Dde I restriction fragment length polymorphism of the α2-adrenoceptor gene does not correlate with blood pressure in the F2 generation obtained from crossing stroke-prone spontaneously hypertensive rats and Wistar—Kyoto rats


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Abstract

ObjectiveA pathogenetic role of altered α2-adrenoceptors in essential hypertension has been suggested, based on studies in humans and animals. To examine the role of the α2-adrenoceptor in genetically hypertensive rats, we compared the α2-adrenoceptor genes of stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats by restriction fragment length polymorphism analysis using human α2-adrenoceptor probes (α2-C10) and Dde I restriction endonuclease, and conducted a genetic cosegregation study.MethodFive 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 α2C10 as a probe and the DMA from the F2 generation.ResultsA 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 α2-adrenoceptor genotype.ConclusionThis study demonstrated that the α2-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.

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