Tissue-specific regulation of renin expression exists, with submandibular gland renin being androgen-dependent while renal renin is not.
Animal data on androgen effects should not inform human hypertension management; leaves open tissue-specific renin regulation mechanisms.
How local renin expression is regulated in many tissues has yet to be defined. In the present studies the ontogeny of renin in submandibular gland (SMG) and kidney of CD-1 mice was examined in order to determine whether renal and extrarenal renin are similarly expressed. In males, submandibular gland (SMG) renin and renin secretory rate increase at puberty as androgen rises. The ratio of secreted forms (1-chain renin cf. 2-chain) seen on Western blots shows predominance of 1-chain prior to puberty and 2-chain thereafter. This androgen influence on renin processing and secretion was supported by reversion to prepubertal patterns with castration of adult males and by conversion to male pattern in androgen treated females which otherwise have low renin levels. In contrast, renal renin remains unchanged throughout development. The influence of ontogeny on renal and SMG renin mRNA was examined by Northern analysis using renin cDNA: SMG renin mRNA increases from near zero to high levels at puberty while renal renin mRNA level is high throughout. Taken together, these data suggest that SMG renin is influenced by androgens, whereas renal renin is not. Apparent differences in tissue renin regulation may have important implications for local function of this enzyme.
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Ingelfinger et al. (1986) studied this question.
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