Maeda Y, Terada Y, Nonoguchi H, Knepper M A
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892.
Am J Physiol. 1992 Aug;263(2 Pt 2):F319-27. doi: 10.1152/ajprenal.1992.263.2.F319.
The inner medullary collecting duct (IMCD) of the rat consists of two structurally and functionally distinct segments, i.e., the initial and the terminal IMCD. To identify factors that may regulate the transport function in the IMCD segments, we assessed whether catecholamines, carbachol, prostaglandin E2 (PGE2), bradykinin, glucagon, calcitonin, parathyroid hormone, or epidermal growth factor affects adenosine 3',5'-cyclic monophosphate (cAMP) production in microdissected tubules in the presence and absence of arginine vasopressin (AVP, 0.1 nM). All experiments were performed in the presence of 3-isobutyl-1-methylxanthine, and cAMP was measured by radioimmunoassay. Epinephrine (greater than or equal to 50 nM) and clonidine (greater than or equal to 1 microM) markedly decreased AVP-induced cAMP levels in both IMCD segments. However, phenylephrine did not show an effect. The inhibitory effect of epinephrine was blocked by yohimbine (50 nM) but not by prazosin (50 nM). In isolated perfused terminal IMCDs, epinephrine inhibited AVP-stimulated urea permeability. Isoproterenol (1 microM), in the absence of AVP, caused a significant increase in cAMP level only in the initial IMCD. Propranolol (1 microM) inhibited this isoproterenol effect, but atenolol did not. Dopamine (less than or equal to 1 microM) had no effect on cAMP levels in either IMCD segment. Carbachol, PGE2, and the various peptide hormones had no effect on cAMP levels (+/- AVP) in either IMCD segment. We conclude that an adrenergic beta 2-receptor is present only in the initial IMCD, where its occupation increases cAMP production. We conclude also that an adrenergic alpha 2-receptor is present in both IMCD segments, where its occupation inhibits AVP-induced cAMP production.(ABSTRACT TRUNCATED AT 250 WORDS)
大鼠的髓质内集合管(IMCD)由两个结构和功能不同的节段组成,即起始段和终末段IMCD。为了确定可能调节IMCD节段转运功能的因素,我们评估了儿茶酚胺、卡巴胆碱、前列腺素E2(PGE2)、缓激肽、胰高血糖素、降钙素、甲状旁腺激素或表皮生长因子在有无精氨酸加压素(AVP,0.1 nM)的情况下对显微解剖小管中3',5'-环磷酸腺苷(cAMP)生成的影响。所有实验均在3-异丁基-1-甲基黄嘌呤存在的情况下进行,cAMP通过放射免疫测定法进行测量。肾上腺素(≥50 nM)和可乐定(≥1 μM)显著降低了两个IMCD节段中AVP诱导的cAMP水平。然而,去氧肾上腺素未显示出作用。肾上腺素的抑制作用可被育亨宾(50 nM)阻断,但不能被哌唑嗪(50 nM)阻断。在分离灌流的终末IMCD中,肾上腺素抑制了AVP刺激的尿素通透性。在无AVP的情况下,异丙肾上腺素(1 μM)仅使起始段IMCD中的cAMP水平显著升高。普萘洛尔(1 μM)抑制了这种异丙肾上腺素的作用,但阿替洛尔没有。多巴胺(≤1 μM)对任一IMCD节段中的cAMP水平均无影响。卡巴胆碱、PGE2和各种肽类激素对任一IMCD节段中的cAMP水平(±AVP)均无影响。我们得出结论,肾上腺素能β2受体仅存在于起始段IMCD中,其激活可增加cAMP生成。我们还得出结论,肾上腺素能α2受体存在于两个IMCD节段中,其激活可抑制AVP诱导的cAMP生成。(摘要截短于250字)