Interaction of atrial natriuretic peptide-stimulated guanylate cyclase and vasopressin-stimulated calcium signaling pathways in the glomerular mesangial cell.
Interaction of atrial natriuretic peptide-stimulated guanylate cyclase and vasopressin-stimulated calcium signaling pathways in the glomerular mesangial cell.
复制标题
肾小球系膜细胞中心钠肽刺激的鸟苷酸环化酶和加压素刺激的钙信号通路的相互作用。
DOI：
10.1016/0003-9861(88)90506-1
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发表时间：
1988
影响因子：
3.9
通讯作者：
Skorecki,K
中科院分区：
文献类型：
--
作者：
Kremer,S;Troyer,D;Kreisberg,J;Skorecki,K
心房钠尿肽（ANP）的受体已被证明存在于肾小球系膜细胞以及肾小球中的其他细胞类型中。ANP对肾小球血流动力学影响的生化基础尚未明确。使用培养的大鼠肾小球系膜细胞，我们证明了一个浓度依赖性的刺激cGMP的生产在完整的细胞，和鸟苷酸环化酶的膜。尽管存在鸟苷酸环化酶反应，但ANP对基础三磷酸肌醇的产生没有抑制作用，也对基础胞浆钙没有抑制作用。精氨酸加压素刺激IP 3的产生，引起细胞内钙离子的上升，用钙敏感的荧光探针Indo-1测量，并引起系膜细胞收缩。ANP引起轻微但显着的增强加压素刺激的IP 3的生产，但对胞浆钙反应，也对收缩反应没有影响。8-溴GMP同样对钙信号的产生没有影响。这些结果表明，ANP对肾小球血流动力学的影响不是通过改变系膜细胞中钙信号的产生来介导的。相反，钙抑制ANP刺激鸟苷酸环化酶活性。
Receptors for atrial natriuretic peptide (ANP) have been demonstrated in renal mesangial cells as well as other cell types in the glomerulus. The biochemical basis for the effects of ANP on glomerular hemodynamics remains undefined. Using cultured rat glomerular mesangial cells, we demonstrated a concentration-dependent stimulation of cGMP production in intact cells, and of guanylate cyclase in membranes. Despite the presence of a guanylate cyclase response, ANP had no inhibitory effect on basal inositol trisphosphate production nor on basal cytosolic calcium. Arginine vasopressin stimulated IP3production, caused a rise in cytosolic calcium as measured using the calcium-sensitive fluorescent probe Indo-1, and caused mesangial cell contraction. ANP caused a slight but significant enhancement of vasopressin-stimulated IP3production, but had no effect on the cytosolic calcium response nor on the contractile response. 8-Bromoc GMP likewise had no effect on the generation of the calcium signal. These results indicate that the effects of ANP on glomerular hemodynamics are not mediated by an alteration in the generation of the calcium signal in mesangial cells. In contrast, addition of calcium inhibited ANP stimulated guanylate cyclase activity.