Recent Advances in Neurogenic Hypertension

Neurogenic hypertension has been a fixture in the hypertension literature for well over half a century. Early reports documented an increase in arterial blood pressure (ABP) after manipulation of baroreceptor afferent nerve signaling, so the hypertension was clearly of neural origin. Today, neurogenic hypertension often refers to a sympathetically driven increase in ABP. However, it could also refer to increased ABP caused by hormonal outputs of the brain or even any form of hypertension that involves neural signaling. Neurogenic hypertension applies whether the true origin of the hypertension is neural (ie, the primary underlying issue is in the brain or in afferent or efferent nerves) or the origin is non-neural but results in neurally mediated increase in ABP. This is a distinction worth making, as the causative factors are quite distinct. Indeed, the term neurogenic hypertension may encompass too much and relate forms of hypertension that share little in terms of pathogenic mechanism or common mechanistic output. Even if one considers a limited definition of neurogenic hypertension as hypertension resulting from increased sympathetic drive to the cardiovascular system, this could result from an increased activity (or increased relative normal for the given physiological conditions) of different sympathetic nerves with different targets (ie, the sympathetic signature). Yet, what factor(s) increase sympathetic nerve activity (SNA) or enhance neurotransmitter release from sympathetic terminals? If, for example, a circulating substance derived from a certain tissue acted on the brain (or afferent or efferent neurons) to produce a pattern of sympathetic outflow resulting in hypertension, would the hypertension be neurogenic (ie, of neural origin) or neurally mediated hypertension? Nonetheless, primary alterations in neural function can result in hypertension, that is, true neurogenic hypertension. Indeed, several recent advances in understanding central neural control of cardiovascular function have focused on hypertension resulting from specific manipulations in the central nervous system of experimental animals. More typically, however, the recent advances have been in understanding neural changes that may underlie different experimental models of hypertension and how interfering with those neural signals can lower ABP. As noted below, many recent reports apply this approach and shed light on how targeting the brain can be used to treat hypertension. Below, we highlight some recent advances related to neurogenic hypertension, fitting these into this framework. In particular, we focus on recent reports providing new insight into the neural mediation of hypertension associated with high dietary salt intake, obesity, and inflammatory states. We acknowledge several other factors, such as the brain renin–angiotensin system, renal denervation, and altered respiratory–sympathetic coupling, that play important roles but were recently reviewed and lie outside the scope of this brief update.