Elevated Blood Pressure, Pulse Rate and Serum Creatinine in Negro Males Deficient in Glucose-6-Phosphate Dehydrogenase

Wiesenfeld, Stephen L.; Petrakis, Nicholas L.; Sams, Bruce J.; Collen, Morris F.; Cutler, John C.

doi:10.1056/nejm197004302821804

Cited by 25 publications

(17 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The higher blood pressure in E-Hemi mice is consistent with a clinical report showing higher blood pressure in G6PD-deficient men. 23 Higher basal blood pressure in E-Hemi mice might be attributed to less endothelial nitric oxide (NO) production, which may also be because of a lower supply of NADPH. In agreement with this interpretation, NO bioavailability is decreased by inhibiting G6PD activity in endothelial cells in culture.…”

Section: Matsui Et Al G6pd Deficiency and Atherosclerosis 913mentioning

confidence: 99%

See 1 more Smart Citation

Glucose-6-Phosphate Dehydrogenase Deficiency Decreases Vascular Superoxide and Atherosclerotic Lesions in Apolipoprotein E ^−/− Mice

Matsui

Maitland

et al. 2006

ATVB

View full text Add to dashboard Cite

Objective-Glucose-6-phosphate dehydrogenase (G6PD) is a key enzyme in the pentose phosphate pathway that is a major source of cellular NADPH. The purpose of this study was to examine whether G6PD deficiency affects vascular oxidants and atherosclerosis in high-fat fed apolipoprotein (apo) E Ϫ/Ϫ mice. Methods and Results-G6PD-mutant mice whose G6PD activity was 20% of normal were crossbred with apoE Ϫ/Ϫ mice. Among male apoE Ϫ/Ϫ mice that were fed a western-type diet for 11 weeks, G6PD wild-type (E-WT), and G6PD hemizygous (E-Hemi) mice were compared. Basal blood pressure was significantly higher in E-Hemi. However, superoxide anion release, nitrotyrosine, vascular cell adhesion molecule (VCAM)-1, and inducible nitric oxide synthase immunohistochemical staining were less in E-Hemi compared with E-WT aorta. Serum cholesterol level was lower in E-Hemi, but aortic lesion area was decreased in E-Hemi even after adjusting for serum cholesterol. Conclusions-Lower NADPH production in G6PD deficiency may result in lower NADPH oxidase-derived superoxide anion, and thus lower aortic lesion growth. The association of higher blood pressure with lower serum cholesterol levels in this mouse model is indicative of the complex effects that G6PD deficiency may have on vascular disease. Key Words: atherosclerosis Ⅲ genetically altered mice Ⅲ reactive oxygen species Ⅲ NADPH E nhanced vascular superoxide anion production is associated with hypercholesterolemia and may contribute to the initiation and progression of atherosclerosis. 1 Vascular cell-derived superoxide anion mediates oxidative modification of low-density lipoprotein (LDL) 2,3 and oxidized LDL further promotes superoxide production and foam cell formation. 4 Also, reactive oxygen species promote various processes including endothelial dysfunction, smooth muscle cell growth and migration, and induction of adhesion molecules. 5 A major source of superoxide anion in vascular cells is NADPH oxidase, the expression of which is enhanced in atherosclerotic lesions. [5][6][7] Pharmacological inhibition of NADPH oxidase decreased aortic superoxide anion production and atherosclerotic lesions in apoE Ϫ/Ϫ mice, 8 and genetic deficiency in the p47 phox subunit of NADPH oxidase attenuates the inflammatory response to hypercholesterolemia 9 and reduces aortic lesions in apoE Ϫ/Ϫ mice. 10 Glucose-6-phosphate dehydrogenase (G6PD), a key enzyme in the pentose phosphate pathway, provides NADPH for various cellular reactions including glutathione (GSH) recycling, superoxide anion production via NADPH oxidase, NO synthesis, and cholesterol synthesis. Inhibition of G6PD results in decreased production of superoxide and/or NO in granulocytes 11,12 and other cell types including endothelial cells. [13][14][15] In addition, recent studies suggest that the level of pentose phosphate pathway-derived NADPH may regulate vascular superoxide production. 16 Consistent with these studies, we found that G6PD-deficient mice had lower aortic superoxide production and less hypertrophy in response to angio...

show abstract

Section: Matsui Et Al G6pd Deficiency and Atherosclerosis 913mentioning

confidence: 99%

“…18 In various conditions G6PD activity is rapidly upregulated in response to oxidative stress, presumably to maintain GSH in its reduced form. 19 -22 Human G6PD deficiency, the most common genetic enzymopathy, is reported to either enhance or decrease the risk of cardiovascular disease, 23,24 but the mechanisms by which risk might be affected are not known.…”

mentioning

confidence: 99%

Glucose-6-Phosphate Dehydrogenase Deficiency Decreases Vascular Superoxide and Atherosclerotic Lesions in Apolipoprotein E ^−/− Mice

Matsui

Maitland

et al. 2006

ATVB

View full text Add to dashboard Cite

show abstract

“…49 It is not well studied whether cardiovascular risk is affected in people with G6PD deficiency. Although an early report suggested a higher incidence of hypertension, 22 a recent cohort study suggested lower mortality from cardiovascular disease in people with G6PD deficiency. 50 Although human cardiovascular diseases stem from multiple genetic and environmental factors, a decreased role of NADPH oxidase may provide a beneficial effect among people with G6PD deficiency.…”

mentioning

confidence: 96%

“…An early clinical report suggested that blood pressure is increased in G6PD-deficient people, 22 but it is not well studied whether risk for cardiovascular disease is affected by G6PD deficiency. We therefore examined the role of G6PD as a source of NADPH in regulating the vascular response to Ang II infusion by using G6PD-deficient mutant mice.…”

mentioning

confidence: 99%

Glucose-6 Phosphate Dehydrogenase Deficiency Decreases the Vascular Response to Angiotensin II

Matsui

Maitland

et al. 2005

Circulation

View full text Add to dashboard Cite

Background-Glucose-6-phosphate dehydrogenase (G6PD) regulates production of the reduced form of NADPH through the pentose phosphate pathway. G6PD may therefore affect superoxide anion production via vascular NADPH oxidase, which is key in mediating the vascular response to angiotensin II (Ang II). We determined the hypertensive and vascular hypertrophic response to Ang II in G6PD-deficient mice. Methods and Results-Ang II (0.7 mg/kg per day) was infused via subcutaneous osmotic pumps for 6 days in male hemizygote G6PD mutant (G6PD mut ) and wild-type (WT) C3H mice. (1)

show abstract

“…This is because pressure overload induces redox stress in the presence of G6PD deficiency, enhancing the risk potential for crisis [17]. Wiesenfeld et al, [18] in their study, reported an increase in blood pressure amongst G6PD deficiency subjects. Furthermore, G6PD deficient subjects appear to be more susceptible to bacterial infection than normal individuals [19].…”

Section: Introductionmentioning

confidence: 91%

An Assessment of Frequent Haemolytic Crisis in G6PD Deficiency Subjects Linked with Chronic Disease States in Al Ahsa Community, Saudi Arabia

Emeka¹,

Hilal²,

Asif³

et al. 2015

Health

View full text Add to dashboard Cite

The main treatment strategy for glucose-6-phosphate dehydrogenase (G6PD) deficiency is averting the use of oxidative precipitants like drugs or foods that trigger haemolysis. However, subjects could experience acute crisis in a comorbidity state of diabetes, hypertension or infection. In addition, the condition could in turn predispose carriers to these chronic diseases. Aim of the study was to evaluate the frequency of haemolytic crisis in carriers with attendant chronic diseases, and also assess awareness and knowledge of aggravated reactions from these conditions. 282 subjects consented and participated in the study. A cross-sectional semi-structured interview questionnaire conducted from May to August 2013 was adopted. Questions focused on demographics, awareness and when disease was diagnosed, type and frequency of crisis, family history, screening and presence of other diseases and awareness of trigger from these conditions. A total of 69.9% were G6PD deficiency gene carriers and mostly fell within the age group of 31 -40 (43.6%). 75.6% of the carriers were not aware that other disease conditions could exacerbate crisis. Non-drug related crisis was 85.3% compared with 14.7 drug related reactions. Out of the 69.9% carriers, 17.3% are diabetics, 18.3% of them are hypertensive and 25.9% are with bleeding disorders. Also, 29.1% had frequent episodes with bacterial infection. Symptoms experienced that were not drug related included, 44.8% attacks of pallor, 25.3% jaundice, 28.5% with shortness of breath, while 21.7% had dark urine frequently. No routine screening for other diseased conditions was carried out for these subjects despite experiencing frequent crisis that were not drug related. Carriers * Corresponding author. P. Emeka et al. 626with other diseased conditions experienced more non-drug related crisis and were not aware of it.

show abstract

Elevated Blood Pressure, Pulse Rate and Serum Creatinine in Negro Males Deficient in Glucose-6-Phosphate Dehydrogenase

Cited by 25 publications

References 6 publications

Glucose-6-Phosphate Dehydrogenase Deficiency Decreases Vascular Superoxide and Atherosclerotic Lesions in Apolipoprotein E ^−/− Mice

Glucose-6-Phosphate Dehydrogenase Deficiency Decreases Vascular Superoxide and Atherosclerotic Lesions in Apolipoprotein E ^−/− Mice

Glucose-6 Phosphate Dehydrogenase Deficiency Decreases the Vascular Response to Angiotensin II

An Assessment of Frequent Haemolytic Crisis in G6PD Deficiency Subjects Linked with Chronic Disease States in Al Ahsa Community, Saudi Arabia

Contact Info

Product

Resources

About

Elevated Blood Pressure, Pulse Rate and Serum Creatinine in Negro Males Deficient in Glucose-6-Phosphate Dehydrogenase

Cited by 25 publications

References 6 publications

Glucose-6-Phosphate Dehydrogenase Deficiency Decreases Vascular Superoxide and Atherosclerotic Lesions in Apolipoprotein E −/− Mice

Glucose-6-Phosphate Dehydrogenase Deficiency Decreases Vascular Superoxide and Atherosclerotic Lesions in Apolipoprotein E −/− Mice

Glucose-6 Phosphate Dehydrogenase Deficiency Decreases the Vascular Response to Angiotensin II

An Assessment of Frequent Haemolytic Crisis in G6PD Deficiency Subjects Linked with Chronic Disease States in Al Ahsa Community, Saudi Arabia

Contact Info

Product

Resources

About

Glucose-6-Phosphate Dehydrogenase Deficiency Decreases Vascular Superoxide and Atherosclerotic Lesions in Apolipoprotein E ^−/− Mice

Glucose-6-Phosphate Dehydrogenase Deficiency Decreases Vascular Superoxide and Atherosclerotic Lesions in Apolipoprotein E ^−/− Mice