Martin J R, Quock R M
Life Sci. 1984 Aug 27;35(9):929-36. doi: 10.1016/0024-3205(84)90658-1.
The dopamine agonist apomorphine was more potent in eliciting hypothermia in spontaneously hypertensive rats (SHRs) than in normotensive Wistar rats (NWRs), while normotensive Wistar-Kyoto rats (WKYs) were intermediate in response. Various drug interventions were attempted in an effort to explain the greater sensitivity of SHRs to apomorphine. Haloperidol produced abolition of apomorphine-induced hypothermia in SHRs but at greater doses than required for antagonism of the drug effect in WKYs and NWRs. Chronic hydralazine treatment that reduced the high blood pressure of SHRs failed to appreciably influence the magnitude of apomorphine-induced hypothermia, compared to the response in control SHRs that received no hydralazine. These findings suggested to us that the enhanced hypothermic effect of apomorphine in SHRs was entirely dopamine receptor-mediated and that it was also independent of the high blood pressure. We also found that chronic lithium treatment that had no influence upon apomorphine-induced hypothermia in WKYs and NWRs significantly reduced the drug effect in SHRs. Based on this finding, we suggest that the greater hypothermic effect induced by apomorphine in SHRs might be due to a supersensitivity of hypothermia-mediating dopamine receptors in the hypertensive strain.
多巴胺激动剂阿扑吗啡在自发性高血压大鼠（SHR）中诱发体温过低的作用比在正常血压的Wistar大鼠（NWR）中更强，而正常血压的Wistar-Kyoto大鼠（WKY）的反应则介于两者之间。尝试了各种药物干预措施，以解释SHR对阿扑吗啡的更高敏感性。氟哌啶醇可消除SHR中阿扑吗啡诱导的体温过低，但所需剂量高于拮抗WKY和NWR中药物作用所需的剂量。与未接受肼屈嗪治疗的对照SHR相比，长期使用肼屈嗪治疗可降低SHR的高血压，但对阿扑吗啡诱导的体温过低程度没有明显影响。这些发现向我们表明，阿扑吗啡在SHR中增强的体温过低作用完全是由多巴胺受体介导的，并且也与高血压无关。我们还发现，长期锂治疗对WKY和NWR中阿扑吗啡诱导的体温过低没有影响，但可显著降低SHR中的药物作用。基于这一发现，我们认为阿扑吗啡在SHR中诱导的更强体温过低作用可能是由于高血压品系中体温调节多巴胺受体的超敏反应。
