L‐NAME, a nitric oxide synthase inhibitor, increases the protein expression of both executioner and inhibitor of apoptosis in the placental bed of mid‐to‐late pregnant rats

Abstract

The involvement of nitric oxide (NO) signaling in apoptosis was examined in the placental bed of mid-to-late pregnant rats. Pregnant rats were treated with L-NAME, a nitric oxide synthase inhibitor, by subcutaneous infusion for 48 hours before the examination at day 13.5, 17.5, or 21.5. L-NAME induced apoptosis in the placental bed to a limited extent at days 13.5 and 17.5, but not at day 21.5. When the placental bed was examined at day 17.5, the protein expression of both executioner (C-Cas3) and inhibitor (XIAP) of apoptosis was increased by L-NAME, but they did not co-localized with apoptosis. It was presumed that placental bed apoptosis induced by L-NAME is regulated through the expression of both executioner and inhibitor, possibly involving protein S-nitrosylation.

Enhancing Muscle Intracellular Ca2+ Homeostasis and Glucose Uptake: Passive Pulsatile Shear Stress Treatment in Type 2 Diabetes

“…The mechanism by which pGz causes the reduction in [Ca 2+ ] i is not fully understood; however, it is possible that NO production induced by pGz treatment (i) decreases Ca 2+ release from the sarcoplasmic reticulum by a reduction in the open probability of the ryanodine receptor [30,31]; (ii) modifies the degree of nitrosylation of the ryanodine receptor, reducing the leak of Ca 2+ from intracellular stores (unpublished observations); or (iii) reduces the influx of Ca 2+ through the muscle sarcolemma [32,33]. The effect of pGz on [Ca 2+ ] i was mediated by nitric oxide since the pretreatment stage for 8 days, with L-NAME, a NOS inhibitor [34,35], abolishing the effect elicited by pGz on [Ca 2+ ] i .…”