| Summary: | 碩士 === 國立成功大學 === 生理學研究所 === 85 === Previous studies have demonstrated that vascular responses
to receptor-mediated endothelium-dependent vasodilators are
enhanced in exercise-trained animals. The enhanced endothelium-
dependent relaxation in response to acetylcholine(ACh) appears
to be mediated through an elevation of endothelium-derived
relaxing factor(EDRF)release. In order to characterize the
subtype of muscarinic(M) receptor responsible for the
endothelium-dependent relaxation to ACh and to examine whather
the upregulation of M receptors occurs after exercise training,
the thoracic aortae ofmale Wistar rats were used in this study.
These animals were randomly divided into exercise-trained and
control groups. The trained rats ran on a treadmill with a
moderate intensity for 60 min per day, 5 days per week, 10 weeks
in total. During the training period, resting heart rates and
systolic blood pressure of these animals were determined by a
tail-cuff method to confirm training effects.After 10 weeks of
training, rings of the thoracic aorta were isolated. The
subclass of M receptor on endothelium responsible for ACh-
induced vasorelaxation were pharmacologically identified on the
basis of selective affinity of antagonists,such as pirenzepine
(for M1), gallamine (for M2), and 4-diphenylacetoxy-N-methyl-
piperidine methiodide (4-DAMP, for M3). Whether upregulation of
M receptor occurs after training was studied by the radioligand
binding assay. Our results showed that after exercise training:
(1) the heart rates and systolic blood pressure were lowered;
(2) the sensitivity of thoracic aortae in response to ACh was
increased;(3) ACh-induced vasorelaxation of the thoracic aortae
was mainly mediated by M3 receptor; (4) the major relaxing
factor released from the endothelium of the rat thoracic aorta
upon ACh stimulation was endothelium-derived nitric oxide
(EDNO);(5) the Bmax value of M3 receptor was not changed; (6)
the Kd value of M3 receptor was not changed. Our data suggest
that chronic exercise in rats can enhance ACh-stimulated EDNO
release via M3 receptor on endothelial cells. However, M3
receptorwas not upregulation after exercise training. Other
possible mechanisms, such as the alteration of signal
transduction system, need to be further studied.
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