THE INCREASED K+ LEAK OF MALARIA-INFECTED ERYTHROCYTES IS NOT VIA A CA2+-ACTIVATED K+ CHANNEL

被引：19

作者：

KIRK, K ^{[1
]}

ELFORD, BC ^{[1
]}

ELLORY, JC ^{[1
]}

机构：

[1] JOHN RADCLIFFE HOSP, INST MOLEC MED, OXFORD OX3 9DU, ENGLAND

来源：

BIOCHIMICA ET BIOPHYSICA ACTA | 1992年 / 1135卷 / 01期

关键词：

MALARIA; ERYTHROCYTE; POTASSIUM ION TRANSPORT; CALCIUM ION-ACTIVATED K+ CHANNEL;

D O I：

10.1016/0167-4889(92)90159-9

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Charybdotoxin and nitrendipine both inhibited K+(Rb-86+) influx via the Ca2+-activated channel of uninfected erythrocytes but had no effect on K+(Rb-86+) transport in malaria-infected cells. Activation of the channel in uninfected cells in which the cytoplasmic [Na+]/[K+] ratio was adjusted to be comparable with that of late-stage malaria-infected erythrocytes resulted in a large (nitrendipine-sensitive) increase in K+(Rb-86+) influx. These results suggest that the endogenous Ca2+-activated K+ channel remains inactive in human red cells infected with late-stage parasites. The identity of the pathway which mediates the increased K+-leak in infected erythrocytes remains to be established.

引用

页码：8 / 12

页数：5

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