Rosiglitazone Improves, While Glibenclamide Worsens Blood Pressure Control in Treated Hypertensive Diabetic and Dyslipidemic Subjects via Modulation of Insulin Resistance and Sympathetic Activity

Yosefy, Chaim; Magen, Eliahu; Kiselevich, Ada; Priluk, R.; London, D. R.; Volchek, Lior; Viskoper, Reuven J.

doi:10.1097/00005344-200408000-00011

Cited by 65 publications

(49 citation statements)

References 30 publications

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“…BP was also reduced to a greater extent with rosiglitazone than either metformin or glyburide, particularly DBP. These modest differences in office BP were consistent with previous reports that either used casual BP measurements (23,24) or, more importantly, monitored 24-hour ambulatory BP (25,26). In our study the effect was independent of pre-existing hypertension, or treatment with ACEi, ARBs, or calcium channel blockers over time, or the level of glycemia.…”

Section: ͻ0001supporting

confidence: 92%

Renal Function in Type 2 Diabetes with Rosiglitazone, Metformin, and Glyburide Monotherapy

Lachin

Viberti

Zinman

et al. 2011

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives In ADOPT (A Diabetes Outcomes Prevention Trial), initial monotherapy with rosiglitazone provided more durable glycemic control than metformin or glyburide in patients with recently diagnosed type 2 diabetes. Herein, we examine differences in albumin excretion, renal function (estimated GFR), and BP over 5 years between treatment groups.Design, setting, participants, & measurements A total of 4351 recently diagnosed, drug-naïve patients with type 2 diabetes were treated and followed for up to 5 years with rosiglitazone, metformin, or glyburide and were examined with periodic assessments of albumin/creatinine ratio (ACR), modification of diet in renal disease (MDRD)-estimated GFR, and BP. ResultsThe ACR rose slowly with metformin. It fell with rosiglitazone and less so with glyburide over the first 2 years, and then rose slowly over time. Estimated GFR (eGFR) with all therapies rose into the high normal range over the first 3 to 4 years, more so with rosiglitazone, and then declined, more so with glyburide. Systolic BP was stable over time, values with rosiglitazone being lower, and diastolic BP declined over time, more so with rosiglitazone than with metformin or glyburide. There was no difference among groups in the incidence of emergent albuminuria (ACR Ն30 mg/g), hypertension, or impaired eGFR (Ͻ60 ml/min per 1.73 m 2 ).Conclusions Over a 5-year period, initial monotherapy with rosiglitazone retards the rise of ACR compared with metformin, preserves eGFR compared with glyburide, and lowers BP relative to both comparators.

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Section: ͻ0001supporting

confidence: 92%

Renal Function in Type 2 Diabetes with Rosiglitazone, Metformin, and Glyburide Monotherapy

Lachin

Viberti

Zinman

et al. 2011

Clinical Journal of the American Society of Nephrology

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“…Studies in both animal models of hypertension and in humans with insulin resistance suggest that treatment with thiazolidinediones reduces urinary catecholamines, skin sympathetic nerve activity, and cardiac sympathetic nervous system function (55,59,61). The contribution of sympathetic activation to SLE hypertension has not been previously examined.…”

Section: Discussionmentioning

confidence: 99%

Rosiglitazone decreases blood pressure and renal injury in a female mouse model of systemic lupus erythematosus

Venegas-Pont

Sartori‐Valinotti

Maric

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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-Women with systemic lupus erythematosus (SLE) exhibit a high prevalence of hypertension and renal injury. Rosiglitazone (Rosi), a peroxisome proliferator activator receptor gamma (PPAR␥) agonist, has renal protective and antihypertensive effects. We tested whether Rosi ameliorates hypertension and renal injury in a female mouse model of SLE (NZBWF1). Thirty-week-old SLE and control (NZW/LacJ) mice (n Ն 6/group) were fed Rosi (5 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 in standard chow) or standard chow for 4 wk. SLE mice had increased blood pressure (BP in mmHg) compared with controls (139 Ϯ 4 vs. 111 Ϯ 4, P Ͻ 0.05). Rosi treatment lowered BP in SLE mice (127 Ϯ 4, P Ͻ 0.05) but not in controls (111 Ϯ 4). Urinary albumin (g/mg creatinine) was increased in SLE mice compared with controls (12,396 Ϯ 6,525 vs. 50 Ϯ 6) and reduced with Rosi treatment (148 Ϯ 117). Glomerulosclerosis (% of glomeruli with sclerosis) was reduced in Rosi-treated SLE mice (4.2 Ϯ 1.6 vs. 0.4 Ϯ 0.3, P Ͻ 0.05). Renal monocyte/ macrophage numbers (cell number/1,320 points counted) were reduced in SLE mice treated with Rosi (32.6 Ϯ 11.0 vs. 10.6 Ϯ 3.6, P Ͻ 0.05) but unchanged in controls (3.7 Ϯ 1.6 vs. 3.7 Ϯ 2.0). Renal osteopontin expression, a cytokine-regulating macrophage recruitment, was reduced in Rosi-treated SLE mice. Urinary endothelin (in pg/mg creatinine) was increased in SLE mice compared with controls (1.9 Ϯ 0.59 vs. 0.6 Ϯ 0.04, P Ͻ 0.05) and reduced in SLE mice treated with Rosi (0.8 Ϯ 0.11, P Ͻ 0.05). PPAR␥ protein expression in the renal cortex was significantly lower in SLE mice compared with controls and was unaffected by Rosi. These data suggest that Rosi may be an important therapeutic option for the treatment of SLE hypertension and renal injury. lupus; inflammation; endothelin; glomerulosclerosis; proliferator activated receptor gamma SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) is a chronic autoimmune inflammatory disorder that has a strong predilection for women during their reproductive years. The hallmark of the disease is the production of autoantibodies such as antinuclear antibodies, and more specifically anti-double-stranded DNA (antidsDNA) antibodies. Accumulating evidence indicates that the major cause of death among patients with SLE is cardiovascular disease (17,22,23,26). Indeed, studies have reported that women with SLE are at a 50-fold greater risk for developing cardiovascular disease independent of traditional Framingham Heart Study risk factors (35). One of the major factors contributing to the progression of cardiovascular disease is increased arterial pressure. Importantly, SLE is associated with a high incidence of hypertension (1, 41, 56).The kidneys are prominently affected during SLE in the form of immune complex glomerulonephritis. This occurs in greater than 50% of patients with SLE (18) and is caused, in part, by circulating anti-dsDNA antibody-mediated formation of immune complexes (51). Few advances have been made toward the treatment of SLE and the associated nephritis and hypertension in the past 40 years. Patients with SL...

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“…In subgroup (Ic), rats were given glibenclamide in a dose of 0.04 mg/kg/day orally, 12 and subgroup (Id) rats were given captopril (17.5 mg/kg/day) and served as a standard. 13 Group [II] (STZ-induced diabetes mellitus) rats were rendered diabetic by single intraperitoneal injection of STZ in a dose of 60 mg/kg. 9 The diabetic rats were randomized into three subgroups (48 rats each).…”

Section: Methodsmentioning

confidence: 99%

Comparison between the effect of glibenclamide and captopril on experimentally induced diabetic nephropathy in rats

Akbar

Hagras

Amin

et al. 2012

J Renin Angiotensin Aldosterone Syst

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Hypothesis: This study aimed to elucidate the role of glibenclamide in the prevention of diabetic nephropathy and to compare it with a reference drug captopril in rats. Materials and methods: There were two main groups of rats. Control group (I) was subdivided into four subgroups which received distilled water, vehicle of streptozotocin, glibenclamide or captopril. The streptozotocin-diabetic Group (II) was subdivided into three subgroups: untreated, glibenclamide or captopril treated. Measurement of arterial blood pressure, serum glucose and creatinine levels, 24 h urinary protein and albumin/creatinine ratio, kidney weight and its histological examination were done after 1, 2, 4, 8, 12 and 16 weeks of treatment. Results: In treated diabetic rats captopril reduced blood pressure significantly, while no significant change in the mean arterial blood pressure or blood glucose level was recorded with glibenclamide treatment. Glibenclamide and captopriltreated diabetic rats showed significant decrease in serum creatinine level, urine volume, urinary protein excretion, albumin:creatinine ratio and kidney:body weight ratio compared with the diabetic non-treated group. Histological examination of diabetic kidneys treated with either glibenclamide or captopril showed reduced glomerular hypertrophy, glomerulosclerosis, tubular degeneration and interstitial fibrosis compared with untreated diabetic rats. Conclusion: Glibenclamide attenuated some biochemical and histological changes produced by diabetic nephropathy, despite persistent hyperglycemia and hypertension.

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Rosiglitazone Improves, While Glibenclamide Worsens Blood Pressure Control in Treated Hypertensive Diabetic and Dyslipidemic Subjects via Modulation of Insulin Resistance and Sympathetic Activity

Abstract: Rosiglitazone improved both plasma glucose and blood pressure levels, probably by attenuation of hyperinsulinemia and sympathetic activity, while Glibenclamide worsened blood pressure control possibly by elevation of insulin levels and activation of the sympathetic system.

Cited by 65 publications

References 30 publications

Renal Function in Type 2 Diabetes with Rosiglitazone, Metformin, and Glyburide Monotherapy

Renal Function in Type 2 Diabetes with Rosiglitazone, Metformin, and Glyburide Monotherapy

Rosiglitazone decreases blood pressure and renal injury in a female mouse model of systemic lupus erythematosus

Comparison between the effect of glibenclamide and captopril on experimentally induced diabetic nephropathy in rats

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