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哌唑嗪耐药、育亨宾敏感的α-肾上腺素能受体介导大鼠尾部离体血管床收缩的证据。

Evidence for prazosin-resistant, rauwolscine-sensitive alpha-adrenoceptors mediating contractions in the isolated vascular bed of the rat tail.

作者信息

Templeton A G, Macmillan J, McGrath J C, Storey N D, Wilson V G

机构信息

Institute of Physiology, University of Glasgow, Scotland.

出版信息

Br J Pharmacol. 1989 Jun;97(2):563-71. doi: 10.1111/j.1476-5381.1989.tb11986.x.

Abstract
  1. The postjunctional alpha-adrenoceptors mediating contractions in the isolated vascular bed of the perfused rat tail have been investigated, in the presence and absence of an increase in perfusion pressure by arginine vasopressin (AVP). 2. In the absence of AVP, bolus doses of noradrenaline (NA) and phenylephrine produced pressor responses of similar time course, while UK-14,304 was practically inactive. Responses to noradrenaline were inhibited more by 0.05 microM prazosin than by 1 microM rauwolscine, suggesting the presence of alpha1-adrenoceptors. 3. Following a sustained elevation in perfusion pressure by AVP, both UK-14,304 and NA (the latter in the presence of 0.05 microM prazosin to inhibit alpha 1-adrenoceptors) elicited dose-dependent pressor responses. The maximum response to UK-14,304 under these conditions was approximately 30% of the maximum response to NA in the absence of prazosin and AVP. Responses to phenylephrine were not affected by the AVP-induced increase in vascular tone. 4. In the presence of AVP, pressor responses to UK-14,304 were resistant to 0.05 microM prazosin and susceptible to antagonism by 1 microM rauwolscine (-log Kb 7.65 +/- 0.15). Similarly, responses to NA in the presence of 0.05 microM prazosin and AVP were inhibited by 1 microM rauwolscine. This represents the first demonstration of prazosin-resistant, rauwolscine-sensitive alpha 2-adrenoceptor-mediated responses in the vasculature of the rat tail. 5. These results suggest that in isolated vascular preparations, functional populations of postjunctional alpha 2-adrenoceptors may be 'uncovered' by the presence of AVP.
摘要
  1. 研究了在灌注大鼠尾部离体血管床中,介导收缩的接头后α-肾上腺素能受体,实验分别在有无精氨酸加压素(AVP)引起灌注压力升高的情况下进行。2. 在无AVP时,静脉推注去甲肾上腺素(NA)和去氧肾上腺素产生的升压反应时程相似,而UK-14,304实际上无活性。0.05μM哌唑嗪对去甲肾上腺素反应的抑制作用比对1μM萝芙木碱更强,提示存在α1-肾上腺素能受体。3. 在AVP使灌注压力持续升高后,UK-14,304和NA(后者在存在0.05μM哌唑嗪以抑制α1-肾上腺素能受体的情况下)均引起剂量依赖性升压反应。在这些条件下,UK-14,304的最大反应约为无哌唑嗪和AVP时NA最大反应的30%。去氧肾上腺素的反应不受AVP诱导的血管张力增加的影响。4. 在存在AVP时,对UK-14,304的升压反应对0.05μM哌唑嗪有抗性,而对1μM萝芙木碱的拮抗作用敏感(-log Kb 7.65±0.15)。同样,在存在0.05μM哌唑嗪和AVP时,对NA的反应也被1μM萝芙木碱抑制。这首次证明了在大鼠尾部血管系统中存在对哌唑嗪有抗性、对萝芙木碱敏感的α2-肾上腺素能受体介导的反应。5. 这些结果表明,在离体血管制备物中,接头后α2-肾上腺素能受体的功能群体可能会因AVP的存在而“暴露”出来。

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