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 directed toward blood pressure homeostasis that occur in the endocrine branch of the renin-angiotensin system of mice having one angiotensinogen gene inactivated. No compensatory up-regulation of the remaining normal allele occurs in the liver, the main tissue of angiotensinogen synthesis. No significant changes occur in expression of the genes coding for the angiotensin converting enzyme or the major pressor-mediating receptor for angiotensin, but plasma renin concentration in the mice having only one copy of the angiotensinogen gene is greater than twice wild-type. This increase is mediated primarily by a modest increase in the proportion of renal glomeruli producing renin in their juxtaglomerular apparatus and by four times wild-type numbers of renin-producing cells along afferent arterioles of the glomeruli rather than by up-regulating renin production in cells already committed to its synthesis.
D000483:Alleles; D000808:Angiotensinogen / Q000235:genetics*; D000818:Animals; D001160:Arterioles / Q000378:metabolism; D002455:Cell Division; D006706:Homeostasis; D007668:Kidney / Q000166:cytology*; D007678:Kidney Glomerulus / Q000098:blood supply / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D016133:Polymerase Chain Reaction; D011945:Receptors, Angiotensin / Q000235:genetics; D012083:Renin / Q000096:biosynthesis*; D012084:Renin-Angiotensin System / Q000502:physiology*; D018631:ras Proteins / Q000378:metabolism