Effects of age and exercise on endothelium dependent dilation of the posterior communicating cerebral artery /
Age-related changes in the intrinsic function of cerebral vasculature may contribute to development of cerebrovascular disease with age. The purpose of this study was two-fold: 1) to examine mechanisms of responsiveness of the posterior cerebral communicating artery (PCoA) to acetylcholine (ACh) w...
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| Format: | Thesis Book |
| Language: | English |
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[Place of publication not identified] :
[publisher not identified] ;
2004.
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| Subjects: | |
| Online Access: | http://proxy.library.tamu.edu/login?url=http://proquest.umi.com/pqdweb?did=766020701&sid=1&Fmt=2&clientId=2945&RQT=309&VName=PQD |
| Summary: | Age-related changes in the intrinsic function of cerebral vasculature may contribute to development of cerebrovascular disease with age. The purpose of this study was two-fold: 1) to examine mechanisms of responsiveness of the posterior cerebral communicating artery (PCoA) to acetylcholine (ACh) with aging, and 2) to examine the effects of exercise training on the ACh responses of aged rats. We hypothesized that aging would decrease nitric oxide (NO) dependent dilation to ACh and that exercise training would increase ACh-induced dilation through an increase in endothelial nitric oxide synthase (eNOS) activity in PCoA. Responses to ACh in pressurized PCoAs were examined under control conditions and in the presence of 10[mu]m indomethacin (INDO), a cyclooxygenase (COX) inhibitor, 100[mu]M 1-(2-trifluoromethylphenyl) imidazole (TRIM), a neuronal nitric oxide synthase (nNOS) inhibitor, and TRIM + INDO, aminoguanidine (AG), an inducible NOS (iNOS) inhibitor, and AG + INDO. ACh-induced dilation was equivalent in PCoAs from aged rats (n=28) and young rats (n=21). The superoxide dismutase mimetic TIRON increased dilation in aged (n=9) rats (p=0.021), but had no effect in young rats (n=6). Neuronal NOS inhibition significantly decreased the ACh-induced dilation in both aged (n=11) and young (n=8) rats (p<0.05). Aminoguanidine inhibited the response to ACh in aged (n=8; p=0.03), but not young (n=10) rats. Indomethacin did not further increase inhibition by TRIM or AG. Non-specific NOS and COX co-inhibition eliminated the ACh-induced response in young and aged rat PCoA (p<0.05). Exercise training tended to increase sensitivity to ACh in aged (n=15) rats (p=0.11) and increased maximal ACh-induced dilation in young (n=17) rats (p=0.05). Following training, TRIM had no effect on the response to ACh (aged rats n=11; young n=9). In aged rats, training eliminated the inhibitory effect of AG (aged n=15)(young n=9). In both young and aged exercise trained groups, non-specific co-inhibition of NOS and COX eliminated the ACh-induced response of PCoA. In both aged and young rats, nNOS contributes to the ACh induced dilatory response. Aging increases the iNOS mediation of the response; exercise training results in a shift in NOS-mediated signaling, reducing the iNOS and nNOS contribution, implying enhancement of the eNOS mediated dilation. |
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| Item Description: | Vita. "Major Subject: Kinesiology". |
| Physical Description: | x, 75 leaves : illustrations ; 28 cm. Issued also on microfiche from University Microfilm Inc. |
| Bibliography: | Includes bibliographical references (leaves 65-74). |