Cyclosporine promotes glomerular endothelin binding in Vivo

Midori Awazu, Masanori Sugiura, Tadashi Inagami, Lekuni Ichikawa, Valentina Kon

研究成果: Article査読

29 被引用数 (Scopus)

抄録

It has previously been shown that administration of cyclosporine causes a prompt (within 15 min after infusion) increase in circulating level of endothelin 1 and a pattern of glomerular hypoperfusion and hypofiltration which can be ameliorated with antiendothelin antibody. We now show that 60 min after cyclosporine, serum endothelin 1 level falls to <2.55 ± 0.31 pg/mL (N = 6), a value comparable to that found in normal animals (<2 pg/mL). The study presented here also examines whether sustained cyclosporine-induced glomerular dysfunction is associated with altered endothelin receptor characteristics. Saturation and competitive inhibition binding studies in isolated glomerular membranes showed two binding sites. Of these, the density of the low-affinity site was affected by cyclosporine treatment (851 ± 117 versus 425 ± 61 fmol/mg of protein; P< 0.05; N= 6) without a change in equilibrium dissociation constant, KD. The high-affinity site was not affected. The receptor characteristics of another vasoconstrictor, angiotensin II, were not affected by cyclosporine. In addition, there was no difference in endothelin binding sites in hepatic tissue between cyclosporine and control rats. These results raise the intriguing possibility that cyclosporine-induced glomerular dysfunction involves upregulation of endothelin binding sites and that altered endothelin receptors appear specific to the kidney.

本文言語English
ページ(範囲)1253-1258
ページ数6
ジャーナルJournal of the American Society of Nephrology
1
11
出版ステータスPublished - 1991 5

ASJC Scopus subject areas

  • Nephrology

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