Hoffmann P, Delle M, Thorén P
Department of Physiology, University of Gothenburg, Sweden.
Acta Physiol Scand. 1990 Oct;140(2):191-8. doi: 10.1111/j.1748-1716.1990.tb08991.x.
In a previous study, electrically induced contractions of the gastrocnemius muscle in conscious spontaneously hypertensive rats were shown to induce a blood pressure reduction of 15-20 mmHg lasting several hours. We showed in that study that endogenous opioid systems were involved. In this study, drugs with selective affinity for different opioid receptors were used to analyse further the involvement of endogenous opioid systems in the post-stimulatory drop in blood pressure in spontaneously hypertensive rats. Prestimulatory intracerebroventricular administration of beta-FNA (a mu-receptor antagonist) did not significantly influence the response at all, nor did a lower intravenous dose of naloxone reverse the post-stimulatory drop in blood pressure. High-dose naloxone (15 mg kg-1) increased post-stimulatory blood pressure by around 10 mmHg. About 50% of the drop thus remained after this treatment. A similar, partial reversal of the decreased blood pressure was seen after intravenous administration of a delta-receptor antagonist, ICI 154,129. However, the depressor response was completely reversed by a low intravenous dose of MR 2266 BS (a kappa-receptor antagonist). These results suggest that the reduction in blood pressure after muscle stimulation is mainly mediated by the opioid kappa-receptor. A certain involvement of the delta-receptor is also indicated.
在先前的一项研究中，已表明有意识的自发性高血压大鼠的腓肠肌电诱发收缩会使血压降低15 - 20 mmHg，并持续数小时。我们在该研究中表明内源性阿片系统参与其中。在本研究中，使用对不同阿片受体具有选择性亲和力的药物，进一步分析内源性阿片系统在自发性高血压大鼠刺激后血压下降中的作用。刺激前脑室内注射β - FNA（一种μ受体拮抗剂）根本没有显著影响该反应，较低静脉剂量的纳洛酮也没有逆转刺激后血压的下降。高剂量纳洛酮（15 mg·kg⁻¹）使刺激后血压升高约10 mmHg。经过这种处理后，约50%的血压下降仍然存在。静脉注射δ受体拮抗剂ICI 154,129后，也观察到了类似的血压下降部分逆转情况。然而，低静脉剂量的MR 2266 BS（一种κ受体拮抗剂）完全逆转了降压反应。这些结果表明，肌肉刺激后血压的降低主要由阿片κ受体介导。也表明了δ受体有一定参与。
