Published Online
on April 28, 2003

A more recent version of this article appeared on June 1, 2003

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Submitted on October 21, 2002
Revised on November 15, 2002

Decreases in ANP Secretion by Lysophosphatidylcholine Through Protein Kinase C

Jeong Hee Han; Chunhua Cao; Sung Zoo Kim; Kyung Woo Cho; and Suhn Hee Kim^*

From the Department of Physiology, Institute for Medical Sciences, Chonbuk National University Medical School, Jeonju, Korea.

^* To whom correspondence should be addressed. E-mail: shkim{at}moak.chonbuk.ac.kr.

Abstract--Lysophosphatidylcholine (LPC) is an endogenous phospholipid released from the cell membrane during ischemia, and it has potent, local effects on cardiac tissues. LPC has been implicated in arrhythmogenesis during ischemia by increasing intracellular Ca²⁺. However, it is not known whether LPC influences atrial release of atrial natriuretic peptide (ANP). The aim of this study was to investigate the effect of LPC on ANP secretion from isolated, perfused, beating rat atria. LPC (10 and 30 µmol/L) caused decreases in ANP secretion in a dose-dependent manner, with slight increases in intra-atrial pressure and extracellular fluid (ECF) translocation. Therefore, the ANP secretion in terms of ECF translocation was markedly decreased by LPC. The order of the suppressive effect of ANP release was stearoyl-LPC>LPC>myristoyl-LPC=lauroyl-LPC. Staurosporine and wortmannin significantly attenuated suppression of the ANP release and an increase in intra-atrial pressure by LPC. High extracellular Mg²⁺ also attenuated the LPC-induced suppression of ANP release. However, other protein kinase C inhibitors such as chelerythrine, GF 109203X, and tamoxifen citrate did not affect LPC-induced suppression of ANP release. In single atrial myocytes, LPC caused increases in intracellular Ca²⁺ in a dose-dependent manner. The order of an increase in intracellular Ca²⁺ by LPC was stearoyl-LPC>LPC>myristoyl-LPC=lauroyl-LPC. An increase in intracellular Ca²⁺ by LPC was attenuated by staurosporine. These results suggest that LPC-induced suppression of ANP release through protein kinase C/Ca²⁺ and phosphoinositol-3-kinase might in part play an important role in the development of hypertension.

Key words: atrial natriuretic factor • phospholipases • extracellular space • calcium • protein kinases • heart

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