Oxytocin is synthesized and released in the heart and vasculature, tissues that also express
oxytocin receptors. Although it has been established this intrinsic cardiovascular
oxytocin system is important in normal homeostatic cardiac and vascular regulation, a role for this system in cardiovascular pathophysiology has not been investigated. The current study examined the influence of
oxytocin on mechanisms in
atherogenesis, oxidative stress, and
inflammation in cultured human vascular cells, THP-1 monocytes, and macrophages.
Oxytocin receptor protein and
mRNA expression,
NADPH-dependent
superoxide activity, and
interleukin-6 secretion were measured. Results demonstrated
oxytocin receptor protein and
mRNA in THP-1 monocytes and macrophages. Incubation of cells at physiological levels of
oxytocin significantly decreased basal and stimulated
NADPH-dependent
superoxide activity in vascular cells, monocytes, and macrophages by 24-48%.
Oxytocin also attenuated
interleukin-6 secretion from stimulated THP-1 macrophages and endothelial cells by 56 and 26%, respectively. These findings suggest that
oxytocin attenuates vascular oxidative stress and
inflammation, two important pathophysiological processes in
atherosclerosis. The fact that
oxytocin receptors are found in monocytes and macrophages, and
oxytocin decreases both
superoxide production and release of a proinflammatory
cytokine from these cells, suggests a potentially larger role for
oxytocin in the attenuation of disease.