|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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).
This article has been cited by other articles:
![]() |
J. H. Lee, S. Xia, and L. Ragolia Upregulation of AT2 receptor and iNOS impairs angiotensin II-induced contraction without endothelium influence in young normotensive diabetic rats Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2008; 295(1): R144 - R154. [Abstract] [Full Text] [PDF] |
||||
![]() |
D.-F. Yeih, L.-Y. Lin, H.-I Yeh, Y.-J. Lai, F.-T. Chiang, C.-D. Tseng, S.-H. Chu, and Y.-Z. Tseng Temporal changes in cardiac force- and flow-generation capacity, loading conditions, and mechanical efficiency in streptozotocin-induced diabetic rats Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H867 - H874. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Matsumoto, T. Kobayashi, K. Wakabayashi, and K. Kamata Cilostazol improves endothelium-derived hyperpolarizing factor-type relaxation in mesenteric arteries from diabetic rats Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H1933 - H1940. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Kobayashi, K. Taguchi, T. Yasuhiro, T. Matsumoto, and K. Kamata Impairment of PI3-K/Akt Pathway Underlies Attenuated Endothelial Function in Aorta of Type 2 Diabetic Mouse Model Hypertension, December 1, 2004; 44(6): 956 - 962. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |