 4-week treatment with SOL1, losartan or hydralazine. We then compared effects of inhibition of NO synthase (NOS) (100 μM L-NAME), blockade of ET A -and ET B -receptors (10 μM bosentan) and stimulation of the endothelium with 0.001-10 μM acetylcholine (ACh) in isolated third-order mesenteric resistance arteries. Losartan and hydralazine significantly lowered blood pressure. Losartan decreased the media-to-lumen ratio of resistance arteries. L-NAME (1) increased arterial contractile responses to K + (5.9-40 mM) in the losartan, SOL1 and vehicle group and (2) increased the sensitivity to phenylephrine (PHE; 0.16-20 μM) in the SOL1 group but not in the losartan, hydralazine and vehicle group. Relaxing responses to ACh in the absence or presence of L-NAME during contractions induced by either 10 μM PHE or 40 mM K + were not altered by any in vivo treatment. Acute treatment with bosentan did, however, significantly improve maximal relaxing responses involving endothelium-derived nitric oxide and -hyperpolarizing factors in the SOL1 group but not in the losartan, hydralazine or vehicle group. Thus, chronic inhibition of NEP/ECE improved basal endothelial function but did not alter blood pressure, resistance artery structure and stimulated endothelium-dependent relaxing responses in 32-week-old SHR.

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“…However, the exact molecular mechanism of hypertension remains unknown. It has been suggested that increased blood pressure is probably the reason or/and result of vascular endothelial dysfunction [2]. Vascular endothelium plays an important role in the regulation of blood pressure by secreting various vasoactive substances.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol affects histone 3 lysine 27 methylation of vessels and blood biomarkers in DOCA salt-induced hypertension

et al. 2014

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Hypertension is a risk factor for the cardiovascular diseases. Although, several drugs are used to treat hypertension, the success of the antihypertensive therapy is limited. Resveratrol decreases blood pressure in animal models of hypertension. This study researched the mechanisms behind the effects of resveratrol on hypertension. Hypertension was induced by using the deoxycorticosterone acetate (DOCA)-induced (15 mg/kg twice per week, subcutaneously) salt-sensitive hypertension model of Wistar rats. Hypertension caused a decrease in endotheliumdependent relaxations of the isolated thoracic aorta. Resveratrol treatment (50 mg/l in drinking water) prevented DOCA salt-induced hypertension, but did not improve endothelial dysfunction. Plasma nitric oxide (NO), asymmetric dimethylarginine (ADMA), total antioxidant capacity (TAC) and hydrogen sulfide (H 2 S) levels were not changed by DOCA salt application. However, treatment of resveratrol significantly decreased ADMA and increased TAC and H 2 S levels. NO level in circulation was not significantly changed by resveratrol. DOCA salt application and resveratrol treatment also caused an alteration in the epigenetic modification of vessels. Staining pattern of histone 3 lysine 27 methylation (H3K27me3) in the aorta and renal artery sections was changed. These results show that preventive effect of resveratrol on DOCA salt-induced hypertension might due to its action on the production of some blood biomarkers and the epigenetic modification of vessels that would focus upon new aspect of hypertension prevention and treatment.

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Endothelial dysfunction: a strategic target in the treatment of hypertension?

Cited by 150 publications

References 91 publications

Pharmacotherapy and analysis of gaseous mediators in hypertensive patients

Pharmacotherapy and analysis of gaseous mediators in hypertensive patients

Dual NEP/ECE inhibition improves endothelial function in mesenteric resistance arteries of 32-week-old SHR

Resveratrol affects histone 3 lysine 27 methylation of vessels and blood biomarkers in DOCA salt-induced hypertension

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