Hypertension and the Insulin Resistance Syndrome of Rats

Klimeš, I; Seböková, E

doi:10.1111/j.1749-6632.1997.tb51819.x

Cited by 4 publications

(6 citation statements)

References 217 publications

(256 reference statements)

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“…The hereditary hypertriglyceridemic (hHTg) rat represents a unique animal model of the human insulin resistance syndrome where hypertension is one of its prominent features 5,36,37 . In this study, we confirmed earlier findings 38,39 that both systolic BP (157 ± 5.5 versus 115 ± 3.4 mmHg) and diastolic BP (131 ± 3.9 versus 95 ± 3.9 mmHg) were highly significantly increased in hHTg rats.…”

Section: Sympathoadrenal Activity In Insulin‐resistant and Hypertensisupporting

confidence: 90%

“…Hyperinsulinemia leads to a dose‐dependent BP increase in rats 5,9 . Euglycemic insulin infusion also has been shown to increase BP, an effect that is reversed by alpha‐and beta‐adrenergic blockade.…”

Section: Hyperinsulinemiamentioning

confidence: 99%

“…In rats, both acute and chronic hyperinsulinemia lead to an increase in blood pressure (BP) 6–8 . The mechanisms of insulin‐induced changes in BP regulation could involve several factors—activation of catecholaminergic systems, sodium‐fluid retention, modulation of cation transport, vasculopathy, etc 5 . Moreover, several investigators have indicated a role for the sympathoneural system in insulin‐mediated BP changes 7,9–13 .…”

mentioning

confidence: 99%

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Hyperinsulinemia and Sympathoadrenal System Activity in the Rat^a

Květňanský

Rusnak

Gašperíková

et al. 1997

Annals of the New York Academy of Sciences

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A relationship between hyperinsulinemia, insulin resistance, and hypertension has been described; however, it is still not completely clear whether these phenomena are causally related (for review, see references 1-5).In rats, both acute and chronic hyperinsulinemia lead to an increase in blood pressure (BP).G8 The mechanisms of insulin-induced changes in BP regulation could involve several hctors-activation of catecholaminergic systems, sodium-fluid retention, modulation of cation transport, vasculopathy, etc.5 Moreover, several investigators have indicated a role for the sympathoneural system in insulin-mediated BP ~hanges.~+~-'3 Thus, one of the important ways by which hyperinsulinemia could increase BP is the activation of the sympathoadrenal system. However, the mechanism by which hyperinsulinemia could affect sympathoadrenal system activity remains unclear. Therefore, the aim of this contribution, which represents a review with

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Section: Sympathoadrenal Activity In Insulin‐resistant and Hypertensisupporting

confidence: 90%

Section: Hyperinsulinemiamentioning

confidence: 99%

mentioning

confidence: 99%

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Hyperinsulinemia and Sympathoadrenal System Activity in the Rat^a

Květňanský

Rusnak

Gašperíková

et al. 1997

Annals of the New York Academy of Sciences

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“…This phenomenon is compatible with the well-known insulin resistance of SHR. 26 Because eNOS phosphorylation by AKT occurs after translocation of the cytosolic AKT to the membranes by means of a scaffold that contains heat-shock protein 90 and eNOS itself, [27][28][29] we explored whether AKT moved into the membranes after EC stimulation. Both agonists were able to increase the membrane content of the kinase in WKY ECs (Figure 4).…”

Section: Akt Assessment In Wky and Shr Ecsmentioning

confidence: 99%

AKT Participates in Endothelial Dysfunction in Hypertension

et al. 2004

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Background-In hypertension, reduced nitric oxide production and blunted endothelial vasorelaxation are observed. It was recently reported that AKT phosphorylates and activates endothelial nitric oxide synthase and that impaired kinase activity may be involved in endothelial dysfunction. Methods and Results-To identify the physiological role of the kinase in normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), we used adenoviral vectors to transfer the human AKT1 gene selectively to the common carotid endothelium. In vitro, endothelial vasorelaxations to acetylcholine, isoproterenol, and insulin were blunted in control carotids from SHR compared with WKY rats, and human AKT1 overexpression corrected these responses. Similarly, blood flow assessed in vivo by Doppler ultrasound was reduced in SHR compared with WKY carotids and normalized after AKT1 gene transfer. In primary cultured endothelial cells, we evaluated AKT phosphorylation, activity, and compartmentalization and observed a mislocalization of the kinase in SHR. Conclusions-We conclude that AKT participates in the settings of endothelial dysfunction in SHR rats by impaired membrane localization. Our data suggest that AKT is involved in endothelium dysfunction in hypertension.

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“…These studies indicate that hypertensives tend to be hyperinsulinemic and insulin resistant in comparison with normotensive individuals, and that the relationship between insulin resistance and hypertension is independent of BMI, age, or magnitude of glucose tolerance. The association between hypertension and insulin resistance has also been documented in several rodent models of hypertension (99). In addition human population studies have demonstrated strong positive associations between blood pressure and markers of insulin resistance in both normotensive and hypertensive individuals (81,89,90,100).…”

Section: Diagnostic Features Of Pih: Analogies To Irsmentioning

confidence: 89%

Pregnancy‐induced hypertension and insulin resistance, evidence for a connection

Innes¹,

Wimsatt²

1999

Acta Obstet Gynecol Scand

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PIH, the most common complication of pregnancy, remains a major source of maternal-child morbidity and mortality. Yet the etiology of this disorder is still little understood. There is now a growing body of evidence linking PIH and insulin resistance. Both proteinuric and non-proteinuric PIH predict future essential hypertension, and to a lesser extent, diabetes, disorders strongly related to glucose intolerance and insulin resistance. PIH is associated with diabetes, occurring in up to 50% of diabetic pregnancies. PIH is characterized by the same features that define IRS, including hypertension, dyslipidemia, disruption of endothelial and platelet function and related disturbances of prostanoid synthesis, coagulation and fibrinolytic abnormalities, hyperuricemia, atherosclerotic changes, and obesity. During the last decade, controlled studies by at least 11 different research groups in nine countries have established significant positive associations between both proteinuric and nonproteinuric PIH and various measures of insulin resistance. In particular, prospective investigations by at least five groups of investigators have indicated that relative hyperinsulinemia, glucose intolerance, and insulin insensitivity predict the subsequent development of PIH. These and other studies suggest that insulin resistance may play a causal role in the pathogenesis of PIH, and that some aspects of PIH may represent an early manifestation of IRS, precipitated by the profound metabolic and hemostatic challenges of gestation.

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Hypertension and the Insulin Resistance Syndrome of Rats

Cited by 4 publications

References 217 publications

Hyperinsulinemia and Sympathoadrenal System Activity in the Rat^a

Hyperinsulinemia and Sympathoadrenal System Activity in the Rat^a

AKT Participates in Endothelial Dysfunction in Hypertension

Pregnancy‐induced hypertension and insulin resistance, evidence for a connection

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Hypertension and the Insulin Resistance Syndrome of Rats

Cited by 4 publications

References 217 publications

Hyperinsulinemia and Sympathoadrenal System Activity in the Rata

Hyperinsulinemia and Sympathoadrenal System Activity in the Rata

AKT Participates in Endothelial Dysfunction in Hypertension

Pregnancy‐induced hypertension and insulin resistance, evidence for a connection

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Hyperinsulinemia and Sympathoadrenal System Activity in the Rat^a

Hyperinsulinemia and Sympathoadrenal System Activity in the Rat^a