Impaired Hypothalamic Regulation of Sympathetic Outflow in Primary Hypertension.
10.1007/s12264-018-0316-5
- Author:
Jing-Jing ZHOU
1
;
Hui-Jie MA
1
;
Jian-Ying SHAO
1
;
Hui-Lin PAN
1
;
De-Pei LI
2
Author Information
1. Division of Anesthesiology and Critical Care, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
2. Department of Medicine, Center for Precision Medicine, University of Missouri, Columbia, MO, 65212, USA. lidep@health.missouri.edu.
- Publication Type:Journal Article
- Keywords:
Essential hypertension;
Hypothalamus;
Paraventricular nucleus;
Sympathetic nervous system;
Synaptic plasticity
- MeSH:
Animals;
Blood Pressure;
physiology;
Excitatory Postsynaptic Potentials;
physiology;
Humans;
Hypertension;
physiopathology;
Hypothalamus;
physiology;
Neurons;
physiology;
Paraventricular Hypothalamic Nucleus;
physiology
- From:
Neuroscience Bulletin
2019;35(1):124-132
- CountryChina
- Language:English
-
Abstract:
The hypothalamic paraventricular nucleus (PVN) is a crucial region involved in maintaining homeostasis through the regulation of cardiovascular, neuroendocrine, and other functions. The PVN provides a dominant source of excitatory drive to the sympathetic outflow through innervation of the brainstem and spinal cord in hypertension. We discuss current findings on the role of the PVN in the regulation of sympathetic output in both normotensive and hypertensive conditions. The PVN seems to play a major role in generating the elevated sympathetic vasomotor activity that is characteristic of multiple forms of hypertension, including primary hypertension in humans. Recent studies in the spontaneously hypertensive rat model have revealed an imbalance of inhibitory and excitatory synaptic inputs to PVN pre-sympathetic neurons as indicated by impaired inhibitory and enhanced excitatory synaptic inputs in hypertension. This imbalance of inhibitory and excitatory synaptic inputs in the PVN forms the basis for elevated sympathetic outflow in hypertension. In this review, we discuss the disruption of balance between glutamatergic and GABAergic inputs and the associated cellular and molecular alterations as mechanisms underlying the hyperactivity of PVN pre-sympathetic neurons in hypertension.
