Function and Localization of Epithelial Sodium Channels in Vasopressin and Oxytocin Neurons

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© 2015 by John Wiley & Sons, Ltd. All rights reserved. Blood pressure is largely controlled by the central nervous system via sympathetic nerve activity and neurohypophysial hormone secretions. Because magnocellular neurosecretory cells (MNCs) are directly involved in neurohypophysial hormone secretions and influence sympathetic nerve activity, MNCs play a pivotal role in blood pressure homeostasis. Antidiuretic and vasoconstriction effects of vasopressin during osmotic and cardiovascular challenges are well known. However, vasopressin also influences blood pressure by regulating epithelial Na+ channel (ENaC) activity in the kidney. ENaCs are non-voltage-dependent and amiloride-sensitive Na+ channels and are known for the rate-limiting step regulating trans-epithelial Na+ reabsorption in the aldosterone-sensitive distal nephron. Thus, ENaCs in the kidney directly contribute to Na+ and water homeostasis and influence blood volume and pressure. Intriguingly, the presence of ENaCs in the brain had been suggested for nearly 20 years since administration into the brain of ENaC blockers, amiloride, or its analog benzamil, attenuated sympathetic activity and hypertension in several animal models of hypertension. More recently, ENaCs were found in several structures in the brain including MNCs in the supraoptic nucleus (SON) and paraventricular nucleus (PVN). Considering the facts that MNCs regulate neurohypophysial hormone secretions and influence sympathetic nerve activity, these findings strongly imply that ENaCs in MNCs are at least partly involved in the development of hypertension. Despite the importance of ENaCs in MNCs, we currently know little about their physiological roles there. In this chapter, I discuss the electrophysiological properties of ENaCs in MNCs, their putative physiological significance, and their possible regulation.

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Neurophysiology of Neuroendocrine Neurons

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