title: Dde I restriction fragment length polymorphism of the alpha 2-adrenoceptor gene does not correlate with blood pressure in the F2 generation obtained from crossing stroke-prone spontaneously hypertensive rats and Wistar-Kyoto rats.
abstract: OBJECTIVE
  A pathogenetic role of altered alpha 2-adrenoceptors in essential hypertension has been suggested, based on studies in humans and animals. To examine the role of the alpha 2-adrenoceptor in genetically hypertensive rats, we compared the alpha 2-adrenoceptor genes of stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats by restriction fragment length polymorphism analysis using human alpha 2-adrenoceptor probes (alpha 2-C10) and Dde I restriction endonuclease, and conducted a genetic cosegregation study.
  
  
  METHODS
  Five female WKY rats were bred with five male SHRSP. Eight pairs of F1 rats were mated in brother-sister pairs to yield an F2 population of 84 rats. Systolic blood pressure was determined by tail-cuff sphygmomanometry. Direct arterial blood pressure was taken under ether anaesthesia just before the rats were killed. Southern blots were performed using alpha 2C10 as a probe and the DNA from the F2 generation.
  
  
  RESULTS
  A restriction fragment length polymorphism of the SHRSP allele of a 1.6-kb fragment and a WKY rat allele of a 0.9-kb fragment with a common band of 1.3 kb in SHRSP and WKY rats was found, as reported previously. The distribution of the genotype based on restriction fragment length polymorphism conformed to a 1:2:1 ratio in F2 rats, as expected for a Mendelian trait. There was no significant difference in the blood pressure of F2 rats with respect to alpha 2-adrenoceptor genotype.
  
  
  CONCLUSIONS
  This study demonstrated that the alpha 2-adrenoceptor gene restriction fragment length polymorphism distribution is a Mendelian trait in the F2 rats of crossed SHRSP and WKY rats, but failed to show genetic cosegregation of this restriction fragment length polymorphism with blood pressure in this generation.
authors.affiliation: Second Department of Internal Medicine, Yokohama City University, School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Kobayashi
authors.forename: S
authors.initials: S
authors.lastname: Umemura
authors.forename: N
authors.initials: N
authors.lastname: Hirawa
authors.forename: T
authors.initials: T
authors.lastname: Iwamoto
authors.forename: S
authors.initials: S
authors.lastname: Yamaguchi
authors.forename: K
authors.initials: K
authors.lastname: Tamura
authors.forename: I
authors.initials: I
authors.lastname: Takasaki
authors.forename: M
authors.initials: M
authors.lastname: Ishii
mesh_terms: D000483:Alleles; D000818:Animals; D001794:Blood Pressure / Q000235:genetics* / Q000502:physiology; D002561:Cerebrovascular Disorders / Q000235:genetics; D003433:Crosses, Genetic; D004247:DNA / Q000235:genetics; D015252:Deoxyribonucleases, Type II Site-Specific; D005260:Female; D006973:Hypertension / Q000235:genetics* / Q000503:physiopathology; D008297:Male; D012150:Polymorphism, Restriction Fragment Length; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D018341:Receptors, Adrenergic, alpha-2 / Q000235:genetics* / Q000502:physiology
chemical_list: D018341:Receptors, Adrenergic, alpha-2; D004247:DNA; C027908:endodeoxyribonuclease DdeI; D015252:Deoxyribonucleases, Type II Site-Specific