Deth R C, Payne R A, Peecher D M
Section of Pharmacology, College of Pharmacy and Allied Health Professions, Northeastern University, Boston, Mass.
Blood Vessels. 1987;24(6):321-33. doi: 10.1159/000158709.
Furosemide-induced inhibition of 86Rb uptake was measured in rat and rabbit aorta and compared with its ability to inhibit contractions induced by alpha-adrenergic agonists. In both rat and rabbit tissues, furosemide defined a portion of 86Rb uptake (IC50 = 2.5 microM) which was distinct from the ouabain-sensitive fraction. Furosemide-sensitive 86Rb uptake was [Cl-]ext dependent and required Na+ and K+ for optimal activity, suggesting that it reflected a Na+-K+ cotransport process. Furosemide-sensitive 86Rb uptake was found to be greater in HEPES buffer than in bicarbonate buffer. Phenylephrine-induced contractions of rat and rabbit aorta were inhibited by furosemide; however, rat responses were far more sensitive. Agonist-induced uptake of 45Ca was reduced by furosemide in rat aorta, but not in rabbit aorta. Agonist-induced 45Ca efflux stimulation was reduced in both species. These findings indicate the presence in arteries of a furosemide-sensitive, Cl-dependent Na+-K+ cotransport process. Along with other monovalent transport processes, it may modulate Ca2+ availability and thereby influence arterial contractility.
在大鼠和兔主动脉中测量了呋塞米诱导的86Rb摄取抑制，并将其与抑制α-肾上腺素能激动剂诱导的收缩的能力进行比较。在大鼠和兔组织中，呋塞米界定了一部分86Rb摄取（IC50 = 2.5 microM），这部分摄取与哇巴因敏感部分不同。呋塞米敏感的86Rb摄取依赖于细胞外[Cl-]，且最佳活性需要Na+和K+，这表明它反映了一种Na+-K+共转运过程。发现呋塞米敏感的86Rb摄取在HEPES缓冲液中比在碳酸氢盐缓冲液中更大。呋塞米抑制了去氧肾上腺素诱导的大鼠和兔主动脉收缩；然而，大鼠的反应更为敏感。呋塞米降低了大鼠主动脉中激动剂诱导的45Ca摄取，但对兔主动脉没有影响。两种动物中激动剂诱导的45Ca外流刺激均降低。这些发现表明动脉中存在一种呋塞米敏感、Cl-依赖的Na+-K+共转运过程。与其他单价转运过程一起，它可能调节Ca2+的可用性，从而影响动脉收缩性。
