Genetic and endocrine control of renin activity in the submaxillary gland of the mouse.
Alleles, Animal, Castration, Chromosome-Mapping, Comparative-Study, Crosses-Genetic, Enzyme-Induction, Female, Hypophysectomy, Male, Mice, Mice-Inbred-Strains, Renin: ge, me, Species-Specificity, Stanolone, Submandibular-Gland: en, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S
Biochem-Genet. 1981 Jun; 19(5-6):509-23.
GM26414, AM03892, NO1CP33255
Basal activity of submaxillary gland (SMG) renin is high in female mice that carry the Rnrs allele and is induced to higher levels by treatment with dihydrotestosterone (DHT). To determine whether the difference in basal activity between high (Rnrs/Rnrs) and low (Rnrb/Rnrb) strains is due to enhanced sensitivity of Rnrs/Rnrs strains to endogenous androgen, we first studied the effect of several types of endocrine ablation on SMG renin in young female mice, and second, we removed normal androgen receptor protein by introducing the X-linked Tfm gene. Adrenalectomy with or without castration had no effect on basal SMG renin; hypophysectomy decreased basal renin activity 400-fold but did not abolish responsiveness to DHT. Loss of androgen receptor did not affect basal renin activity but did prevent enhancement by DHT. Basal and induced renin activities in L.AKR(Alll)/Cy, a congenic strain homozygous for Rnrs introduced from AKR/J into the background of C57L/J, an Rnrb/Rnrb type strain, are intermediate between levels observed in the original strains. We conclude that (1) the basal level of SMG renin is regulated directly or indirectly by some pituitary hormone(s) but not by androgen, (2) androgen induction of renin activity requires a normal androgen receptor, and (3) major gene(s) that regulate basal as well as induced SMG renin are in a circumscribed region of chromosome 1.
Wilson, C M.; Cherry, M; Taylor, B A.; and Wilson, J D., " Genetic and endocrine control of renin activity in the submaxillary gland of the mouse." (1981). Faculty Research 1980 - 1989. 131.
Please contact the Joan Staats Library for information regarding this document.