Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The spontaneously hypertensive rat (SHR) has a Y chromosome locus that increases blood pressure. This locus requires an androgen receptor and testosterone for maximum expression. Steroid sulfatase (STS) catalyzes the conversion of steroid sulfates to their active nonconjugated form. In some mammals the steroid sulfatase locus (Sts) is on the Y chromosome, although the rat Sts is on the X chromosome. We measured STS activity levels in SHR and normotensive Wistar Kyoto (WKY) males. SHR had significantly higher STS activity in testes, adrenal gland, liver, and hypothalamus. The Km values for STS in the two strains were not significantly different; thus, activity differences were likely due to differences in enzyme amounts. STS activity was measured in the backcross strains SHR/y and SHR/a to test and/or confirm a Y chromosome influence on STS. STS activity levels in these strains were intermediate between those of SHR and WKY. Because the blood pressures of SHR/y and SHR/a were also intermediate between SHR and WKY, the STS activity could be a secondary response to the hypertension. An alternative hypotheses is that a regulatory locus in addition to the structural locus is responsible for STS activity levels, and this regulatory locus is on the rat Y chromosome. Further study is needed to discriminate between these possibilities, and until the second hypothesis can be eliminated, the Sts locus or its modifier loci remain a potential component of the Y chromosome hypertensive locus.
Steroids 1995 Oct
PMID:Steroid sulfatase and the Y chromosome hypertensive locus of the spontaneously hypertensive rat. 853 76

The following review examines the role of the SHR Y chromosome and specifically the Sry gene complex in hypertension and potential mechanisms that involve the sympathetic nervous system and renin-angiotensin system. There are consistent gender differences in hypertension, with a greater proportion of males affected than females in most mammalian populations. Our earlier studies demonstrated that a portion of the gender differences in blood pressure (BP) in the SHR rat mapped to the SHR Y chromosome. In rats, males with the SHR Y chromosome have higher BP than females, or males with a different Y chromosome. Consistent with these results, several human population studies have confirmed a Y chromosome effect on BP. Our more recent studies focus on a transcription factor, Sry, as the locus involved in not only BP modulation but effects on other phenotypes. The Sry locus is an evolutionarily conserved locus on the mammalian Y chromosome responsible for testis determination and is a transcription factor. The Sry locus contains a highly conserved High Mobility Group (HMG) box region responsible for DNA binding. Mutations in the HMG box result in sex reversal. We have found multiple functional copies of Sry in SHR and WKY male rats. There is abundant evidence that testes determination may not be Sry's only function as it is expressed in the brain, kidney and adrenal gland of adult males. These findings have potential implications for gender physiology research which involves, the sympathetic nervous system, renin-angiotensin system, androgen receptor regulation and prostate physiology.
Steroids 2010 Nov
PMID:Review of the Y chromosome, Sry and hypertension. 1991 67