Peysner K, Forsling M L
Department of Gynaecology, UMDS, St. Thomas' Campus, London, U.K.
J Physiol Pharmacol. 1991 Sep;42(3):317-26.
Conscious rats were given i. p. polyethylene glycol (PEG) or dextran injections to compare their efficacy in inducing moderate hypovolaemia. Dextran was found unsuitable, producing large variability in the plasma vasopressin (AVP) concentrations. Putative neurotransmitters involved in the AVP response to hypovolaemia and in basal release were examined using opioid, and beta-adrenoceptor and dopamine receptor-blocking agents. A dose of PEG was chosen to produce a decrease in blood volume of approx 14.5% giving plasma AVP concentrations of 19.0 +/- 4.6 pmol/l. Naloxone and phenoxybenzamine failed to influence AVP release under both hypovolaemic and basal conditions. Prazosin also failed to influence the AVP response. In contrast propranolol elevated the plasma AVP concentrations in both conditions. Haloperidol enhanced basal AVP release but did not influence release during hypovolaemia. Guanethidine pretreatment partially blocked the response to hypovolaemia, but did not affect basal plasma AVP. Thus it appears that aminergic pathways have an inhibitory influence on AVP release under hypovolaemic and basal conditions. However, endogenous opioids do not appear to contribute significantly to the hypovolaemic response.
给清醒大鼠腹腔注射聚乙二醇（PEG）或右旋糖酐，以比较它们诱导中度血容量不足的效果。发现右旋糖酐不合适，它会使血浆血管加压素（AVP）浓度产生很大差异。使用阿片类药物、β-肾上腺素能受体阻滞剂和多巴胺受体阻滞剂，研究了参与AVP对血容量不足反应和基础释放的假定神经递质。选择一定剂量的PEG以使血容量减少约14.5%，血浆AVP浓度为19.0±4.6 pmol/l。纳洛酮和苯氧苄胺在血容量不足和基础条件下均未能影响AVP释放。哌唑嗪也未能影响AVP反应。相比之下，普萘洛尔在两种情况下均提高了血浆AVP浓度。氟哌啶醇增强了基础AVP释放，但在血容量不足时不影响释放。胍乙啶预处理部分阻断了对血容量不足的反应，但不影响基础血浆AVP。因此，似乎胺能途径在血容量不足和基础条件下对AVP释放具有抑制作用。然而，内源性阿片类物质似乎对血容量不足反应的贡献不大。
