Massfelder T, Saussine C, Simeoni U, Enanga B, Judes C, Helwig J J
Laboratoire de Physiologie Cellulaire Rénale, Université Louis Pasteur, Strasbourg, France.
Life Sci. 1993;53(11):875-81. doi: 10.1016/0024-3205(93)90439-a.
Studies were conducted to test whether parathyroid hormone-related protein (PTHrP) is able to stimulate adenylate cyclase activity in isolated rabbit glomeruli. Maximal stimulations were reached at 10(-7) M of human PTHrP-(1-34) or rat PTH-(1-34) and showed a 3-3.3 fold increase over basal activity. The potency (EC50) values were close to 10(-9) M. The guanyl nucleotide GTP, at 10(-5) M, potentiated the effect of PTH and PTHrP but reduced their potency. The combined effect of maximal concentrations of PTHrP and PTH was not additive, and the PTH antagonist [Nle8.18, Tyr34]-bPTH-(3-34)amide inhibited both PTHrP- and PTH-stimulated adenylate cyclase activities. These findings suggest that PTHrP could affect glomerular function through changes in glomerular cAMP content by interaction with PTH receptors.
开展了多项研究以测试甲状旁腺激素相关蛋白（PTHrP）是否能够刺激分离出的兔肾小球中的腺苷酸环化酶活性。在10⁻⁷M的人PTHrP-（1-34）或大鼠PTH-（1-34）时达到最大刺激，且相较于基础活性显示出3至3.3倍的增加。效价（EC50）值接近10⁻⁹M。10⁻⁵M的鸟苷酸GTP增强了PTH和PTHrP的作用，但降低了它们的效价。PTHrP和PTH最大浓度的联合作用并非相加性的，并且PTH拮抗剂[Nle8,18,Tyr34]-bPTH-（3-34）酰胺抑制了PTHrP和PTH刺激的腺苷酸环化酶活性。这些发现表明，PTHrP可能通过与PTH受体相互作用改变肾小球cAMP含量来影响肾小球功能。
