Role of ET<sub>A</sub> receptors in experimental ANG II-induced hypertension in rats

Ballew, Jennifer R.; Fink, Gregory D.

doi:10.1152/ajpregu.2001.281.1.r150

Cited by 37 publications

(45 citation statements)

References 21 publications

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“…8,34 Briefly, kidneys were immersed in 4% buffered formalin solution overnight at room temperature, transferred to 70% ethanol for 24 hours, and paraffin-embedded. Sections were stained with primary antibodies specific for T cells (CD3, 1:2500; Santa Cruz Biotechnology) overnight at 4°C and detection with the immunocruz staining system (Santa Cruz Biotechnology) or monocytes/macrophages (F4/80, 1:100; Serotec or RM0029, 1:100; Abcam) overnight at 4°C and detection with horseradish peroxidase-conjugated secondary antibodies (Serotec and Abcam, respectively) for 1 hour at room temperature and detection with polymer conjugated secondary antibody (BioCare Medical).…”

Section: Immunohistochemical Analysesmentioning

confidence: 99%

ETA Activation Mediates Angiotensin II-Induced Infiltration of Renal Cortical T Cells

Boesen

Krishnan

Pollock

et al. 2011

Journal of the American Society of Nephrology

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Section: Immunohistochemical Analysesmentioning

confidence: 99%

ETA Activation Mediates Angiotensin II-Induced Infiltration of Renal Cortical T Cells

Boesen

Krishnan

Pollock

et al. 2011

Journal of the American Society of Nephrology

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“…9,19 Starting at week 3, some of the DOCA-salt rats received ABT-627 (Abbott Laboratories), a selective ET A receptor antagonist, 2 mg · kg body wt Ϫ1 · d Ϫ1 in drinking water for 2 weeks. 20 Blood pressure was measured in conscious rats by the noninvasive tail-cuff method. The vessels were collected between weeks 4 and 5 after DOCA implantation.…”

Section: Doca-salt Hypertensive Rats and In Vivo Pharmacological Intementioning

confidence: 99%

Endothelin-1 Increases Vascular Superoxide via Endothelin _A –NADPH Oxidase Pathway in Low-Renin Hypertension

Fink²,

Watts³

et al. 2003

Circulation

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305

269

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Background-Angiotensin II-induced hypertension is associated with NAD(P)H oxidase-dependent superoxide production in the vessel wall. Vascular superoxide level is also increased in deoxycorticosterone acetate (DOCA)-salt hypertension, which is associated with a markedly depressed plasma renin activity because of sodium retention. However, the mechanisms underlying superoxide production in low-renin hypertension are undefined. Methods and Results-This study investigated (1) whether and how endothelin-1 (ET-1), which is increased in DOCA-salt hypertensive rats, contributes to arterial superoxide generation and (2) the effect of gene transfer of manganese superoxide dismutase and endothelial nitric oxide synthase. Both superoxide and ET-1 levels were significantly elevated in carotid arteries of DOCA-salt rats compared with that of the sham-operated controls. ET-1 concentration-dependently stimulated superoxide production in vitro in carotid arteries of normotensive rats. The increase in arterial superoxide in both ET-1-treated normotensive and DOCA-salt rats was reversed by a selective ET A receptor antagonist, ABT-627, the flavoprotein inhibitor diphenyleneiodonium, and the NADPH oxidase inhibitor apocynin but not by the nitric oxide synthase inhibitor N -L-arginine methyl ester or the xanthine oxidase inhibitor allopurinol. Furthermore, in vivo blockade of ET A receptors significantly reduced arterial superoxide levels, with a concomitant decrease of systolic blood pressure in DOCA-salt rats. Ex vivo gene transfer of manganese superoxide dismutase or endothelial nitric oxide synthase also suppressed superoxide levels in carotid arteries of DOCA-salt rats. Conclusions-These findings suggest that ET-1 augments vascular superoxide production at least in part via an ET A /NADPH oxidase pathway in low-renin mineralocorticoid hypertension.

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“…Endothelin synthesis can be upregulated by Ang II, 47 and ET A receptors have been shown to mediate Ang II hypertension in animal studies. 48,49 Testosterone treatment of women also increases plasma endothelin levels. 36 Just as endothelin can cause oxidative stress, endothelin also increases in response to oxidative stress.…”

Section: Does Endothelin Play a Role In Postmenopausal Hypertension?mentioning

confidence: 99%

Novel Mechanisms Responsible for Postmenopausal Hypertension

2004

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Abstract-Blood pressure increases in many women after menopause. Hypertension is one of the major risk factors for cardiovascular disease. However, the mechanisms responsible for the postmenopausal increase in blood pressure are yet to be elucidated. Various humoral systems have been proposed to play a role in postmenopausal hypertension, such as changes in estrogen/androgen ratios, increases in endothelin and oxidative stress, and activation of the renin-angiotensin system (RAS). In addition, obesity, type II diabetes, and activation of the sympathetic nervous system are common in postmenopausal women and may also play important roles. However, progress in elucidating the mechanisms responsible for postmenopausal hypertension has been hampered by the lack of a suitable animal model. The aging female spontaneously hypertensive rat (SHR) exhibits many of the characteristics found in postmenopausal women. In this review, some of the possible mechanisms that could play a role in postmenopausal hypertension are discussed, as well as the characteristics of the aged female SHR as a model to study. Key Words: endothelin Ⅲ renin-angiotensin system Ⅲ oxidative stress Ⅲ obesity Ⅲ diabetes mellitus Ⅲ sympathetic nervous system B efore menopause, blood pressure is typically lower in women than in age-matched men. 1 In aging men and women, systolic and diastolic blood pressures increase, although in later years the diastolic plateaus or even declines. [1][2][3] However, in postmenopausal women, the prevalence of hypertension and cardiovascular disease risk increases regardless of ethnic origin. Results from the National Health and Nutrition Examination Survey (NHANES III) showed that in Hispanic women and non-Hispanic black women, the prevalence of hypertension was similar to, or higher than, that in men by age 60 years. 4 In non-Hispanic white populations, the prevalence of hypertension was higher in women than in men by age 70 years. 4 The increase in blood pressure in postmenopausal women does not occur as soon as the ovary becomes senescent, but rather over a number of years. 5 The mechanisms responsible for the increased blood pressure in women after menopause are not known. This review focuses on the use of the spontaneously hypertensive rat as a model of postmenopausal hypertension and evaluates the possible mechanistic roles of the sex hormones, oxidative stress, endothelin, renin-angiotensin system (RAS), weight gain, and sympathetic activation in postmenopausal hypertension. Animal Model for the Study of Postmenopausal HypertensionThe elucidation of mechanisms responsible for postmenopausal hypertension has been stunted by lack of an animal model. Sheep, rabbits, nonhuman primates, rats, and mice have been used as models of various menopausal changes; 6 however, to our knowledge, there is no animal model of naturally occurring postmenopausal hypertension. There have been attempts to mimic menopause by ovariectomizing animals; 7,8 however, these have rarely taken into account the effect of aging and cessation of ova...

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Role of ET_A receptors in experimental ANG II-induced hypertension in rats

Cited by 37 publications

References 21 publications

ETA Activation Mediates Angiotensin II-Induced Infiltration of Renal Cortical T Cells

ETA Activation Mediates Angiotensin II-Induced Infiltration of Renal Cortical T Cells

Endothelin-1 Increases Vascular Superoxide via Endothelin _A –NADPH Oxidase Pathway in Low-Renin Hypertension

Novel Mechanisms Responsible for Postmenopausal Hypertension

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Role of ETA receptors in experimental ANG II-induced hypertension in rats

Cited by 37 publications

References 21 publications

ETA Activation Mediates Angiotensin II-Induced Infiltration of Renal Cortical T Cells

ETA Activation Mediates Angiotensin II-Induced Infiltration of Renal Cortical T Cells

Endothelin-1 Increases Vascular Superoxide via Endothelin A –NADPH Oxidase Pathway in Low-Renin Hypertension

Novel Mechanisms Responsible for Postmenopausal Hypertension

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Role of ET_A receptors in experimental ANG II-induced hypertension in rats

Endothelin-1 Increases Vascular Superoxide via Endothelin _A –NADPH Oxidase Pathway in Low-Renin Hypertension