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(Hypertension. 2004;43:243.)
© 2004 American Heart Association, Inc.

Scientific Contributions

Attenuation of Lysophosphatidylcholine-Induced Suppression of ANP Release From Hypertrophied Atria

Jeong Hee Han; Chunhua Cao; Soo Mi Kim; Feng Lian Piao; Suhn Hee Kim

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

Correspondence to Suhn Hee Kim, MD, PhD, 2-20 Keum-Am-Dong-San, Department of Physiology, Chonbuk National University Medical School, Jeonju 561-180, Korea. e-mail shkim{at}moak.chonbuk.ac.kr

Lysophosphatidylcholine (LPC) is an endogenous phospholipid released from the cell membrane during ischemia, and it has potent cardiac effects, including inhibition of atrial natriuretic peptide (ANP) release. The aim of this study was to investigate the effects of LPC on hemodynamics and ANP release in hypertrophied atria and to define its mechanism. Isolated, perfused, beating, hypertrophied atria from monocrotaline-treated rats were used. LPC (30 µmol/L), a mixture of stearoyl-LPC, palmitoyl-LPC, and oleoyl-LPC, caused suppression of ANP release, which was markedly attenuated in hypertrophied atria compared with nonhypertrophied atria. Suppression of ANP release by stearoyl-LPC, palmitoyl-LPC, or oleoyl-LPC was also attenuated in hypertrophied atria. The potency appeared to be dependent on the species of fatty acid residue of LPC. Changes in ANP release by LPC, palmitoyl-LPC, and oleoyl-LPC were positively correlated with the degree of cardiac hypertrophy, but that by stearoyl-LPC was not. Changes in ANP release by LPC also were negatively correlated with changes in pulse pressure. Stearoyl-LPC caused an increase in intracellular Ca²⁺ in single, atrial myocytes in a concentration-dependent manner, which was markedly attenuated in hypertrophied atrial myocytes. These results suggest that attenuation of LPC-induced suppression of ANP release from hypertrophied atria might partly be related to changes in pulse pressure in terms of cardiac hypertrophy and/or disturbance of intracellular Ca²⁺ regulation.

Key Words: calcium • hypertrophy • natriuretic peptides • hypertension

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