Role of vasopressin in the paraventricular nucleus of hypothalamus on hyperosmolality-induced sympathoexcitation

Abstract

Homeostasis is the property of a biological system regulates its internal environment (mileu interieur) in order to maintain a stable and constant condition. Among the different mechanisms that preserve the biological homeostasis, a major of them is the control of body water and minerals levels, known as osmoregulation. The increase in plasma osmolality, also called hyperosmolality, is an electrolyte imbalance in which the solute concentration in plasma is increased. Hyperosmolality is able to affect the sympathetic autonomic outflow and the PVN is one of the key brain regions strictly involved in control of the sympathetic activity during osmotic stimuli. The PVN is composed by two distinct subgroups of neurons (parvo and magnocellular). Parvocellular neurons (PCN) project to pre-motor sympathetic neurons located in the rostral ventrolateral medulla (RVLM) and/or pre-ganglionic sympathetic neurons in the intermediolateral cell column (IML) of the spinal cord, two important brain areas involved in the control of sympathetic outflow. The magnocellular neurons (MCN) of PVN projects to the posterior pituitary and they are responsible for the synthesis and release of vasopressin (VP). The VP is a nonapeptide with hormonal and neurotransmitter activity. In the central nervous system the VP is either synaptic released from collaterals axon or nonsynaptic released from the somatodendritic regions of magnocellular neurons and has its effects by acting via V1 receptors. It is well established in the literature that osmotic stimuli (water deprivation) was able to evoke different responses at the distinct subgroups of the PVN neurons level and that VP may play an important role as a neuromodulator in this responses. Although, it has been already showing a dendritic release of the VP within PVN nothing is known about the functional role of this neurotransmitter/neuromodulator on hyperosmolality-induced sympathoexcitation at this nuclei level. Therefore, the goal of this study is to investigate the role of endogenous vasopressin, through its action within PVN neurons, on sympathetic outflow induced by hyperosmolality. (AU)