Gonadal steroid regulation of renal injury in renal wrap hypertension

Ji, Hong; Menini, Stefano; Mok, Koby; Zheng, Wei; Pesce, Carlo; Kim, James; Mulroney, Susan E.; Sandberg, Kathryn

doi:10.1152/ajprenal.00032.2004

Cited by 61 publications

(51 citation statements)

References 23 publications

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“…Previous studies utilizing the ovariectomy model of menopause have demonstrated the dramatic impact that the loss of estrogen has on the development of hypertension in several rodent models, e.g., ANG II, renal wrap, and high-salt diet (13,24,39). In the present study, we demonstrate that during the transition from perimenopause into menopause the hypertensive response to ANG II infusion is augmented in female mice.…”

Section: Discussionsupporting

confidence: 67%

ANG II-induced hypertension in the VCD mouse model of menopause is prevented by estrogen replacement during perimenopause

Pollow

Romero-Aleshire

Sánchez

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Pollow DP, Romero-Aleshire MJ, Sanchez JN, Konhilas JP, Brooks HL. ANG II-induced hypertension in the VCD mouse model of menopause is prevented by estrogen replacement during perimenopause. Am J Physiol Regul Integr Comp Physiol 309: R1546 -R1552, 2015. First published October 21, 2015 doi:10.1152/ajpregu.00170.2015.-Premenopausal females are resistant to the development of hypertension, and this protection is lost after the onset of menopause, resulting in a sharp increase in disease onset and severity. However, it is unknown how a fluctuating ovarian hormone environment during the transition from perimenopause to menopause impacts the onset of hypertension, and whether interventions during perimenopause prevent disease onset after menopause. A gradual transition to menopause was induced by repeated daily injections of 4-vinylcyclohexene diepoxide (VCD). ANG II (800 ng·kg Ϫ1 ·min Ϫ1 ) was infused into perimenopausal and menopausal female mice for 14 days. A separate cohort of mice received 17␤-estradiol replacement during perimenopause. ANG II infusion produced significantly higher mean arterial pressure (MAP) in menopausal vs. cycling females, and 17␤-estradiol replacement prevented this increase. In contrast, MAP was not significantly different when ANG II was infused into perimenopausal and cycling females, suggesting that female resistance to ANG II-induced hypertension is intact during perimenopause. ANG II infusion caused a significant glomerular hypertrophy, and hypertrophy was not impacted by hormonal status. Expression levels of aquaporin-2 (AQP2), a collecting duct protein, have been suggested to reflect blood pressure. AQP2 protein expression was significantly downregulated in the renal cortex of the ANG II-infused menopause group, where blood pressure was increased. AQP2 expression levels were restored to control levels with 17␤-estradiol replacement. This study indicates that the changing hormonal environment in the VCD model of menopause impacts the severity of ANG II-induced hypertension. These data highlight the utility of the ovary-intact VCD model of menopause as a clinically relevant model to investigate the physiological mechanisms of hypertension that occur in women during the transition into menopause.aquaporin-2; glomerular hypertrophy; collecting duct; estrogen PREMENOPAUSAL FEMALES are resistant to the development of hypertension, and this protection is lost after the onset of menopause, resulting in a sharp increase in disease incidence and severity (20). Similarly, resistance to ANG II-induced hypertension has been demonstrated in female rodents. Ovariectomy (the abrupt induction of menopause via the removal of gonads) removes this resistance to ANG II, resulting in a robust ANG II-induced hypertensive response (39). Pharmacological inhibition or genetic ablation of estrogen receptors also increases the hypertensive response to ANG II infusion, suggesting that the loss of 17␤-estradiol signaling during menopause is in part responsible for the shift in blood pressure regulation (40).R...

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Section: Discussionsupporting

confidence: 67%

ANG II-induced hypertension in the VCD mouse model of menopause is prevented by estrogen replacement during perimenopause

Pollow

Romero-Aleshire

Sánchez

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This group has not determined whether there are sex differences in oxidative stress in their model, however. In contrast, Ji and colleagues (30) reported that, in rats with "renal wrap hypertension" and high-salt diet, there was no difference in blood pressure between males and females. Despite the lack of a difference in blood pressure in this latter study, the males exhibited higher levels of oxidative stress, as determined by measuring urinary malondialdehyde, renal cortical NADPH oxidase activity, and expression of NADPH oxidase subunit p22 phox .…”

Section: Oxidative Stress In Other Animal Models Of Hypertensionmentioning

confidence: 89%

Sex differences in control of blood pressure: role of oxidative stress in hypertension in females

Lopez‐Ruiz¹,

Sartori‐Valinotti²,

Yanes³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Lopez-Ruiz A, Sartori-Valinotti J, Yanes LL, Iliescu R, Reckelhoff JF. Sex differences in control of blood pressure: role of oxidative stress in hypertension in females. Am J Physiol Heart Circ Physiol 295: H466 -H474, 2008. First published June 20, 2007 doi:10.1152/ajpheart.01232.2007.-In general, blood pressure is higher in normotensive men than in age-matched women, and the prevalence of hypertension in men is also higher until after menopause, when the prevalence of hypertension increases for women. It is likely then that the mechanisms by which blood pressure increases in men and women with aging may be different. Although clinical trials to reduce blood pressure with antioxidants have typically not been successful in human cohorts, studies in male rats suggest that oxidative stress plays an important role in mediating hypertension. The exact mechanisms by which oxidative stress increases blood pressure have not been completely elucidated. There may be several reasons for the discrepancies between clinical and animal studies. In this review, the data obtained in selected clinical and animal studies are discussed, and the hypothesis is put forward that oxidative stress may not be as important in mediating hypertension in females as has been shown previously in male rats. Furthermore, it is likely that differences in genetics, age, length of time with hypertension, endothelial dysfunction, and sex are all factored in to modulate the responses to antioxidants in humans. As such, future clinical trials should be designed and powered to evaluate the effects of oxidative stress on blood pressure separately in men and women.F 2-isoprostanes WITH THE USE OF AMBULATORY blood pressure monitoring, it is now well accepted that blood pressure is higher in men than age-matched premenopausal women, and that, following menopause, this trend reverses, such that the incidence of hypertension in postmenopausal women is similar to or higher than in men (5, 69). A comparison of the data from the National Health and Nutrition Examination Survey (NHANES) III (1988III ( -1994 with data from NHANES IV (1999 -2002) revealed that the prevalence of hypertension is currently stable in men, and their blood pressures are well controlled with medication. In contrast, in women, the incidence of hypertension is progressively increasing, and blood pressure is often higher in women than in age-matched men (35). Furthermore, blood pressure in women is not well controlled with medication, despite typically higher levels of compliance compared with men (35). These disturbing statistics suggest that mechanisms responsible for hypertension in men and women may be different, and it is imperative that physicians and scientists begin to determine what these differences are to better treat hypertension in both men and women. Oxidative Stress and Hypertension in Humans: Clinical TrialsThe role that oxidative stress plays in mediating hypertension has been the focus of a significant amount of research in recent years. Several clinical trials have be...

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“…Sexual dimorphism in response to renal disease has been noted for many years. There are gender differences in many renal disease models, including age-related glomerular injury (Baylis 1994), hypertension (Ji et al 2005), polycystic kidney disease (Stringer et al 2005) and diabetic nephropathy (Tomiyoshi et al 2002). In recent years experimental science is now producing tantalizing clues that gender differences also play a role in the kidney's response to ischemia.…”

mentioning

confidence: 99%

Gender Differences in the Susceptibility to Renal Ischemia-Reperfusion Injury in BALB/c Mice

Wang

Batteux

et al. 2009

Tohoku J. Exp. Med.

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Gonadal steroid regulation of renal injury in renal wrap hypertension

Cited by 61 publications

References 23 publications

ANG II-induced hypertension in the VCD mouse model of menopause is prevented by estrogen replacement during perimenopause

ANG II-induced hypertension in the VCD mouse model of menopause is prevented by estrogen replacement during perimenopause

Sex differences in control of blood pressure: role of oxidative stress in hypertension in females

Gender Differences in the Susceptibility to Renal Ischemia-Reperfusion Injury in BALB/c Mice

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