Chronic hypoxia alters effects of endothelin and angiotensin on K+ currents in pulmonary arterial myocytes

Research output: Contribution to journalArticle

Abstract

We tested the hypothesis that chronic hypoxia alters the regulation of K+ channels in intrapulmonary arterial smooth muscle cells (PASMCs). Charybdotoxin-insensitive, 4-aminopyridine-sensitive voltage-gated K+ (K(V,CI)) and Ca2+activated K+ (K(Ca)) currents were measured in freshly isolated PASMCs from rats exposed to 21 or 10% O2 for 17-21 days. In chronically hypoxic PASMCs, K(V,CI) current was reduced and K(Ca) current was enhanced. 4-Aminopyridine (10 mM) depolarized both normoxic and chronically hypoxic PASMCs, whereas charybdotoxin (100 nM) had no effect in either group. The inhibitory effect of endothelin (ET)-1 (10-7 M) on K(V,CI) current was significantly reduced in PASMCs from chronically hypoxic rats, whereas inhibition by angiotensin (ANG) II (10-7 M) was enhanced. Neither ET-1 nor ANG II altered K(Ca) current in normoxic PASMCs; however, both stimulated K(Ca) current at positive potentials in chronically hypoxic PASMCs. These results suggest that although modulation of K(V,CI) and K(Ca) channels by ET- 1 and ANG II is altered by chronic hypoxia, the role of these channels in the regulation of resting membrane potential was not changed.

Original languageEnglish (US)
Pages (from-to)L431-L439
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume277
Issue number3 21-3
StatePublished - Sep 1 1999

Keywords

  • Calcium-activated potassium current
  • Membrane potential
  • Voltage-gated potassium current

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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