Rebas E, Lachowicz-Ochedalska A, Pawlikowski M
Department of Biochemistry, Institute of Physiology and Biochemistry, Institute of Endocrinology, Medical University of Łódź.
J Physiol Pharmacol. 2004 Mar;55(1 Pt 1):107-11.
Angiotensin II (Ang II) is known to modulate tyrosine kinases (PTKs) activity in pituitary tumor cells. It is known that AngII is acting via AT1 receptors in many tissues. The aim of this study was to see whether 3-8 fragment of AngII, called angiotensin IV (AngIV) has a similar effect on tyrosine kinase activity in normal pituitary gland and what type of angiotensin receptor is involved in this process. The homogenates of normal rat pituitaries was a source of enzymes. The PTKs activity was determined using the synthetic substrate poly GluTyr and gamma-(32)P-ATP. Ang IV was found to increase the PTK activity in the rat anterior pituitary tissue, with the maximal effect at concentration of 10(-10) M. AngII was ineffective at all concentrations studied. Losartan, a selective AT1 receptor blocker, added together with Ang IV abolished the effect of the latter, however losartan diminished also the PTK activity when applied together with Ang II, but only when it was added immediately before, but not after, the addition of Ang II. The involvement of a non-classic AT1-like receptor is suggested.
已知血管紧张素II(Ang II)可调节垂体肿瘤细胞中的酪氨酸激酶(PTK)活性。众所周知,AngII在许多组织中通过AT1受体发挥作用。本研究的目的是观察血管紧张素II的3 - 8片段,即血管紧张素IV(AngIV)对正常垂体中酪氨酸激酶活性是否有类似作用,以及该过程涉及何种类型的血管紧张素受体。正常大鼠垂体匀浆是酶的来源。使用合成底物聚谷氨酸酪氨酸和γ - (32)P - ATP测定PTK活性。发现Ang IV可增加大鼠垂体前叶组织中的PTK活性,在浓度为10(-10)M时效果最佳。在所有研究浓度下,AngII均无作用。与Ang IV一起添加的选择性AT1受体阻滞剂氯沙坦消除了后者的作用,然而,氯沙坦与Ang II一起应用时也会降低PTK活性,但仅在紧接Ang II添加之前而非之后添加时才会出现这种情况。提示存在非经典的AT1样受体参与其中。