A comparison of the development of renal hypertension in male and female rats

OKUNIEWSKI, Rachel; Davis, Elizabeth A.; JARROTT, Bevyn; WIDDOP, Robert E.

doi:10.1042/cs19970303

Cited by 16 publications

(14 citation statements)

References 23 publications

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“…Many studies have demonstrated that estrogen replacement therapy reduces the risk of cardiovascular disease in postmenopausal women (2). Animal studies also demonstrate gender differences in the development of cardiovascular diseases (3)(4)(5). Thus, circulating endogenous estrogen is proposed to protect against cardiovascular disease.…”

Section: Introductionmentioning

confidence: 99%

Estrogen and Enalapril attenuate the Development of Right Ventricular Hypertrophy induced by Monocrotaline in Ovariectomized Rats

et al. 2003

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INTRODUCTIONGender differences in the development of cardiovascular diseases have been documented in both human and animal studies. The rate of incidence of cardiovascular disease is lower in premenopausal women than in men, but increases sharply in postmenopausal women (1). Among the clinical consequences of postmenopausal estrogen deficiency, the deaths associated with cardiovascular diseases represent the largest concern in public health. Many studies have demonstrated that estrogen replacement therapy reduces the risk of cardiovascular disease in postmenopausal women (2). Animal studies also demonstrate gender differences in the development of cardiovascular diseases (3-5). Thus, circulating endogenous estrogen is proposed to protect against cardiovascular disease. However, mechanisms by which estrogen induces its protective effects are not fully understood.Various vasoactive substances and growth factors have been implicated in cardiac and vascular remodeling, as well as further degenerative transformation of these tissues (6). A critical role of the cardiac renin-angiotensin system (RAS), among others, has been recognized (7,8). Increased activity of the cardiac RAS has been confirmed both in humans (9) and animal models of cardiac failure (10, 11), whereas inhibition of the RAS decreased ventricular remodeling and improved cardiac function (12, 13).Cardiac hypertrophy is known to be one of the most critical risk factors of heart diseases. It has been demonstrated that monocrotaline (MCT) treatment produces pulmonary hypertension and right ventricular (RV) hypertrophy in male rats but not in female rats (4, 14). We previously found enhanced gene expressions of the cardiac RAS in the hypertrophied RV of male rats (15). The present study evaluated 1) the importance of the ovairan function and the RAS in the progression of the pulmonary hypertension, and 2) RV hypertrophy in MCT treated rats. We examined the cardiac expression of genes that contribute to the pathogenesis of cardiac hypertrophy, such as the RAS components, TGF-1, and endothelin-1 as well as histological changes in the lung and heart. Although this MCT rat model has no human equivalent, as a study design, we used a system of MCT-induced cardiopulmonary dysfunction to investigate possible beneficial effects of estrogen and inhibition of angiotensin converting enzyme. J Korean Med Sci 2003; 18: 641-8 ISSN 1011-8934 Copyright � The Korean Academy of Medical Sciences 641 Estrogen and Enalapril attenuate the Development of Right Ventricular Hypertrophy induced by Monocrotaline in Ovariectomized RatsThe present study evaluated the importance of ovarian functions and the reninangiotensin system in the progression of the right ventricular (RV) hypertrophy. Female Sprague-Dawley rats were bilaterally ovariectomized (Ovx) and injected with monocrotaline (MCT, 60 mg/kg, sc). Four weeks after MCT-treatment, only the male and Ovx female rats showed marked RV hypertrophy. The hypertrophied RV of the male-MCT and Ovx-MCT rats exhibited remarkably elevate...

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Section: Introductionmentioning

confidence: 99%

Estrogen and Enalapril attenuate the Development of Right Ventricular Hypertrophy induced by Monocrotaline in Ovariectomized Rats

et al. 2003

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“…In contrast some authors found no change in the weight of the clipped kidney, while they also found an increase in the contralateral kidney [14,15]. Sham-operated rats showed as expected no difference in kidney weight [16,17]. …”

Section: Discussionmentioning

confidence: 98%

Renin, endothelial no synthase and endothelin gene expression in the 2Kidney-1clip goldblatt model of long-term renovascular hypertension

Reinhold

Uihlein

et al. 2009

Eur J Med Res

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Objective Numerous reports have shown the influence of renin, nitric oxide (NO) and the endothelin (ET) systems for regulation of blood pressure and renal function. Furthermore, interactions between these peptides have been reported. Aim of our study was to investigate the relative contribution of these compounds in long-term renovascular hypertension/renal ischemia. Methods Hypertension/left-sided renal ischemia was induced using the 2K1C-Goldblatt rat model. Renal renin, ET-1, ET-3 and endothelial NO synthase (eNOS) gene expression was measured by means of RNAse protection assay at different timepoints up to 10 weeks after induction of renal artery stenosis. Results Plasma renin activity and renal renin gene expression in the left kidney were increased in the clipped animals while eNOS expression was unchanged. Furthermore, an increase in ET-1 expression and a decrease of ET-3 expression was detected in early stenosis. Conclusions While renin is obviously involved in regulation of blood pressure and renal function in unilateral renal artery stenosis, ET-1, ET-3 and endothelium derived NO do not appear to play an important role in renal adaptation processes in long-term renal artery stenosis, although ET-1 and ET-3 might be involved in short-term adaptation processes.

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“…To our knowledge, only 1 study using 2K1C hypertensive rats has analyzed estrous cyclicity and suggests a similar distribution of cycle stages between 2K1C hypertensive and normotensive female rats. 27 However, this assumption was based on the collection of the vaginal smears only at the completion of the study and based on the observation that all stages of the estrous cycle were represented at that point. Because of our daily checks of estrous cyclicity, we believe that the data presented here provide a more comprehensive look at estrous cycling in the 2K1C model.…”

Section: Hypertension and Estrous Cyclementioning

confidence: 99%