Key result
In 45-kb human renin transgenic mice, sodium-deficient diet, ACE inhibition, and beta1-adrenergic stimulation significantly increased both human and mouse plasma renin concentrations.
The 45-kb hREN transgenic mouse model demonstrates appropriate physiological regulation of human renin synthesis and secretion, validating its use for studying the human renin-angiotensin system.
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Validates hREN transgenic mice for renin studies; leaves open clinical translation pending human data.
To create physiological models of the human renin-angiotensin system in transgenic animals, the component genes should be expressed in the correct tissues and cells and respond appropriately to physiological stimuli. We recently showed that mice carrying a 45-kb human renin genomic fragment, containing approximately 25 kb 5'-flanking DNA and 6 kb 3'-flanking DNA, express the transgene in a highly cell- and tissue-specific pattern. More importantly, in contrast to previous models, human renin in the circulating plasma of these mice is derived exclusively from the kidneys. In the present study, we tested the responses of both human and mouse renal renin expression and secretion of the 45-kb hREN transgenic mice to a variety of physiological and pharmacological stimuli. A sodium-deficient diet, angiotensin-converting enzyme inhibition, and beta1-adrenergic stimulation each increased both human and mouse plasma renin concentration significantly, whereas elevated blood pressure and/or increased plasma angiotensin II levels suppressed them. Human and mouse renal renin mRNA levels changed similarly but to a lesser degree. These studies demonstrate that human renin synthesis and secretion respond appropriately in 45-kb hREN mice to physiological stimuli. This most likely results from appropriate cell-specific expression of the transgene conferred by the extended transgene flanking sequences.
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Yan et al. (1998) studied this question. Physiological and pharmacological stimuli (sodium-deficient diet, ACE inhibition, beta1-adrenergic stimulation) was evaluated on Human and mouse plasma renin concentration and renal renin mRNA levels. In 45-kb human renin transgenic mice, sodium-deficient diet, ACE inhibition, and beta1-adrenergic stimulation significantly increased both human and mouse plasma renin concentrations.
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