Effect of amurinone on human pulmonary artery in vitro

S. Ono; S. Ueda; T. Sakuma; M. Noda; T. Tabata; Y. Hoshikawa; Y. Ashino; T. Tanita; K. Koike; S. Fujimura

Effect of amurinone on human pulmonary artery in vitro

S. Ono, S. Ueda, T. Sakuma, M. Noda, T. Tabata, Y. Hoshikawa, Y. Ashino, T. Tanita, K. Koike, S. Fujimura

IDAC - Division of Cancer Science

Tohoku University

Research output: Contribution to journal › Article › peer-review

Abstract

We studied the effect of amurinone, a phosphodiesterase inhibitor, on human pulmonary arterial smooth muscle in vitro. Amurinone caused dose-dependent relaxation of pulmonary arterial strips precontracted with 60 mM KCl. Preincubation with either meclofenamate (31 μM), a cyclooxygenase inhibitor, or L-N(G)-nitroarginine (100 μM), an endothelium-derived relaxing factor (EDRF) production inhibitor, failed to inhibit amurinone-induced pulmonary vasodilation. The cyclic AMP (cAMP) levels in the supernatant of the lung vessel homogenates significantly increased after incubation with amurinone. These results indicate that amurinone causes relaxation of human pulmonary artery in vitro, and suggest a role for cAMP in the mechanisms of amurinone-induced pulmonary vasodilation.

Original language	English
Pages (from-to)	650-654
Number of pages	5
Journal	Respiratory Investigation
Volume	32
Issue number	7
Publication status	Published - 1994

Keywords

amurinone
human pulmonary artery
pulmonary hypertension
tissue bioassay

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This output contributes to the following UN Sustainable Development Goals (SDGs)

Cite this

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abstract = "We studied the effect of amurinone, a phosphodiesterase inhibitor, on human pulmonary arterial smooth muscle in vitro. Amurinone caused dose-dependent relaxation of pulmonary arterial strips precontracted with 60 mM KCl. Preincubation with either meclofenamate (31 μM), a cyclooxygenase inhibitor, or L-N(G)-nitroarginine (100 μM), an endothelium-derived relaxing factor (EDRF) production inhibitor, failed to inhibit amurinone-induced pulmonary vasodilation. The cyclic AMP (cAMP) levels in the supernatant of the lung vessel homogenates significantly increased after incubation with amurinone. These results indicate that amurinone causes relaxation of human pulmonary artery in vitro, and suggest a role for cAMP in the mechanisms of amurinone-induced pulmonary vasodilation.",

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T1 - Effect of amurinone on human pulmonary artery in vitro

AU - Ono, S.

AU - Ueda, S.

AU - Sakuma, T.

AU - Noda, M.

AU - Tabata, T.

AU - Hoshikawa, Y.

AU - Ashino, Y.

AU - Tanita, T.

AU - Koike, K.

AU - Fujimura, S.

PY - 1994

Y1 - 1994

N2 - We studied the effect of amurinone, a phosphodiesterase inhibitor, on human pulmonary arterial smooth muscle in vitro. Amurinone caused dose-dependent relaxation of pulmonary arterial strips precontracted with 60 mM KCl. Preincubation with either meclofenamate (31 μM), a cyclooxygenase inhibitor, or L-N(G)-nitroarginine (100 μM), an endothelium-derived relaxing factor (EDRF) production inhibitor, failed to inhibit amurinone-induced pulmonary vasodilation. The cyclic AMP (cAMP) levels in the supernatant of the lung vessel homogenates significantly increased after incubation with amurinone. These results indicate that amurinone causes relaxation of human pulmonary artery in vitro, and suggest a role for cAMP in the mechanisms of amurinone-induced pulmonary vasodilation.

AB - We studied the effect of amurinone, a phosphodiesterase inhibitor, on human pulmonary arterial smooth muscle in vitro. Amurinone caused dose-dependent relaxation of pulmonary arterial strips precontracted with 60 mM KCl. Preincubation with either meclofenamate (31 μM), a cyclooxygenase inhibitor, or L-N(G)-nitroarginine (100 μM), an endothelium-derived relaxing factor (EDRF) production inhibitor, failed to inhibit amurinone-induced pulmonary vasodilation. The cyclic AMP (cAMP) levels in the supernatant of the lung vessel homogenates significantly increased after incubation with amurinone. These results indicate that amurinone causes relaxation of human pulmonary artery in vitro, and suggest a role for cAMP in the mechanisms of amurinone-induced pulmonary vasodilation.

KW - amurinone

KW - human pulmonary artery

KW - pulmonary hypertension

KW - tissue bioassay

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JO - Respiratory Investigation

JF - Respiratory Investigation

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ER -

Effect of amurinone on human pulmonary artery in vitro

Abstract

Keywords

UN SDGs

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