Nitric oxide up-regulates the expression of calcium-dependent potassium channels in the supraoptic nuclei and neural lobe of rats following dehydration.

Nitric oxide (NO) is a gas molecule to signal neurotransmission in the hypothalamo-neurohypophysial system during osmotic regulation. We previously reported that osmotic stimulation increased nitric oxide synthase (NOS) activity in the supraoptic nuclei (SON) and neural lobe. The aim of this study is to define the role of NO in the regulation of Ca(2+)-activated K(+) channels (BK channels) expression in the magnocellular system following dehydration. We used Western blot analysis and quantitative immunocytochemistry to conduct the experiment in rats. In the immunoblot study, we found that water deprivation significantly increased the expression of BK channels in the SON and neural lobes. Dehydration also enhanced the profiles of neurons expressing vasopressin and oxytocin significantly. In about 70% of these neurons, BK channels were co-localized in the same neuron, and their expression increased significantly during dehydration. We further examined the effects of intracerebroventricular administration of sodium nitroprusside (a donor of NO) and L-NAME (an inhibitor of NO synthase) on expression of BK channels in the SON. We found that compared to animals treated with the donor of NO, there were significant decreases in the expression of BK proteins in animals receiving L-NAME. These results suggest that NO may enhance the expression of BK channels in the supraoptic nuclei and neural lobe of rats following dehydration.