Involvement of Ras-regulated myosin light chain phosphorylation in the captopril effects in spontaneously hypertensive rats.

Background: Early treatment with captopril prevents the development of hypertension by inhibiting the generation of angiotensin II and smooth muscle contraction. Although smooth muscle contraction is regulated by myosin light chain phosphorylation (MLC-P), the role of MLC-P in captopril effects in hypertension has not been described. Therefore, we treated spontaneously hypertensive rats (SHR) with captopril and investigated the effects of this agent on downstream signaling.

Inhibiting myosin light chain kinase retards the growth of mammary and prostate cancer cells.

We have previously shown that ML-7, which inhibits myosin light chain kinase (MLCK), induces apoptosis in transformed and non-transformed cells. We have extended these studies and found that ML-7 stimulates the ability of etoposide to induce apoptosis in Mm5MT mouse mammary adenocarcinoma cells and Mat-Ly-Lu rat prostate cancer cells in vitro. ML-7 was also found to have a chemopreventive effect using an in vitro mouse mammary organ culture model.