1988Journal of HypertensionRequires access

The effects of vasoactive agents on the proliferation of vascular smooth muscle cells grown in vitro

Satoru Kuriyama, Koji Nakamura, Yoshihiko Kaguchi, Masayuki Kimura, H Tamura, Katsura Tamai, Takao Hashimoto, Tadashi Miyahara

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Abstract

The present study was designed to investigate the effect of vasoactive agents on cellular proliferation in serially passed cultured vascular smooth muscle cells (VSMC). A substantial reduction in the number of vascular smooth muscle cells was observed with the addition of nifedipine, nicorandil, bunazocine and labetalol compared with that in a control sample. Furthermore, noradrenaline significantly increased the number of vascular smooth muscle cells. In contrast, neither propranolol nor captopril had any effect on number of vascular smooth muscle cells. The cell size, measured as water volume of vascular smooth muscle cells based on the equilibrium distribution of 3-O-(14C-methyl)-D-glucose, did not differ between treatments with the above-mentioned agents. It is suggested that in addition to a known calcium-mediated mechanism, an alpha-receptor-mediated property could be involved in the proliferation of vascular smooth muscle cells and that clinical use of a calcium antagonist or an alpha-blocker might be useful to prevent the hyperproliferation of vascular smooth muscle cells commonly seen in the vascular walls of patients with hypertension.

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The present study was designed to investigate the effect of vasoactive agents on cellular proliferation in serially passed cultured vascular smooth muscle cells (VSMC). A substantial reduction in the number of vascular smooth muscle cells was observed with the addition of nifedipine, nicorandil, bunazocine and labetalol compared with that in a control sample. Furthermore, noradrenaline significantly increased the number of vascular smooth muscle cells. In contrast, neither propranolol nor captopril had any effect on number of vascular smooth muscle cells. The cell size, measured as water volume of vascular smooth muscle cells based on the equilibrium distribution of 3-O-(14C-methyl)-D-glucose, did not differ between treatments with the above-mentioned agents. It is suggested that in addition to a known calcium-mediated mechanism, an alpha-receptor-mediated property could be involved in the proliferation of vascular smooth muscle cells and that clinical use of a calcium antagonist or an alpha-blocker might be useful to prevent the hyperproliferation of vascular smooth muscle cells commonly seen in the vascular walls of patients with hypertension.

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Available abstract

The present study was designed to investigate the effect of vasoactive agents on cellular proliferation in serially passed cultured vascular smooth muscle cells (VSMC). A substantial reduction in the number of vascular smooth muscle cells was observed with the addition of nifedipine, nicorandil, bunazocine and labetalol compared with that in a control sample. Furthermore, noradrenaline significantly increased the number of vascular smooth muscle cells. In contrast, neither propranolol nor captopril had any effect on number of vascular smooth muscle cells. The cell size, measured as water volume of vascular smooth muscle cells based on the equilibrium distribution of 3-O-(14C-methyl)-D-glucose, did not differ between treatments with the above-mentioned agents. It is suggested that in addition to a known calcium-mediated mechanism, an alpha-receptor-mediated property could be involved in the proliferation of vascular smooth muscle cells and that clinical use of a calcium antagonist or an alpha-blocker might be useful to prevent the hyperproliferation of vascular smooth muscle cells commonly seen in the vascular walls of patients with hypertension.

Key concepts: Vascular smooth muscle, Medicine, Internal medicine, Endocrinology, Nifedipine, Myocyte, Propranolol, Mural cell

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