Neural Control of Non-vasomotor Organs in Hypertension

Abstract

Hypertension affects over 25 % of the population with the incidence continuing to rise, due in part to the growing obesity epidemic. Chronic elevations in sympathetic nerve activity (SNA) are a hallmark of the disease and contribute to elevations in blood pressure through influences on the vasculature, kidney, and heart (i.e., neurogenic hypertension). In this regard, a number of central nervous system mechanisms and neural pathways have emerged as crucial in chronically elevating SNA. However, it is important to consider that "sympathetic signatures" are present, with differential increases in SNA to regional organs that are dependent upon the disease progression. Here, we discuss recent findings on the central nervous system mechanisms and autonomic regulatory networks involved in neurogenic hypertension, in both non-obesity- and obesity-associated hypertension, with an emphasis on angiotensin-II, salt, oxidative and endoplasmic reticulum stress, inflammation, and the adipokine leptin.

Keywords: Autonomic; Blood pressure; Brain; Central nervous system; Sympathetic nerve activity.

Fig. 1

The control of regional sympathetic outflow to target organs is dependent upon the integration of signaling mechanisms and factors within integrated neural networks. These CNS pathways include circumventricular organs situated outside of the blood brain barrier (red), along with hypothalamic and hindbrain autonomic nuclei. Not shown are afferent reflex inputs, which also modulate activity within these networks. See text for additional details. Ang-II angiotensin II, AP area postrema, CVLM caudal ventral lateral medulla, ER endoplasmic reticulum, IML intermediolateral nucleus, MnPO median preoptic nucleus, NTS, nucleus tractus solitarii, OVLT organum vasculosum lamina terminalis, PP posterior pituitary, PVN paraventricular nucleus of the hypothalamus, ROS reactive oxygen species, RVLM rostral ventral lateral medulla, SFO subfornical organ, SON supraoptic nucleus