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[Inhibition of voltage-gated K+ current in rat intrapulmonary arterial smooth muscle cells by endothelin-1].
Yao Xue Xue Bao. 2004 Jan; 39(1):9-12.YX

Abstract

AIM

To investigate the role of endothelin-1 (ET-1) in the physiological and pathophysiological regulating mechanisms of voltage-gated K+ current (IKV) inhibition in rat intrapulmonary arterial smooth muscle cells (PASMCs).

METHODS

Single PASMCs were obtained with acute enzyme (collagnase plus papain) dispersing method. Using whole cell patch-clamp technique in freshly isolated rat PASMCs, the effect of ET-1 on voltage-gated K+ current was recorded.

RESULTS

ET-1 (1 x 10(-9) mol.L-1) and the voltage-dependent K+ (KV)-channel antagonist 4-aminopyridine (4AP), but not the Ca(2+)-activated K(+)-channel antagonist tetraethylammonium (TEA), caused membrane depolarization. The effect of ET-1 on membrane potential persisted in cells in which intracellular Ca2+ was buffered with 1,2-bis (2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA). ET-1 (1 x 10(-9) mol.L-1) caused a significant reversible inhibition of KV current, which began 4.0 s after application of ET-1, was much earlier than the effect of membrane depolarization of PASMCs (15s). ET-1 (1 x 10(-10) to 1 x 10(-7) mol.L-1) caused a concentration-dependent inhibition of K+ current (mV, from 136 to 40 pA/pF). The percent inhibition was 71% at 1 x 10(-7) mol.L-1 (n = 6). The effect of ET-1 (1 x 10(-9) mol.L-1) on K+ current was weaker under conditions free of Ca2+ than containing Ca2+. At a test potential of mV, free of Ca2+ conditions reduced the maximum inhibitory effect of ET-1 from 71% to 50%.

CONCLUSION

ET-1 modulated pulmonary vascular reactivity by depolarizing membrane potential and inhibiting the K+ current of PASMCs. The effect of ET-1 on PASMCs membrane potential and the inhibition of K+ current were independent of Ca2+, but the inhibition of K+ current was much greater under conditions containing Ca2+ than free of Ca2+.

Authors+Show Affiliations

Pulmonary Disease Laboratory of Ministry of Health of China, Affiliated Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China. zaiwenfan@163.netNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Research Support, Non-U.S. Gov't

Language

chi

PubMed ID

15127573

Citation

Fan, Zai-wen, et al. "[Inhibition of Voltage-gated K+ Current in Rat Intrapulmonary Arterial Smooth Muscle Cells By Endothelin-1]." Yao Xue Xue Bao = Acta Pharmaceutica Sinica, vol. 39, no. 1, 2004, pp. 9-12.
Fan ZW, Zhang ZX, Xu YJ. [Inhibition of voltage-gated K+ current in rat intrapulmonary arterial smooth muscle cells by endothelin-1]. Yao Xue Xue Bao. 2004;39(1):9-12.
Fan, Z. W., Zhang, Z. X., & Xu, Y. J. (2004). [Inhibition of voltage-gated K+ current in rat intrapulmonary arterial smooth muscle cells by endothelin-1]. Yao Xue Xue Bao = Acta Pharmaceutica Sinica, 39(1), 9-12.
Fan ZW, Zhang ZX, Xu YJ. [Inhibition of Voltage-gated K+ Current in Rat Intrapulmonary Arterial Smooth Muscle Cells By Endothelin-1]. Yao Xue Xue Bao. 2004;39(1):9-12. PubMed PMID: 15127573.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Inhibition of voltage-gated K+ current in rat intrapulmonary arterial smooth muscle cells by endothelin-1]. AU - Fan,Zai-wen, AU - Zhang,Zhen-xiang, AU - Xu,Yong-jian, PY - 2004/5/7/pubmed PY - 2004/8/3/medline PY - 2004/5/7/entrez SP - 9 EP - 12 JF - Yao xue xue bao = Acta pharmaceutica Sinica JO - Yao Xue Xue Bao VL - 39 IS - 1 N2 - AIM: To investigate the role of endothelin-1 (ET-1) in the physiological and pathophysiological regulating mechanisms of voltage-gated K+ current (IKV) inhibition in rat intrapulmonary arterial smooth muscle cells (PASMCs). METHODS: Single PASMCs were obtained with acute enzyme (collagnase plus papain) dispersing method. Using whole cell patch-clamp technique in freshly isolated rat PASMCs, the effect of ET-1 on voltage-gated K+ current was recorded. RESULTS: ET-1 (1 x 10(-9) mol.L-1) and the voltage-dependent K+ (KV)-channel antagonist 4-aminopyridine (4AP), but not the Ca(2+)-activated K(+)-channel antagonist tetraethylammonium (TEA), caused membrane depolarization. The effect of ET-1 on membrane potential persisted in cells in which intracellular Ca2+ was buffered with 1,2-bis (2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA). ET-1 (1 x 10(-9) mol.L-1) caused a significant reversible inhibition of KV current, which began 4.0 s after application of ET-1, was much earlier than the effect of membrane depolarization of PASMCs (15s). ET-1 (1 x 10(-10) to 1 x 10(-7) mol.L-1) caused a concentration-dependent inhibition of K+ current (mV, from 136 to 40 pA/pF). The percent inhibition was 71% at 1 x 10(-7) mol.L-1 (n = 6). The effect of ET-1 (1 x 10(-9) mol.L-1) on K+ current was weaker under conditions free of Ca2+ than containing Ca2+. At a test potential of mV, free of Ca2+ conditions reduced the maximum inhibitory effect of ET-1 from 71% to 50%. CONCLUSION: ET-1 modulated pulmonary vascular reactivity by depolarizing membrane potential and inhibiting the K+ current of PASMCs. The effect of ET-1 on PASMCs membrane potential and the inhibition of K+ current were independent of Ca2+, but the inhibition of K+ current was much greater under conditions containing Ca2+ than free of Ca2+. SN - 0513-4870 UR - https://www.unboundmedicine.com/medline/citation/15127573/[Inhibition_of_voltage_gated_K+_current_in_rat_intrapulmonary_arterial_smooth_muscle_cells_by_endothelin_1]_ DB - PRIME DP - Unbound Medicine ER -