title: Insulin receptor exon 11+/- isoform mRNA in spontaneously hypertensive and adrenocorticotropin-hypertensive rats.
abstract: OBJECTIVE
  To test the hypothesis that insulin resistance of the spontaneously hypertensive rat (SHR) and adrenocorticotropin-hypertensive rat is related to a difference in the proportion of the functionally different, alternatively spliced exon 11 isoforms of the insulin receptor.
  
  
  METHODS
  We determined the proportions of mRNA for the exon 11+ and exon 11- isoforms in various tissues of SHR and Wistar-Kyoto rats aged 3, 6, 9 and 12 weeks, which span the pre-hypertensive phase through to established hypertension, as well as in Sprague-Dawley rats with adrenocorticotropin-induced hypertension and Sprague-Dawley controls.
  
  
  METHODS
  Detection of mRNA involved a reverse-transcriptase polymerase chain reaction technique specific for each isoform and quantification was by slot and dot blot hybridization.
  
  
  RESULTS
  Mean proportions of exon 11+ mRNA in SHR, Wistar-Kyoto rats, adrenocorticotropin-hypertensive rats and Sprague-Dawley control rats at each age were 95% for liver, 82% for adipose tissue, 77% for kidney, 66% for adrenal, 53% for heart, 26% for cerebral cortex, 23% for hypothalamus, and 3% for skeletal muscle. There was also no difference in concentration of total insulin receptor mRNA.
  
  
  CONCLUSIONS
  The absence of any difference in proportions of insulin receptor mRNA isoforms argues against the hypothesis that an alteration of differential splicing plays a role in the models of hypertension studied.
authors.affiliation: Department of Physiology and Institute for Biomedical Research, The University of Sydney, New South Wales, Australia.
authors.forename: Y
authors.initials: Y
authors.lastname: Lou
authors.forename: R Y
authors.initials: RY
authors.lastname: Zee
authors.forename: M
authors.initials: M
authors.lastname: Li
authors.forename: B J
authors.initials: BJ
authors.lastname: Morris
mesh_terms: D000324:Adrenocorticotropic Hormone; D017398:Alternative Splicing; D000818:Animals; D001483:Base Sequence; D018076:DNA, Complementary / Q000235:genetics; D005091:Exons; D006973:Hypertension / Q000139:chemically induced / Q000235:genetics* / Q000378:metabolism*; D007333:Insulin Resistance / Q000235:genetics; D008297:Male; D012333:RNA, Messenger / Q000235:genetics* / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D011972:Receptor, Insulin / Q000235:genetics*
chemical_list: D018076:DNA, Complementary; D012333:RNA, Messenger; D000324:Adrenocorticotropic Hormone; D011972:Receptor, Insulin