Central sympatholytic therapy has anti-inflammatory properties in hypertensive postmenopausal women

Pöyhönen‐Alho, Maritta; Manhem, Karin; Katzman, Per; Kibarskis, Aleksandras; Antikaínen, Riitta; Erkkola, Risto; Tuomilehto, Jaakko; Ebeling, Pertti; Kaaja, Risto

doi:10.1097/hjh.0b013e328311cf37

Cited by 45 publications

(36 citation statements)

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“…In addition to its efficacy as an antihypertensive, moxonidine has been shown to improve indices of glycaemic control, aspects of the plasma lipid profile, and inflammatory markers [14–16]. Furthermore, its use has been associated with reduction in body weight [16–21].…”

Section: Introductionmentioning

confidence: 99%

Improved Hypertension Control with the Imidazoline Agonist Moxonidine in a Multinational Metabolic Syndrome Population: Principal Results of the MERSY Study

Чазова

Schlaich

2013

International Journal of Hypertension

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This study was designed to assess the effects of moxonidine on blood pressure and aspects of the metabolic syndrome in racially diverse population of patients encountered in routine medical practice. Physicians collected data on a minimum of three consecutive patients with uncontrolled essential hypertension and criteria for metabolic syndrome, eligible to receive moxonidine (0.2–0.4 mg once daily) for 6 months, either as monotherapy or as adjunct therapy to current antihypertensive treatment. Systolic and diastolic blood pressure (BP) declined by an average of 24.5 + 14.3 mmHg and 12.6 + 9.1 mmHg, respectively. BP responder rates defined as attaining BP < 140/90 mmHg were significantly (P < 0.001) and substantially higher among younger patients, nonpostmenopausal women, and patients receiving monotherapy. While potentially relevant improvements in the entire cohort were observed in regard to body weight (−2.1 ± 5.4 kg), fasting plasma glucose (from 6.8 to 6.2 mmol/L), and triglycerides (2.4 to 2.0 mmol/L), statistically significant changes in metabolic parameters could only be detected in subgroup analyses. Moxonidine therapy reduced blood pressure and improved rates of blood pressure control in this group of patients. While the observed trend towards improvement in various metabolic parameters merits further investigation, the overall effect of moxonidine treatment is consistent with a reduction of total cardiovascular risk in this hypertensive metabolic syndrome cohort.

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Section: Introductionmentioning

confidence: 99%

Improved Hypertension Control with the Imidazoline Agonist Moxonidine in a Multinational Metabolic Syndrome Population: Principal Results of the MERSY Study

Чазова

Schlaich

2013

International Journal of Hypertension

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“…Rilmenidine and clonidine were shown to reduce acute paw edema induced by carrageenan-, formalin-, serotonin or histamine in rats, an effect mediated most likely by alpha2-adrenoceptors (Gyires et al 2009;Holsapple et al 1984;Kulkarni et al 1986). Moxonidine reduced systemic low-grade inflammation in hypertensive postmenopausal overweight women (Pöyhönen-Alho et al 2008). …”

Section: Discussionmentioning

confidence: 99%

“…Moxonidine reduced the level of the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) in the serum of hypertensive postmenopausal women (Pöyhönen-Alho et al 2008). …”

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confidence: 99%

Analysing the effect of I1 imidazoline receptor ligands on DSS-induced acute colitis in mice

et al. 2016

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Imidazoline receptors (IRs) have been recognized as promising targets in the treatment of numerous diseases, and moxonidine and rilmenidine, agonists of I1-IRs are widely used as antihypertensive agents. Some evidence suggests that IR ligands may induce anti-inflammatory effects acting on I1-IRs or other molecular targets, which could be beneficial in patients with inflammatory bowel disease (IBD). On the other hand, several IR ligands may stimulate also alpha2-adrenoceptors, which was earlier shown to inhibit, but in more recent studies to rather aggravate colitis. Hence, this study aimed to analyse for the first time the effect of various I1-IR ligands on intestinal inflammation. Colitis was induced in C57BL/6 mice by adding dextran sulfate sodium (DSS) to the drinking water for 7 days. Mice were treated daily with different IR ligands; moxonidine and rilmenidine (I1-IR agonists), AGN 192403 (highly selective I1-IR ligand, putative antagonist), efaroxan (I1-IR antagonist), as well as with the endogenous IR agonists agmatine and harmane. It was found that moxonidine and rilmenidine at clinically relevant doses, similarly to the other IR ligands, do not have a significant impact on the macroscopic and histological signs of DSS-evoked inflammation. Likewise, colonic myeloperoxidase and serum interleukin-6 levels remained unchanged in response to these agents. Thus, our study demonstrates that imidazoline ligands do not influence significantly the severity of DSS-colitis in mice and suggest that they probably neither affect the course of IBD in humans. However, the translational value of these findings needs to be verified with other experimental colitis models and human studies.

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“…These are important regulators of cardiovascular risk. Therefore, it is very intriguing to evaluate the effects of central sympathetic blockade on parameters of inflammation in the context of overweight hypertensive subjects, as done by Pö yhö nen-Alho et al in this issue of the Journal [1].…”

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confidence: 97%

Addressing the relationship between sympathetic activity and inflammation

Hausberg¹,

Hillebrand²,

Kisters³

2008

Journal of Hypertension

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In this issue of the Journal, Maritta K. Pö yhö nen-Alho and coworkers present an intriguing study on the effects of differential antihypertensive medication (central-sympatholytic agent versus b-blocker) on insulin sensitivity and markers of inflammation in hypertensive overweight postmenopausal women [1].A total of 87 women not taking any medication including hormone-replacement therapy were enrolled into the study. They were randomized to antihypertensive treatment with either atenolol 50 mg per day or moxonidine 0,3 mg twice daily.The authors applied assays for C-reactive protein (CRP), interleukin (IL)-6, tumor necrosis factor-alpha (TNFa), TNFa-RII and adiponectin and measured insulin sensitivity with an oral glucose tolerance test and calculation of the insulin-sensitivity index. The authors observed an increase in TNFa in the atenolol group as opposed to a decrease in TNFa in the moxonidine group. Adiponectine decreased in the atenolol-treated women and did not change significantly in women receiving moxonidine. The other parameters did not change with either treatment. Thus, the authors were able to show that a central sympatholytic agent reduces the level of a proinflammatory cytokine without affecting adiponectin levels in hypertensive overweight postmenopausal women.This study has intriguing findings as it relates pharmacological-central blockade of the sympathetic nervous system to a reduction in inflammatory markers. Peripheral b blockade did not have these beneficial effects. The effects of moxonidine were observed in a population of hypertensive overweight postmenopausal women -thus a population likely to have increased sympathetic tone and increased markers of inflammation [2,3]. The effects of moxonidine were not attributable to a more pronounced decrease in blood pressure with moxonidine.

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Central sympatholytic therapy has anti-inflammatory properties in hypertensive postmenopausal women

Abstract: We believe that centrally acting sympatholytic agent moxonidine is beneficial in the treatment of postmenopausal women with hypertension by reducing inflammatory cytokine TNFalpha without changing protective adiponectin level.

Cited by 45 publications

References 47 publications

Improved Hypertension Control with the Imidazoline Agonist Moxonidine in a Multinational Metabolic Syndrome Population: Principal Results of the MERSY Study

Improved Hypertension Control with the Imidazoline Agonist Moxonidine in a Multinational Metabolic Syndrome Population: Principal Results of the MERSY Study

Analysing the effect of I1 imidazoline receptor ligands on DSS-induced acute colitis in mice

Addressing the relationship between sympathetic activity and inflammation

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