Hypertension remains a leading risk factor for morbidity and mortality from cardiovascular disease. Elevated sympathetic nerve activity contributes to the development and maintenance of hypertension, but the central mechanisms that lead to chronic increases in sympathetic nerve activity remain unresolved (Guyenet, 2006). Understanding these mechanisms requires detailed anatomical and physiological mapping of the relevant neurocircuitry. Recent studies highlight the importance of the paraventricular nucleus of the hypothalamus (PVN) in mediating acute and chronic increases in sympathetic nerve activity under multiple conditions including hypertension and heart failure (Benarroch, 2005; Guyenet, 2006). However, the PVN seems to have minimal influence on resting sympathetic nerve activity under normal conditions, which raises the important question: what inputs turn on the PVN (Dampney et al. 2005)? Recent investigations are increasing our understanding of the regulation of PVN neuronal activity. In this issue of The Journal of Physiology, Shi et al. (2008) demonstrate that a direct neural connection originating in the organum vasculosum of the laminae terminalis (OVLT) and terminating in the PVN mediates activation of PVN neurons by hyperosmolality.
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