Abstract
By stably integrating the mouse Ren-2 renin gene into the rat genome, transgenic rats, e.g. TGR (mREN2)27 are obtained, which express the transgene in a tissue-specific manner and translate it to biologically active renin. The search for pathophysiological mechanisms initiating hypertension in TGR (mREN2) 27 rats focuses on the expression and function of renin in tissues involved in cardiovascular regulation. The major function of the renin-angiotensin system is the regulation of blood pressure, water and electrolyte balance. Its effector peptide, angiotensin II, is a strong vasopressor, which in addition stimulates the synthesis of several adrenal steroids particularly that of aldosterone, in the zona glomerulosa. TGR (mREN2) 27 rats developed hypertension-related alterations in various tissues. In the aorta, coronaries, and renal arteries, an increase of vascular wall thickness and perivascular fibrosis was observed. In the kidney of TGR (mREN2)27 rats, expression of the rat renin gene and that of the Ren-2 gene is high at the prenatal and neonatal stage.
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