NERVE GROWTH-FACTOR SYNTHESIS IN VASCULAR SMOOTH-MUSCLE

被引:73
作者
CREEDON, D
TUTTLE, JB [1 ]
机构
[1] UNIV VIRGINIA, HLTH SCI CTR, DEPT NEUROSCI, BOX 230, CHARLOTTESVILLE, VA 22908 USA
[2] UNIV VIRGINIA, HLTH SCI CTR, DEPT PHYSIOL, CHARLOTTESVILLE, VA 22908 USA
关键词
GROWTH SUBSTANCES; VASCULAR SMOOTH MUSCLE; NEURONS; SYMPATHETIC NERVOUS SYSTEM;
D O I
10.1161/01.HYP.18.6.730
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Details of the interdependent, trophic relation between smooth muscle and its neural innervation are not well known despite suggestions that neural influences may contribute significantly to hypertensive and other cardiovascular disease. Vascular smooth muscle is a major target of innervation by neurons of the sympathetic nervous system. Sympathetic neurons depend on a constant supply of the potent neurotrophic peptide nerve growth factor. Nerve growth factor regulates an impressive list of neuronal and perhaps muscle properties, yet its source in vessels and the determinants of its synthesis are not known. We have taken advantage of the cytoarchitecture of the aorta to demonstrate that vascular smooth muscle cells synthesize nerve growth factor. The survival of cultured sympathetic neurons is supported in a nerve growth factor-dependent manner by co-culture with pure rat aortic vascular smooth muscle cells. Furthermore, pure smooth muscle cell cultures contain nerve growth factor-specific messenger RNA. Levels of messenger nucleic acid coding for nerve growth factor in smooth muscle are regulated by contractile agonists (angiotensin II, arginine vasopressin) and the adrenergic agonist phenylephrine. This suggests a link between muscle activity and growth factor production. Secretion of nerve growth factor protein by vascular smooth muscle was measured using a sensitive two-site immunoassay. Secretion is highest during muscle growth. Secretion is elevated by angiotensin II and arginine vasopression but slightly inhibited by phenylephrine. These results suggest that cultured vascular smooth muscle can serve as a useful model in which to study the cellular regulation of trophic factor synthesis in health and disease.
引用
收藏
页码:730 / 741
页数:12
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