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Endocrinology Vol. 139, No. 11 4576-4580
Copyright © 1998 by The Endocrine Society

ARTICLES

Production and Secretion of Adrenomedullin in Cultured Rat Cardiac Myocytes and Nonmyocytes: Stimulation by Interleukin-1ß and Tumor Necrosis Factor-{alpha}1

Takeshi Horio, Toshio Nishikimi, Fumiki Yoshihara, Noritoshi Nagaya, Hisayuki Matsuo, Shuichi Takishita and Kenji Kangawa

Division of Hypertension, Department of Medicine (T.H., S.T.), and Research Institute (T.N., F.Y., N.N., H.M., K.K.), National Cardiovascular Center, Suita, Osaka 565-8565, Japan

Address correspondence and requests for reprints to: Takeshi Horio, M.D., Division of Hypertension, Department of Medicine, National Cardiovascular Center, 5–7-1, Fujishirodai, Suita, Osaka 565-8565, Japan.

The present study investigated the secretion level and gene expression of adrenomedullin (AM), a novel vasorelaxant peptide, in cultured neonatal rat cardiac myocytes and nonmyocytes, and the effects of interleukin-1ß (IL-1ß) and tumor necrosis factor-{alpha} (TNF{alpha}) on its production and secretion in these cells. Under serum-free conditions, both myocytes and nonmyocytes secreted immunoreactive (ir-) AM into the culture medium in a time-dependent manner. The secretion rates of ir-AM from myocytes and nonmyocytes per 105 cells were almost equivalent. The expression of AM messenger RNA was also observed in cultured myocytes and nonmyocytes. The peptide secretion and messenger RNA level of AM in cardiac myocytes were increased after stimulation with IL-1ß. In nonmyocytes, IL-1ß and TNF{alpha} remarkably augmented both the release of ir-AM into the medium and AM gene expression after 24 and 48 h of incubation. These observations indicate that cardiac ventricular cells (i.e. myocytes and nonmyocytes) actively produce AM and also suggest that cytokines such as IL-1ß and TNF{alpha} regulate the gene expression and secretion of this peptide in the ventricles. On the basis of these results and the findings that IL-1ß and TNF{alpha} are involved in heart failure and cardiac hypertrophy, AM may play a role as an autocrine/paracrine modulator in some cardiac disorders.




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