Hirata Y, Emori T, Ohta K, Shichiri M, Marumo F
Second Department of Internal Medicine, Tokyo Medical and Dental University, Japan.
Eur J Pharmacol. 1989 May 30;164(3):603-6. doi: 10.1016/0014-2999(89)90273-2.
Long-term (24 h) pretreatment of cultured rat vascular smooth muscle cells with 100 nM angiotensin and 1 microM vasopressin induced a marked reduction of the maximal binding capacity of atrial natriuretic peptide (ANP) receptors in a fashion similar to that induced by phorbol ester. The down-regulation of the receptors induced by vasoconstrictors and phorbol ester was concomitantly associated with an attenuation of ANP-stimulated cGMP accumulation. These data suggest that vasoconstrictor-induced activation of protein kinase C is involved in the mechanism of heterologous down-regulation of vascular ANP receptors.
用100纳摩尔血管紧张素和1微摩尔血管加压素对培养的大鼠血管平滑肌细胞进行长期（24小时）预处理，可导致心房利钠肽（ANP）受体的最大结合能力显著降低，其方式类似于佛波酯所诱导的情况。血管收缩剂和佛波酯所诱导的受体下调与ANP刺激的环磷酸鸟苷（cGMP）积累减弱同时发生。这些数据表明，血管收缩剂诱导的蛋白激酶C激活参与了血管ANP受体异源下调的机制。
