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Am J Physiol Heart Circ Physiol 279: H388-H396, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 1, H388-H396, July 2000

Effects of cardiotrophin-1 on hemodynamics and endocrine function of the heart

Ichiro Hamanaka1, Yoshihiko Saito1, Toshio Nishikimi2, Tatsuo Magaribuchi3, Shigeki Kamitani1, Koichiro Kuwahara1, Masahiro Ishikawa1, Yoshihiro Miyamoto1, Masaki Harada1, Emiko Ogawa1, Noboru Kajiyama1, Nobuki Takahashi1, Takehiko Izumi1, Gotaro Shirakami3, Kenjiro Mori3, Yoshito Inobe1, Ichiro Kishimoto1, Izuru Masuda1, Kazuhiko Fukuda3, and Kazuwa Nakao1

1 Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto, Japan 606-8507; 2 Hypertension Research Laboratory, National Cardiovascular Center Research Institute, 5-7-1 Fujishiro-dai, Suita, Osaka, Japan 565-8565; and 3 Department of Anesthesiology, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto, Japan 606-8507

Cardiotrophin-1 (CT-1), a member of the interleukin-6 superfamily of cytokines, possesses hypertrophic actions and atrial natriuretic peptide (ANP)-producing activity in vitro. The goal of our study is to elucidate whether CT-1 affects the cardiovascular system in vivo. Intravenous injection of CT-1 (4-100 µg/kg) in conscious rats evoked significant declines in blood pressure and reflex increases in heart rate (HR) in a dose-dependent manner. CT-1 induced no significant change in cardiac output (from 260.7 ± 11.0 to 264.7 ± 26.6 ml · min-1 · kg-1, P = not significant), which was compatible with the results from isolated perfused rat hearts; HR, change in pressure over time, left ventricular developed pressure, and perfusion pressure were unaffected. Northern blot and RT-PCR analyses revealed that CT-1 increased expression of inducible nitric oxide synthase (iNOS) in lung and aorta but not in heart or liver. Pretreatment with aminoguanidine, a specific iNOS inhibitor, inhibited both iNOS mRNA production and the depressor effect of CT-1. Interestingly, CT-1 increased ventricular expression of ANP and brain natriuretic peptide (BNP). The data demonstrate that CT-1 elicits its hypotensive effect via a nitric oxide-dependent mechanism and that CT-1 induces ANP and BNP mRNA expression in vivo.

blood pressure; nitric oxide synthase; natriuretic peptide


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