1996 Fiscal Year Final Research Report Summary
Modification in the peripheral arteriole alpha-adrenoceptor subtype by congestive heart failure.
Project/Area Number |
07670822
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
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Research Institution | Hyogo College of Medicine |
Principal Investigator |
TATEISHI Jun Hyogo College of Medicine, Faculty of Medicine, Lecturer, 医学部, 講師 (60163490)
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Project Period (FY) |
1995 – 1996
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Keywords | congetive heart failure / alpha1-adrenoceptor / alpha2-adrenoceptor / L-type voltage dependent Ca^<2+> channel / ATP-sensitive K^+ channel / microcirculation |
Research Abstract |
The first aim of this study is to clarify the role of alpha1-and alpha2-adrenoceptor (AR) in the peripheral arteriole of rats with congestive heart failure (CHF). CHF was induced in WKY rats by left anterior coronary artery ligation. Sham-operated rats served as a control. An arteriole (phi100um) was dissected out from the cremaster and was inserted glass micropippettes from both ends, and was perfused by Krebs solution in tissue bath 4 weeks after operation. We evaluated responses in the arterioles from CHF rats to alpha1-agonists (phenylphrine : PE) and alpha2-agonists (UK-14,304 : UK), compared with those of a control. Concentration-response curves (CRC) to PE in CHF was shifted to the right compared with a control (EC_<50> ; CHF : 0.97uM,cont. : 0.30uM). Maximal contraction to PE was increased in CHF compared with a control (vs cont ; 142%). CRC to UK in CHF was shifted to the left compared with a control (EC_<50> ; CHF : 0.05uM,cont. : 0.26uM). Maximal contraction to UK was decreased in CHF compared with a control (vs cont. ; 76%). Our data shows that in CHF,maximal arteriole constriction of alpha1-AR increased but the affinity of alpha1-AR decreased, in contrast, maximal arteriole constriction of alpha2-AR decreased but the affinity of alpha2-AR increased. alpha1-and alpha2-AR may play the different roles in the regulation of the peripheral arteriolar responses in CHF.The second goal of this study is to test the mechanism of the alteration of alpha2 arteriole constriction in CHF.The CRCs of Bay K-8644, L-type voltage-dependent Ca^<2+> channel (VDCC) agonist, were tested CHF and control rats. There was no significant difference between two groups. This date suggest that alpha2 arteriole constriction was altered in CHF through mechanism that involve between alpha2-AR and VDCC.
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