Inflammation and Hypertension: New Understandings and Potential Therapeutic Targets

Miguel, Carmen De; Rudemiller, Nathan P.; Abais, Justine M.; Mattson, David L.

doi:10.1007/s11906-014-0507-z

Cited by 204 publications

(161 citation statements)

References 107 publications

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“…Consistent with this observation, a study showed that increased plasma levels of IL-1β, a cytokine involved in monocyte activation, precedes changes in BP in HTN [50]. Furthermore, IL-6, MCP-1 and especially TNF-α were shown to be essential for the pathologic effects of Ang II on the vasculature by increasing oxidative stress, activating fibroblasts and attracting T cells [47, 51]. …”

Section: Discussionmentioning

confidence: 80%

“…The innate immune pathway not only responds to exogenous pathogens but can be also activated by damage-associated molecular patterns (DAMPs) released endogenous by stressed, damaged or necrotic cells [46]. DAMPs are present in cardiovascular diseases during HTN [47]. AT 1 activation was shown to induce p53-dependent apoptosis of cultured rat cardiomyocytes, which might lead the release of DAMPs [48].…”

Section: Discussionmentioning

confidence: 99%

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Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation

Antoniak

Cardenas²,

Buczek³

et al. 2016

Cardiology

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Background: Angiotensin II (Ang II) plays an important role in cardiovascular disease. It also leads to the activation of coagulation. The coagulation protease thrombin induces cellular responses by activating protease-activated receptor 1 (PAR-1). We investigated whether PAR-1 contributes to Ang II-induced cardiovascular remodeling and inflammation. Methods and Results: PAR-1^+/+ (wild-type; WT) and PAR-1^-/- mice were infused with Ang II (600 ng/kg/min) for up to 4 weeks. In WT mice, this dose of Ang II did not cause a significant increase in blood pressure but it did cause pathological changes in both the aorta and the heart. Ang II infusion resulted in vascular remodeling of the aorta, demonstrated by a significant increase in medial wall thickening and perivascular fibrosis. Importantly, both parameters were significantly attenuated by PAR-1 deficiency. Furthermore, perivascular fibrosis around coronary vessels was reduced in Ang II-treated PAR-1^-/- mice compared to WT mice. In addition, PAR-1 deficiency significantly attenuated Ang II induction of inflammatory cytokines and profibrotic genes in the aortas compared to WT mice. Finally, PAR-1 deficiency had no effect on Ang II-induced heart hypertrophy. However, the heart function measured by fractional shortening was less impaired in PAR-1^-/- mice than in WT mice. Conclusion: Our data indicate that PAR-1 plays a significant role in cardiovascular remodeling mediated by a blood pressure-independent action of Ang II.

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Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation

Antoniak

Cardenas²,

Buczek³

et al. 2016

Cardiology

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“…production of free radicals outweighing their scavenging, is one of the systemic pathological processes, related to endothelium. Inflammation in the vascular wall is another example, synthesis of pro-inflammatory cytokines and recruitment of inflammatory cells, with hypertension being considered even as inflammatory disease now [5, 6]. …”

Section: Introductionmentioning

confidence: 99%

Effects of Aspirin on Endothelial Function and Hypertension

2016

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Purpose of reviewEndothelial dysfunction is intimately related to the development of various cardiovascular diseases, including hypertension, and is often used as a target for pharmacological treatment. The scope of this review is to assess effects of aspirin on endothelial function and their clinical implication in arterial hypertension.Recent findingsEmerging data indicate the role of platelets in the development of vascular inflammation due to the release of proinflammatory mediators, for example, triggered largely by thromboxane. Vascular inflammation further promotes oxidative stress, diminished synthesis of vasodilators, proaggregatory and procoagulant state. These changes translate into vasoconstriction, impaired circulation and thrombotic complications. Aspirin inhibits thromboxane synthesis, abolishes platelets activation and acetylates enzymes switching them to the synthesis of anti-inflammatory substances.SummaryAspirin pleiotropic effects have not been fully elucidated yet. In secondary prevention studies, the decrease in cardiovascular events with aspirin outweighs bleeding risks, but this is not the case in primary prevention settings. Ongoing trials will provide more evidence on whether to expand the use of aspirin or stay within current recommendations.

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“…The role of inflammation as an important underlying process contributing to the initiation and progression of atherosclerosis and its clinical manifestations is well established [3][4][5][6] . Recent data indicated a strong relationship between essential HT and the inflammatory process.…”

Section: -1 Htmentioning

confidence: 99%

Do antilipidemic agents reduce blood pressure?

2018

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Abstract:Currently, the prevalence of hypertension (HT), diabetes mellitus (DM), and hyperlipidemia (HL) is high, and these diseases are important risk factors for cardiovascular disease (CVD). Furthermore, patients with CVD often have more than one of these diseases. Generally, patients take multiple drugs for each disease. Therefore, clinicians must pay attention to drug interactions. Although HT, DM, and HL are different diseases, they share some of the same pathophysiological mechanisms and ultimately lead to the same cardiovascular events.Currently, most patients with CVD are treated with 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors (statins), and various beneficial pleiotropic effects of statins have been reported since the 1990s.In this review, we evaluate the additional effects of antihyperlipidemic agents on blood pressure (BP).

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Inflammation and Hypertension: New Understandings and Potential Therapeutic Targets

Cited by 204 publications

References 107 publications

Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation

Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation

Effects of Aspirin on Endothelial Function and Hypertension

Do antilipidemic agents reduce blood pressure?

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