Abstract
The central nervous system (CNS) in concert with the heart and vasculature is essential to maintaining cardiovascular (CV) homeostasis. In recent years, our understanding of CNS control of blood pressure regulation (and dysregulation leading to hypertension) has evolved substantially to include (i) the actions of signaling molecules that are not classically viewed as CV signaling molecules, some of which exert effects at CNS targets in a non-traditional manner, and (ii) CNS locations not traditionally viewed as central autonomic cardiovascular centers. This review summarizes recent work implicating immune signals and reproductive hormones, as well as gasotransmitters and reactive oxygen species in the pathogenesis of hypertension at traditional CV control centers. Additionally, recent work implicating non-conventional CNS structures in CV regulation is discussed.
Highlights
According to the World Health Organization (WHO), cardiovascular (CV) disease accounts for approximately 17 million deaths a year worldwide[1], of which more than half (9.4 million) are attributable to complications of hypertension[2]
A recent study demonstrating that acute microinjection of relaxin-2 into the paraventricular nucleus (PVN) increased sympathetic outflow and blood pressure (BP) in spontaneously hypertensive rats (SHRs), whereas chronic PVN administration caused a profound increase in BP in normotensive rats[74], supports the conclusion that there are multiple central targets for this reproductive hormone/neurotransmitter
Further study of the actions of traditional CV signals within these non-traditional CV central nervous system (CNS) centers may elucidate previously unknown roles of these regions in normal CV regulation. In this brief review, we have highlighted some emerging new perspectives which over the past 20 years contributed new and important information to the evolution of our understanding of CNS mechanisms involved in central CV control
Summary
According to the World Health Organization (WHO), cardiovascular (CV) disease accounts for approximately 17 million deaths a year worldwide[1], of which more than half (9.4 million) are attributable to complications of hypertension[2]. A recent study demonstrating that acute microinjection of relaxin-2 into the PVN increased sympathetic outflow and BP in SHR, whereas chronic PVN administration caused a profound increase in BP in normotensive rats[74], supports the conclusion that there are multiple central targets for this reproductive hormone/neurotransmitter This same study revealed that neutralization of endogenous relaxin reduced BP in SHR but had no significant effect in WKY74, suggesting a role for relaxin in the pathogenesis of hypertension. Superoxide dismutase (SOD), an enzyme that metabolizes superoxide, overexpression in the brain abolished the hypertensive response normally observed in response to icv ANG II administration[119], whereas specific SOD3 deletion in the SFO increased baseline BP and potentiated ANG II-induced increases in BP120 This same study showed that ROS in the SFO leads to infiltration by activated lymphocytes in the peripheral vasculature[120], linking oxidative stress in the CNS with immune activation in the periphery, which in concert would serve to intensify hypertension. Further study of the actions of traditional CV signals (such as ANG II) within these non-traditional CV CNS centers may elucidate previously unknown roles of these regions in normal CV regulation
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