Moxonidine in the treatment of overweight and obese patients with the metabolic syndrome: a postmarketing surveillance study

Sharma, Arya M.; Wagner, Todd H.; Marsalek, Parvaneh

doi:10.1038/sj.jhh.1001676

Cited by 55 publications

(41 citation statements)

References 23 publications

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“…The imidazoline binding agents, such as rilmenidine and moxonidine, which inhibit sympathetic outflow, might also be expected to increase weight, but surprisingly do not. Weight loss of 1 to 2 kg is typically seen, despite sympathetic inhibition, 95 perhaps because of the reduction in neurogenic vasoconstriction in skeletal muscle producing a favorable effect on insulin resistance and hyperinsulinemia. 81,82 The evidence is conflicting concerning the capacity of renin-angiotensin system blockade to inhibit sympathetic activity.…”

Section: Antihypertensive Drugsmentioning

confidence: 99%

Mechanisms of Sympathetic Activation in Obesity-Related Hypertension

et al. 2006

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O besity prevalence is soaring in industrialized countries and progressively increasing in the developing world. Altered patterns of nutrition and reduction in work-related energy expenditure have led to obesity becoming a truly global health issue. The central thermodynamic formulation for the origins of obesity, a mismatched energy balance equation, with an excess of dietary calorie intake over body energy expenditure, is a first step in the understanding of this phenomenon but leaves the diverse causal issues unexplored.Dietary calorie intake is modified by multiple social, economic, and cultural issues. Similarly, the reduction in energy expenditure in recent decades has complex origins, deriving from demographic and social change, which includes thirdworld transition from a labor-intensive agricultural economy to an industrial base, the introduction of household labor-saving devices, the popularity of transportation modes not reliant on physical effort, and from changed recreational habits, particularly in childhood (computer games instead of physical games). The prevalence of childhood obesity is escalating, having whimsically but not entirely unrealistically been attributed to "potato chips and computer chips."Obesity and hypertension are intimately associated, and both very commonly coexist in individual patients with insulin resistance, hyperinsulinemia, and hyperlipidemia, this clustering of adverse health factors 1 being designated the metabolic syndrome. The pathophysiological mechanisms by which obesity leads to hypertension remain uncertain. Understanding these processes might, perhaps, provide a more rational basis for drug treatment of obesity-related hypertension. Attempts at reduction in body weight, although pivotal in the treatment of obesity-related hypertension, more often than not fail, so that antihypertensive drug therapy is often needed.This review analyses the proposition that obesity is characterized by activation of the sympathetic nervous system and that obesity-related hypertension is, in fact, neurogenic, being initiated and sustained by neural mechanisms. At one time, this idea would have been held to fly in the face of both reason and empirical evidence, because the sympathetic nervous system is thermogenic and promotes negative energy balance and weight loss, 2 and in earlier experimental models of obesity, sympathetic nervous activity was found to be suppressed. 3 Consideration of these earlier and very influential experimental models of obesity, many of which involved brain lesions inhibiting both sympathetic nervous outflow and satiety, will now be the starting point for this review. Hypothalamic Models of Experimental ObesityVentromedial hypothalamic injury in rats can cause obesity either with or without hyperphagia. 3,4 The observation that hypothalamic ablation can cause obesity without overeating, but associated with sympathetic nervous suppression, led Bray et al 3 to propose that the sympathetic nervous system underactivity commonly present in animal models of obesity...

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Section: Antihypertensive Drugsmentioning

confidence: 99%

Mechanisms of Sympathetic Activation in Obesity-Related Hypertension

et al. 2006

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“…• Стабилизацию/снижение массы тела (моксо-нидин и периндоприл снижают ИМТ) [25][26][27][28][29][30] • Коррекцию метаболических нарушений (мок-сонидин и периндоприл оказывают благоприятное влияние на липидный обмен) [31][32][33].…”

Section: для чего нужная новая комбинация блокаторов раас с агонистамunclassified

“…• Уменьшение инсулинорезистентности (моксо-нидин и периндоприл улучшают чувствительность тканей к инсулину [28][29][30], причем этот эффект мок-сонидина доказан для разных популяций пациентов с АГ) [27,36,37].…”

Section: для чего нужная новая комбинация блокаторов раас с агонистамunclassified

Combination of Ace Inhibitor With Agonist of I1 -Imidazoline Receptors: New Opportunities for Antihypertensive Therapy

Недогода¹

2016

Russ J Cardiol

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“…The antihypertensive effectiveness of moxonidine is comparable to hydrochlorothiazide, angiotensin-converting enzyme inhibitor, and ␣-and ␤-blockers. 28 Although clonidine lowers resting energy expenditure 29 in normal volunteers, moxonidine appears to have a positive metabolic effect, inducing a 1-to 2-kg weight loss 30 (in uncontrolled studies) and improving insulin sensitivity. 31,32 This effect, however, has not been reported with rilmenidine.…”

Section: Central Sympatholytics In the Treatment Of Obesity-associatementioning

confidence: 99%

Should We Target the Sympathetic Nervous System in the Treatment of Obesity-Associated Hypertension?

Biaggioni

2008

Hypertension

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A n estimated 60% to 70% of hypertension may be attributed to obesity. 1 As our population increases in weight and girth, obesity-associated hypertension will be an increasing medical problem, contributing to greater health care costs and reversing the gains that we have achieved in the treatment of hypertension. Considering that 30% of hypertensive subjects are undiagnosed, 40% remain untreated, and, of those being treated, 65% do not meet treatment goals, 2 the opening of the spigot of obesityassociated hypertension will result in an ever-growing number of patients with uncontrolled hypertension, particularly because obesity is a predictor of poor blood pressure control. 3 It is important, therefore, to understand the pathophysiology of obesity-associated hypertension. This commentary focuses on the role that the sympathetic nervous system plays in this condition and its relevance to treatment. Sympathetic Activity and Obesity-Associated HypertensionLandsberg 4 postulated that obesity induces sympathetic activation as a compensatory mechanism to increase resting energy expenditure and restore energy balance; sympathetically mediated hypertension is the price to pay for this beneficial metabolic effect. A competing MONA LISA (Most Obesities kNown Are Low In Sympathetic Activity) hypothesis postulates that lower sympathetic activity is an initiating event leading to decreased energy expenditure and obesity. 5 In white populations, in whom most of the studies have been done, the preponderance of evidence supports the concept that sympathetic activation accompanies obesity-associated hypertension. There is less agreement about the cause of sympathetic activation; potential culprits include the increase in insulin, leptin, and angiotensin II; the decrease of adiponectin; and the sleep apnea 6,7 associated with obesity. Despite the disparity of these mechanisms, it is interesting that all of them act in the central nervous system to increase sympathetic outflow. This central sympathetic activation is not generalized; rather, it is selectively increased in organs relevant to blood pressure regulation, including the kidney, heart, and skeletal muscle vasculature. 6,8 To determine whether sympathetic activation indeed contributed to obesity-associated hypertension, Wofford et al 9 used combined ␣-and ␤-blockade with doxazosin and atenolol and showed a greater decrease in blood pressure in obese compare with lean hypertensive subjects. We recently used a similar approach, inducing complete but transient autonomic withdrawal with the ganglionic blocker trimethaphan, and showed that most of the increase in blood pressure observed in obese subjects was mediated by the autonomic nervous system. 10 As expected, resting energy expenditure was higher in obese subjects but, in contrast to blood pressure, it remained significantly elevated after autonomic blockade. We found that the increase in energy expenditure was likely because of the increase in muscle mass that usually companies obesity 10 ; in our patients, a 30-kg increa...

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Moxonidine in the treatment of overweight and obese patients with the metabolic syndrome: a postmarketing surveillance study

Cited by 55 publications

References 23 publications

Mechanisms of Sympathetic Activation in Obesity-Related Hypertension

Mechanisms of Sympathetic Activation in Obesity-Related Hypertension

Combination of Ace Inhibitor With Agonist of I1 -Imidazoline Receptors: New Opportunities for Antihypertensive Therapy

Should We Target the Sympathetic Nervous System in the Treatment of Obesity-Associated Hypertension?

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