Down-regulation of endogenous nitric oxide synthase in late-pregnancy and parturition in the rat hypothalamic magnocellular neurons and neurohypophysis.

Several recent lines of evidence suggest that nitric oxide (NO) may be an endogenous inhibitory regulator of the neurosecretory mechanism in magnocellular neurons of the paraventricular and the supraoptic nuclei in the hypothalamus. The NO synthase (NOS) system in the hypothalamo-neurohypophysial-axis is regulated in an activity-dependent manner. The present study examined NOS activity in the magnocellular neurons and neurohypophysis during pregnancy and parturition by using the nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry and assay of the specific NOS enzyme activity, respectively. In the paraventricular and supraoptic nuclei, the density and number of NADPH-diaphorase-positive cells decreased in late-pregnancy and parturition. The specific activity of NOS in the neurohypophysis also decreased in late-pregnancy through parturition, and increased shortly afterward. Together with the ability of a NO donor to significantly delay the progress of parturition when administered centrally in parturient rats, these observations suggest that this down-regulation of NOS activity in the hypothalamo-neurohypophysial axis in late-pregnancy and parturition may be of physiological importance in the onset and/or progress of parturition.