2002 Fiscal Year Final Research Report Summary
The role of calcium ion in vasoreactivity in rat hypertensive pulmonary arteries during recovery from chronic hypoxia
| Project/Area Number |
13670062
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | Mie University |
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Principal Investigator |
MARUYAMA Junko Mie Univ., Medicine, Assistant Prof., 医学部, 講師 (50263017)
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| Co-Investigator(Kenkyū-buntansha) |
MARUYAMA Kazuo Mie Univ., Medicine, Professor, 医学部, 教授 (20181828)
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| Project Period (FY) |
2001 – 2002
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| Keywords | pulmonary hypertension / calcium / nifedipine / rat |
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| Research Abstract |
To study the changes of L type calcium channel-dependent relaxation in structurally remodeled pulmonary arteries with hypoxic pulmonary hypertension and their reversibility during recovery in room air, rats were exposed to hypobaric hypoxia (air at 380 mmHg) for 10 days and then allowed to recover in room air for 3 or 14 days. In isolated endothelium-intact normal extra-pulmonary arteries (EPAs) and intrapulmonary arteries (IPAs), precontracted with PGF_<2α>, nifedipine (L type calcium channel blocker, 10^<-10>-10^<-5> M) caused relaxation in a concentration-dependent manner. The relaxation was markedly augmented in higher concentration in both EPA and IPA rings from hypoxic rats compared with those of normoxic rats. The relaxation response to nifedipine was normalized completely after 3 days recovery in IPA and 14 days in EPA. To further examine the augmented relaxation, we tested response to nifedipine in endothelium-denuded PA rings. The relaxation to nifedipine was augmented in both hypertensive endothelium-denuded IPA and EPAs compared with those of pulmonary hypertensive aretries. There was no difference in recovery process between hypertensive endothelium-intact and -denuded PAs during recovery period. These results suggested that this augmented response was caused by functional alteration associated with L type calcium channel in vascular smooth muscle cells.
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