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2D-adrenoceptor and eNOS in aortae from early and later stages of diabetes in Goto-Kakizaki rats
1 Department of Physiology and Morphology, Institute of Medicinal Chemistry Hoshi University, Shinagawa-ku, Tokyo, Japan
* To whom correspondence should be addressed. E-mail: kamata{at}hoshi.ac.jp.
The aim of the present study was to compare vascular dysfunction between the early- (12-week old) and later- (36-week old) stages of spontaneous diabetes in Goto-Kakizaki (GK) rats. We also evaluated the aortic expressions of the 
2D-adrenoceptor and endothelial nitric oxide synthase (eNOS). Vascular reactivity was assessed in thoracic aortae from age-matched controls and 12- and 36-week GK rats. Using RT-PCR and immunoblots, we also examined the changes in the expressions of the 2D-adrenoceptor and eNOS. In aortae from GK rats (versus those from agematched controls): (a) the relaxation response to acetylcholine (ACh) was enhanced at 12-weeks, but decreased at 36-weeks, (b) the relaxation response to sodium nitroprusside was decreased at both 12- and 36-weeks, (c) norepinephrine (NE)-induced contractility was decreased at 12-weeks, but not at 36-weeks, (d) the
expressions of 1B- and 1D-adrenoceptors were unaffected, while those of the 2D-adrenoceptor and eNOS mRNAs were increased at both 12- and 36-weeks, (e) NE- and ACh-stimulated NOx- (nitrite and nitrate) levels were increased at 12-weeks, although at 36-weeks the ACh-stimulated NOx- was lower while the NE-stimulated NOx- showed no change. These results clearly demonstrate that (i) enhanced AChinduced relaxation and impaired NE-induced contraction, due to an NO overproduction via eNOS and increased 2D-adrenoceptor expression, occur in earlystage
GK rats and (ii) the impaired ACh-induced relaxation in later-stage GK rats is due to reductions in both NO production and NO responsiveness (but not in eNOS
expression).
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