Calcium homeostasis and nerve growth factor secretion from vascular and bladder smooth muscle cells

被引:5
|
作者
Sherer, TB
Clemow, DB
Tuttle, JB
机构
[1] Univ Virginia, Hlth Sci Ctr, Dept Neurosci, Charlottesville, VA 22908 USA
[2] Univ Virginia, Hlth Sci Ctr, Dept Urol, Charlottesville, VA 22908 USA
关键词
hypertension; micturition; neural survival; rat; (WKY; SHR; WKHA; WKHT);
D O I
10.1007/s004419900148
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Bladder and vascular smooth muscle cells cultured from four rat strains (WKY, SHR, WKHA, WKHT) differing in rates of nerve growth factor (NGF) production were used to determine whether a relationship exists between intracellular calcium and NGF secretion. Basal cytosolic calcium was related to basal NGF secretion rates in bladder and vascular smooth muscle cells from all four strains with the exception of WKHT bladder muscle cells. Thrombin is a calcium-mobilizing agent and increases NGF production from vascular but not bladder smooth muscle cells. Strain differences were found in the magnitude of the calcium peak induced by thrombin in vascular smooth muscle cells, but these differences did not correlate with NGF secretion. Thrombin caused a calcium response in bladder smooth muscle cells without influencing NGF production. Quenching the calcium transient with a calcium chelator had no effect on thrombin-inducted NGF secretion rates in vascular smooth muscle cells. Thus, basal intracellular calcium may establish a set point for NGF secretion from smooth muscle. In addition, transient elevations in cytosolic calcium were unrelated to the induction of NGF output.
引用
收藏
页码:201 / 211
页数:11
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