Pro-inflammatory Cytokines and Resistant Hypertension: Potential for Novel Treatments?
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ANTIHYPERTENSIVE AGENTS: MECHANISMS OF DRUG ACTION (ME ERNST, SECTION EDITOR)
Pro-inflammatory Cytokines and Resistant Hypertension: Potential for Novel Treatments? Mariana Rodrigues Pioli 1
&
Ana Paula de Faria 1
# Springer Science+Business Media, LLC, part of Springer Nature 2019
Abstract Purpose of Review To gather data from studies evaluating the pro-inflammatory profile of individuals with resistant hypertension (RH), and bring a clinical update of new and potential complementary therapies to treat inflammation in RH. Recent Findings Increases in pro-inflammatory cytokines are related to elevated blood pressure and target organ damage in RH patients. Clinical and experimental studies have shown that some biological therapies, especially TNF-α inhibitors, regulated pro- and anti-inflammatory cytokines associated with improvements in clinical outcomes, although they are not yet reported in RH. Summary New emerging therapies to treat inflammation in RH, although promising, are still hypotheses that have not been scientifically confirmed in clinical trials. For this reason, inflammation-target treatments, such as the TNF-α and IL-6 inhibitors, should be encouraged for testing as complementary therapies in RH in order to elucidate their potential benefits. Keywords Refractory hypertension . Blood pressure . Cytokines . Inflammation . Biological therapies
Introduction An individual is considered resistant to antihypertensive treatment when they do not achieve optimal blood pressure (BP) levels, despite concomitant use of a calcium channel blocker (CCB), a blocker of the renin-angiotensin system, and a diuretic, at tolerated maximal doses—namely uncontrolled resistant hypertension (RH). Also, the definition includes hypertensive patients who achieve appropriate BP levels, but require ≥ 4 antihypertensive classes, referred to in the literature as controlled RH [1]. True diagnosis of RH includes exclusion of both (i) patients with the white-coat effect and (ii) nonadherence to antihypertensive treatment [1]. The lack of BP control along with coexisting multiple comorbidities, metabolic abnormalities, and target organ damage (TOD) places RH as a high cardiovascular (CV) risk [1]. This article is part of the Topical Collection on Antihypertensive Agents: Mechanisms of Drug Action * Ana Paula de Faria [email protected]; [email protected] 1
Department of Pharmacology, FCM 10 Building, School of Medical Sciences - University of Campinas (FCM-UNICAMP), Tessália Vieira de Camargo, 126, Campinas, SP 13083-970, Brazil
Due to its complex nature, many pathophysiological mechanisms underly the development and progression of the disease; among them, the inflammatory process has played a critical role in the regulation of BP in RH [2, 3]. Antihypertensive therapies such as angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), and mineralocorticoid receptor (MR) antagonists are widely used in RH. Beyond the reduction in BP levels, decrease in plasma levels of some cytokines has
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