Homeostasis in mice with genetically decreased angiotensinogen is primarily by an increased number of renin-producing cells

Here we investigate the biochemical, molecular, and cellular changes direct ed toward blood pressure homeostasis that occur in the endocrine branch of the renin-angiotensin system of mice having one angiotensinogen gene inacti vated. No compensatory up-regulation of the remaining normal allele occurs in tbe liver, the main tissue of angiotensinogen synthesis. No significant changes occur in expression of the genes coding for the angiotensin convert ing enzyme or the major pressor-mediating receptor for angiotensin, but pla sma renin concentration in the mice having only one copy of the angiotensin ogen gene is greater than twice wild-type, This increase is mediated primar ily by a modest increase in the proportion of renal glomeruli producing ren in in their juxtaglomerular apparatus and by four times wild-type numbers o f renin-producing cells along afferent arterioles of the glomeruli rather t han by upregulating renin production in cells already committed to its synt hesis.