Autonomic Regulation of the Cardiovascular System: Diseases, Treatments, and Novel Approaches

Abstract

The autonomic nervous system (ANS) integrates the involuntary physiological activities of visceral organs that are vital for survival. In particular, the ANS controls heart rate, blood pressure, breathing, gastrointestinal contraction and secretion, and electrolyte and fluid homeostasis. Many studies have focused on understanding the neural mechanisms of autonomic dysfunction or neuropathy in pathophysiological states including hypertension, heart failure, orthostatic hypotension, stroke, hypoxia, sleep apnea, diabetes, and metabolic disorders. In these diseases and conditions, the function of the ANS is altered, leading to autonomic neuropathy. The effect of autonomic neuropathy ranges from mild to life-threatening. However, the mechanisms of autonomic neuropathy in the pathological states are not well understood and have yet to be elucidated. For this special issue, the Editor-in-Chief of Neuroscience Bulletin invited Dr. Qing-Hui Chen as a Guest Editor to organize and gather a number of investigators in this field to contribute original research articles that address the underlying neural mechanisms and significance of autonomic dysfunction in the pathogenesis of these diseases and provide potential interventions. Furthermore, the invited review articles contribute to the recent understanding of the mechanisms of autonomic function and dysregulation, which may provide novel approaches and strategies to decipher the complicated autonomic neural network. Hypertension is a devastating cardiovascular disease. In this issue, spontaneous hypertension, salt-sensitive hypertension, and obesity-related hypertension are discussed. Sympathetic overactivity is currently considered as an important mechanism for the development of hypertension. The activation of pre-sympathetic neurons in the hypothalamic paraventricular nucleus (PVN) and the rostral ventrolateral medulla (RVLM), the main source of excitatory synaptic input to sympathetic preganglionic neurons in the spinal cord, both contribute to sympathetic overactivity. Li and colleagues review the cellular and molecular mechanisms underlying the hyperactivity of pre-sympathetic neurons in the PVN which may lead to the increase in sympathetic outflow in spontaneously hypertensive rats (SHRs), a model of primary hypertension [1]. Kang and colleagues examine the antioxidative effect of Metformin (MET) in salt-induced hypertension. Their study suggests that central MET administration reduces sympathetic outflow and arterial pressure (AP) by attenuating oxidative stress, inhibiting the renin-angiotensin system, and restoring the balance between excitatory and inhibitory neurotransmitters in the PVN [2]. Furthermore, Kang and colleagues also show that the increased AP and sympathetic nerve activity (SNA) can be suppressed by blockade of endogenous angiotensin (Ang-1–7) in salt-induced hypertension through the modulation of proinflammatory cytokines and oxidative stress [3]. Using the obesityrelated hypertensive (OH) rat model, Zhou and colleagues investigate the effects of PVN intermedin (IMD) on the sympathetic activation induced by chronic systemic & Zixi Jack Cheng [email protected]