Kuan S I, Judd A M, Jarvis W D, Login I S, MacLeod R M
Department of Medicine, University of Virginia Health Sciences Center, Charlottesville 22908.
Mol Cell Endocrinol. 1990 Sep 10;72(3):239-46. doi: 10.1016/0303-7207(90)90148-2.
The presence of kallikrein activity, bradykinin (BK) and lys-bradykinin (LBK) in the pituitary gland suggests a possible physiological role of kinins therein. We demonstrated that BK and LBK increased prolactin (PRL), but not growth hormone release, from rat anterior pituitary cells cultured in vitro. Such stimulatory effect on PRL secretion appears to involve B2-type BK receptors, as suggested by the antagonizing effect of B6572 (a B2-type BK receptor antagonist) on PRL release. The BK-induced increase in PRL release is associated with an enhanced [3H]arachidonate (AA) efflux, an elevated cytosolic free calcium concentration [(Ca2+]i), and increased inositol phosphate (InsPx) production. Bradykinin and LBK stimulated [3H]AA liberation, [Ca2+]i elevation and PRL release at lower concentrations than those necessary to stimulate InsPx production. Therefore, AA release and [Ca2+]i elevation may be more important to PRL release than is InsPx production. Dopamine (DA) inhibited BK- or LBK-stimulated PRL release and slightly attenuated the stimulated [Ca2+]i response, but had no effect on stimulated [3H]AA efflux and InsPx generation. This study suggests that BK and LBK may have either an autocrine or a paracrine role in regulating PRL secretion, and are subject to modulation by DA.
垂体中激肽释放酶活性、缓激肽（BK）和赖氨酸缓激肽（LBK）的存在表明激肽在其中可能具有生理作用。我们证明，BK和LBK可增加体外培养的大鼠垂体前叶细胞催乳素（PRL）的释放，但不影响生长激素的释放。B6572（一种B2型BK受体拮抗剂）对PRL释放具有拮抗作用，提示对PRL分泌的这种刺激作用似乎涉及B2型BK受体。BK诱导的PRL释放增加与增强的[3H]花生四烯酸（AA）外流、升高的胞质游离钙浓度[Ca2+]i以及增加的肌醇磷酸（InsPx）生成有关。与刺激InsPx生成所需的浓度相比，缓激肽和LBK在较低浓度下即可刺激[3H]AA释放、[Ca2+]i升高和PRL释放。因此，AA释放和[Ca2+]i升高对PRL释放可能比InsPx生成更重要。多巴胺（DA）抑制BK或LBK刺激的PRL释放，并略微减弱刺激的[Ca2+]i反应，但对刺激的[3H]AA外流和InsPx生成无影响。本研究表明，BK和LBK在调节PRL分泌中可能具有自分泌或旁分泌作用，并受DA的调节。
