The vasodilator action of insulin. Implications for the insulin hypothesis of hypertension.

Anderson, Erling A.; Mark, Allyn L.

doi:10.1161/01.hyp.21.2.136

Cited by 228 publications

(110 citation statements)

References 43 publications

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“…Dentre os mecanismos implicados, discute-se o papel da insulina, que, embora seja um vasodilatador (24,31), parece ter um papel indireto sobre os mecanismos pressóricos. Entre estes, destaca-se a sua participação na retenção hidrossalina, diretamente nos túbulos renais ou indiretamente, através do aumento na produção de aldosterona, pela sensibilização das adrenais à angiotensina II (32) e via ativação simpática (27).…”

Section: Fisiopatologia Da Obesidade -Hipertensãounclassified

Obesidade visceral, hipertensão arterial e risco cárdio-renal: uma revisão

Rosa

Zanella

Ribeiro

et al. 2005

Arq Bras Endocrinol Metab

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Arq Bras Endocrinol Metab vol 49 nº 2 Abril 2005 196 RESUMOA maior parte da adversidade atribuída à obesidade é dada pelo risco cardiovascular/coronariano imputado à mesma, particularmente presente nos obesos com distribuição visceral de gordura corporal. O acúmulo de gordura visceral está sabidamente associado à maior prevalência de desarranjos metabólicos, hormonais, inflamatórios e hemodinâmicos, que no conjunto implicarão em maior acometimento da microvasculatura e impacto negativo sobre os órgãos-alvo, particularmente sobre o eixo cárdio-renal. Neste sentido, além da associação clássica com a doença coronariana, têm-se verificado uma associação maior da obesidade visceral com a hipertrofia ventricular esquerda e microalbuminúria, ambos fatores de risco cardiovascular e nefrológico reconhecidos. Assim, a abordagem terapêutica dos pacientes obesos, particularmente dos hipertensos, deve levar em conta a estratificação de risco baseada na distribuição de gordura corporal, o que permitirá uma terapêutica mais adequada, visando-se não só o controle dos fatores de risco como a monitorização do acometimento de órgãos-alvo nestas populações. Great part of obesity adversity is due to its cardiovascular/coronary risk, particularly present in obese with visceral adiposity distribution. Visceral fat deposition is known to be associated with a greater prevalence of metabolic, neurohormonal, inflammatory and hemodynamic disorders, which together will be implicated in microvascular and target organ involvement, particularly to the cardio-renal axis. In this aspect, beyond its classical association with coronary disease, visceral obesity has been associated with left ventricular hypertrophy and microalbuminuria, which are known cardiac and nephrologic risk factors. So, therapeutic tools for obese patients, specially for those with hypertension, must accomplish the risk stratification based on body fat distribution, which will allow a more adequate therapy in terms of risk factors control as well as target organ damage monitoring. AOBESIDADE É ATUALMENTE UMA DOENÇA altamente prevalente e de elevada morbimortalidade para as populações industrializadas (1). Tal risco é particularmente atribuído às implicações cardiovasculares relacionadas à obesidade (2,3), especialmente presentes nos obesos com deposição visceral de gordura, conforme demonstrou-se nos estudos

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Section: Fisiopatologia Da Obesidade -Hipertensãounclassified

Obesidade visceral, hipertensão arterial e risco cárdio-renal: uma revisão

Rosa

Zanella

Ribeiro

et al. 2005

Arq Bras Endocrinol Metab

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“…This may be explained by proliferation of vascular smooth muscle induced by sympathetic stimulation (38) or insulin (6,11,39), or by reduction of insulin-induced vasodilatation due to increased insulin resistance (6,11,(40)(41)(42). Therefore, it is considered that the ZDF rat may be a model of NIDDM associated with major vascular complications.…”

Section: Figurementioning

confidence: 99%

“…Insulin has vasodilative and hypotensive effects (3)(4)(5)(6)(7)(8)(9). It has been reported that hypertension was improved by insulin treatment in patients with DM (10)(11)(12). The antihypertensive effect of insulin was explained either by the secondary action of improved glucose metabolism after insulin treatment or by the direct action on peripheral arterial vessels (4,(10)(11)(12)(13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

“…It has been reported that hypertension was improved by insulin treatment in patients with DM (10)(11)(12). The antihypertensive effect of insulin was explained either by the secondary action of improved glucose metabolism after insulin treatment or by the direct action on peripheral arterial vessels (4,(10)(11)(12)(13)(14)(15)(16). Peripheral arterial resistance is a critical factor for the regulation of diastolic blood pressure, which is increased by atherosclerosis or vasoconstriction (17)(18)(19)(20).…”

Section: Introductionmentioning

confidence: 99%

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Antihypertensive effect of insulin via nitric oxide production in the Zucker diabetic fatty rat, an animal model for non-insulin-dependent diabetes mellitus

Kawaguchi

Koshimura²,

Murakami³

et al. 1999

European Journal of Endocrinology

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It has been reported that insulin treatment improves hypertension in patients with diabetes mellitus. The mechanisms of the antihypertensive effect of insulin, however, remain to be fully elucidated. In the present study, we investigated a possible involvement of nitric oxide (NO) in insulin-induced reduction of blood pressure using the Zucker diabetic fatty (ZDF) rat, an animal model of non-insulin-dependent diabetes mellitus. The animals were divided into three groups and treated for 4 weeks with daily subcutaneous injections of insulin (25 U/kg body weight) with or without oral administration of Lnitro-arginine methyl ester (L-NAME, 50 mg/kg/day body weight as drinking water), an inhibitor of NO synthase (NOS). Saline solution was injected subcutaneously in the control groups. During the experimental period, body weight gain was greater in the insulin-treated groups than in the control groups whereas water intake was considerably decreased in the insulin-treated groups. Insulin treatment resulted in a decrease in plasma glucose and blood pressure, and an increase in both NO metabolites (NOx) in the plasma and NOS activity in the aorta tissue. L-NAME treatment blunted not only the antihypertensive effect of insulin but also the changes in NOx and NOS activity. These findings suggest that insulin reduces blood pressure in the ZDF rat by stimulating NOS activation and NO production.

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“…1,2 A prevailing concept has been that obesity-induced hypertension is secondary to insulin resistance and hyperinsulinemia 3 despite the fact that experimental studies in humans 4 and dogs 5 have challenged this concept. Recently, interest has focused on the role of the kidney and renal sympathetic nerves in obesity-induced hypertension.…”

mentioning

confidence: 99%

Obesity-Induced Hypertension

et al. 1999

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Abstract-Obesity is associated with an increased risk of hypertension. In the past 5 years there have been dramatic advances into the genetic and neurobiological mechanisms of obesity with the discovery of leptin and novel neuropeptide pathways regulating appetite and metabolism. In this brief review, we argue that these mounting advances into the neurobiology of obesity have and will continue to provide new insights into the regulation of arterial pressure in obesity. We focus our comments on the sympathetic, vascular, and renal mechanisms of leptin and melanocortin receptor agonists and on the regulation of arterial pressure in rodent models of genetic obesity. We suggest 3 concepts. First, the effect of obesity on blood pressure may depend critically on the genetic-neurobiological mechanisms underlying the obesity. Second, obesity is not consistently associated with increased blood pressure, at least in rodent models. Third, the blood pressure response to obesity may be critically influenced by modifying alleles in the genetic background. Key Words: leptin Ⅲ melanocortins Ⅲ sympathetic nervous system Ⅲ agouti Ⅲ rats, experimental Ⅲ obesity O besity is a leading risk factor for chronic arterial hypertension. 1,2 A prevailing concept has been that obesity-induced hypertension is secondary to insulin resistance and hyperinsulinemia 3 despite the fact that experimental studies in humans 4 and dogs 5 have challenged this concept. Recently, interest has focused on the role of the kidney and renal sympathetic nerves in obesity-induced hypertension. 5,6 Since the discovery of leptin about 5 years ago, knowledge regarding the genetic and neurobiological mechanisms of obesity has mushroomed. We review here the sympathetic and cardiovascular actions of leptin and melanocortin receptor agonists and the regulation of arterial pressure in murine genetic models of obesity associated with leptin deficiency or resistance and melanocortin-4 receptor antagonism. We argue that the escalating advances regarding the genetic and neurobiological mechanisms of obesity will provide new insights and concepts regarding the regulation of blood pressure in obesity. Two converging lines of evidence prompt this view: first, recent studies implicating renal sympathetic nerves in obesity-induced hypertension 6 and, second, knowledge that the neurobiological mechanisms of obesity involve alterations in sympathetic regulation. 7,8 Sympathetic and Cardiovascular Actions of LeptinLeptin increases thermogenic metabolism in addition to inhibiting appetite. 9,10 Sympathetic nerves have been implicated in the regulation of thermogenesis in brown adipose tissue in rodents. This prompted consideration of the influence of leptin on sympathetic nerves. Collins et al demonstrated that leptin increases norepinephrine turnover in brown adipose tissue, suggesting increased sympathetic activity. 11 We subsequently studied effects of intravenous infusion of leptin on regional sympathetic nerve activity recorded directly with microelectrodes in Sprague-Dawley ...

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The vasodilator action of insulin. Implications for the insulin hypothesis of hypertension.

Cited by 228 publications

References 43 publications

Obesidade visceral, hipertensão arterial e risco cárdio-renal: uma revisão

Obesidade visceral, hipertensão arterial e risco cárdio-renal: uma revisão

Antihypertensive effect of insulin via nitric oxide production in the Zucker diabetic fatty rat, an animal model for non-insulin-dependent diabetes mellitus

Obesity-Induced Hypertension

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