Mediators of contraction-evoked skeletal muscle depressor response in anesthetized rats.
Mediators of contraction-evoked skeletal muscle depressor response in anesthetized rats.
复制标题
麻醉大鼠收缩诱发骨骼肌抑制反应的介质。
DOI：
10.1152/jappl.1996.81.2.578
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Mifflin,SW
中科院分区：
文献类型：
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作者：
Toney,GM;Mifflin,SW
在本研究中，肌肉收缩诱发的心血管反应的介质进行了检查在麻醉大鼠。通过使用1 s on-1 s off模式刺激胫神经（运动阈值22.7 +/- 2.3 microA; n = 10）产生后肢小腿三头肌的节律性收缩。在1）毒蕈碱受体阻断剂（硫酸阿托品; 2.0mg/kg静脉注射，n = 5）; 2）用N ω-硝基-L-精氨酸甲酯（L-NAME; 300 μ M/kg静脉注射，n = 7）; 3）β-肾上腺素受体阻断（普萘洛尔; 2.0mg/kg静脉注射，双侧肾上腺切除术4例。节律刺激（10-s）显著降低MAP（P < 0.05），并引起HR小幅下降，但可被神经肌肉阻滞（n = 4）消除。阿托品对MAP或HR收缩反应无影响。L-NAME增加基线MAP（112.2 +/- 2.2至137.1 +/- 4.6 mmHg，P < 0.05）和减弱收缩诱发的MAP降低用苯肾上腺素升高MAP，可使4只大鼠出现L-NAME诱导的反应性障碍（P < 0.05（7-10微克·kg-1·h-1 iv）至与L-NAME产生的水平无差异。双侧肾上腺切除术和普萘洛尔对HR反应没有显著影响，但收缩诱发的MAP下降分别从14.3 +/- 2.9降至7.7 +/- 2.2 mmHg和从13.4 +/- 1.3降至6.3 +/- 3.1 mmHg（P < 0.05）。基线MAP无变化。我们的结论是，肾上腺儿茶酚胺，作用于β-肾上腺素受体，有助于显着的收缩引起的降压反应在大鼠。毒蕈碱受体在这种反应中没有明显作用。此外，一氧化氮抑制后收缩的降压反应减弱可能是由于L-NAME的升压作用的间接作用。
In the present study, mediators of muscle contraction-evoked cardiovascular responses were examined in anesthetized rats. Rhythmic contractions of the hindlimb triceps surae muscle were produced by stimulating the tibial nerve (motor threshold 22.7 +/- 2.3 microA; n = 10) by using a 1 s on-1 s off pattern. Mean arterial pressure (MAP) and heart rate (HR) responses were recorded before and after 1) muscarinic receptor blockade (atropine sulfate; 2.0 mg/kg i.v., n = 5); 2) nitric oxide synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME; 300 microM/kg i.v., n = 7); 3) beta-adrenoceptor blockade (propranolol; 2.0 mg/kg i.v., n = 10); and 4) bilateral adrenalectomy (n = 4). Rhythmic stimulation (10-s) significantly reduced MAP (P < 0.05) and elicited small decreases in HR that were abolished by neuromuscular blockade (n = 4). Atropine had no effect on MAP or HR responses to contraction. L-NAME increased baseline MAP (112.2 +/- 2.2 to 137.1 +/- 4.6 mmHg, P < 0.05) and attenuated contraction-evoked reductions of MAP (P < 0.05) without affecting HR. L-NAME-induced response deficits were mimicked in four separate rats by elevating MAP with phenylephrine (7–10 micrograms.kg-1.h-1 iv) to a level not different from that produced by L-NAME. Bilateral adrenalectomy and propranolol did not significantly affect HR responses but reduced contraction-evoked decreases in MAP from 14.3 +/- 2.9 to 7.7 +/- 2.2 mmHg and from 13.4 +/- 1.3 to 6.3 +/- 3.1 mmHg, respectively (P < 0.05). Baseline MAP was unchanged. We conclude that adrenal catecholamines, acting at beta-adrenoceptors, contribute significantly to the contraction-evoked depressor response in rats. No role for muscarinic receptors is evident in this response. Furthermore, attenuation of depressor responses to contraction after nitric oxide inhibition could result from an indirect effect of the pressor actions of L-NAME.