Abnormalities in growth characteristics of aortic smooth muscle cells in spontaneously hypertensive rats.
Author(s) -
Vratislav Hadrava,
Johanne Tremblay,
Pavel Hamet
Publication year - 1989
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.13.6.589
Subject(s) - dna synthesis , endocrinology , medicine , vascular smooth muscle , stimulation , epidermal growth factor , thymidine , cell growth , growth factor , platelet derived growth factor , spontaneously hypertensive rat , cell , biology , smooth muscle , dna , chemistry , platelet derived growth factor receptor , blood pressure , biochemistry , receptor
Comparative studies have shown that cultured vascular smooth muscle cells from spontaneously hypertensive rats (SHR) proliferate to a higher cell number, grow to a greater density, and have greater specific growth rate, particularly at a higher saturation density, than those of the normotensive Wistar-Kyoto (WKY) control rats. The growth difference was not due to varying cell survival nor to attachment ability after passage. The degree of DNA synthesis was estimated by [3H]thymidine incorporation into newly synthesized DNA. [3H]thymidine uptake increased with escalating concentrations of calf serum and reached a plateau at 5% calf serum in WKY rats, whereas an excessive, continuous rise was observed in SHR with up to a 20% concentration. [3H]thymidine incorporation into newly synthesized DNA was tested after stimulation by platelet-derived growth factor and epidermal growth factor. A significantly higher amount of newly synthesized DNA in vascular smooth muscle cells from SHR was noted when the cells were stimulated by platelet-derived growth factor or epidermal growth factor alone, and their simultaneous addition did not significantly change the 50% effective concentration but heightened the maximal response. These data provide evidence of increased aortic smooth muscle cell proliferation from aortas of SHR after mitogen stimulation and suggest a defect in growth stimulatory-inhibitory control.
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