scholarly journals The Sympathetic Nervous System Mitigates CNS Autoimmunity via β2-Adrenergic Receptor Signaling in Immune Cells

Cell Reports ◽  
2019 ◽  
Vol 28 (12) ◽  
pp. 3120-3130.e5 ◽  
Author(s):  
Leandro Pires Araujo ◽  
Juliana Terzi Maricato ◽  
Marcia Grando Guereschi ◽  
Maisa Carla Takenaka ◽  
Vanessa M. Nascimento ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Immune Cells ◽  
Adrenergic Receptor ◽  
Receptor Signaling ◽  
Cns Autoimmunity ◽  
Β2 Adrenergic Receptor ◽  
Sympathetic Nervous

Abnormal Regulation of the Sympathetic Nervous System in α2A-Adrenergic Receptor Knockout Mice

1999 ◽  
Vol 56 (1) ◽  
pp. 154-161 ◽  
Author(s):  
John D. Altman ◽  
Anne U. Trendelenburg ◽  
Leigh MacMillan ◽  
Dan Bernstein ◽  
Lee Limbird ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Knockout Mice ◽  
Adrenergic Receptor ◽  
Sympathetic Nervous

scholarly journals Local sympathetic neurons promote neutrophil egress from the bone marrow at the onset of acute inflammation

2020 ◽  
Vol 32 (11) ◽  
pp. 727-736 ◽  
Author(s):  
Tomoka Ao ◽  
Junichi Kikuta ◽  
Takao Sudo ◽  
Yutaka Uchida ◽  
Kenta Kobayashi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Immune Cells ◽  
Acute Inflammation ◽  
Sympathetic Neurons ◽  
Dependent Manner ◽  
Adrenergic Signaling ◽  
Sympathetic Nervous

Abstract The sympathetic nervous system plays critical roles in the differentiation, maturation and recruitment of immune cells under homeostatic conditions, and in responses to environmental stimuli, although its role in the migratory control of immune cells during acute inflammation remains unclear. In this study, using an advanced intravital bone imaging system established in our laboratory, we demonstrated that the sympathetic nervous system locally regulates neutrophil egress from the bone marrow for mobilization to inflammatory foci. We found that sympathetic neurons were located close to blood vessels in the bone marrow cavity; moreover, upon lipopolysaccharide (LPS) administration, local sympathectomy delayed neutrophil egress from the bone marrow and increased the proportion of neutrophils that remained in place. We also showed that vascular endothelial cells produced C-X-C motif chemokine ligand 1 (CXCL1), which is responsible for neutrophil egress out of the bone marrow. Its expression was up-regulated during acute inflammation, and was suppressed by β-adrenergic receptor blockade, which was accompanied with inhibition of neutrophil egress into the systemic circulation. Furthermore, systemic β-adrenergic signaling blockade decreased the recruitment of neutrophils in the lung under conditions of acute systemic inflammation. Taken together, the results of this study first suggested a new regulatory system, wherein local sympathetic nervous activation promoted neutrophil egress by enhancing Cxcl1 expression in bone marrow endothelial cells in a β-adrenergic signaling-dependent manner, contributing to the recruitment of neutrophils at the onset of inflammation in vivo.

scholarly journals Prenatal cold exposure causes hypertension in offspring by hyperactivity of the sympathetic nervous system

2019 ◽  
Vol 133 (9) ◽  
pp. 1097-1113 ◽  
Author(s):  
Ken Chen ◽  
Dongdong Sun ◽  
Shuang Qu ◽  
Yue Chen ◽  
Jialiang Wang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Cold Exposure ◽  
Sodium Excretion ◽  
Adrenergic Receptor ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Sympathetic Nervous

Abstract Environmental temperature plays a role in the variation of blood pressure. Maternal cold stress could affect the physiological phenotype of the offspring, including blood pressure elevation. In the present study, we found that adult offspring of dams exposed to cold have increased systolic and diastolic blood pressure, and decreased urine volume and sodium excretion, accompanied by increased heart rate and heart rate variability, secondary to increased activity of the sympathetic nervous system. Renal denervation or adrenergic receptor blockade decreased blood pressure and increased sodium excretion. The increase in peripheral sympathetic nerve activity can be ascribed to the central nervous system because administration of clonidine, a centrally acting α2 adrenergic receptor agonist, lowered blood pressure to a greater degree in the prenatal cold-exposed than control offspring. Moreover, these prenatal cold-exposed offspring had hypothalamic paraventricular nucleus (PVN) disorder because magnetic resonance spectroscopy showed decreased N-acetylaspartate and increased choline and creatine ratios in the PVN. Additional studies found that prenatal cold exposure impaired the balance between inhibitory and excitatory neurons. This led to PVN overactivation that was related to enhanced PVN-angiotensin II type 1 (AT1) receptor expression and function. Microinjection of the AT1 receptor antagonist losartan in the PVN lowered blood pressure to a greater extent in prenatal cold-exposed that control offspring. The present study provides evidence for overactive peripheral and central sympathetic nervous systems in the pathogenesis of prenatal cold-induced hypertension. Central AT1 receptor blockade in the PVN may be a key step for treatment of this type hypertension.

Hypertension in l-NAME-treated diabetic rats depends on an intact sympathetic nervous system

2002 ◽  
Vol 282 (4) ◽  
pp. R1070-R1076 ◽  
Author(s):  
Sharyn M. Fitzgerald ◽  
Michael W. Brands
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Adrenergic Receptor ◽  
Pressor Response ◽  
Plasma Renin ◽  
Progressive Increase ◽  
Diabetic Rats ◽  
Nitric Oxide Synthase Inhibitor ◽  
Sympathetic Nervous

We demonstrated previously that induction of diabetes in rats that were treated chronically with the nitric oxide synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME) causes a severe, progressive increase in mean arterial pressure. This study tested the role of the sympathetic nervous system in that response. Rats were instrumented with chronic artery and vein catheters and assigned randomly to four diabetic groups pretreated with vehicle (D), l-NAME (D+L), the α1- and β-adrenergic receptor antagonists terazosin and propranolol (D+B), or l-NAME, terazosin, and propranolol (D+LB). After baseline measurements were taken, rats were pretreated; 6 days later, streptozotocin was administered and 3 wk of diabetes ensued. D+L rats had a marked, progressive increase in arterial pressure that by day 20 was ∼60 mmHg greater than in D rats. The pressor response to l-NAME was significantly attenuated in diabetic rats cotreated with adrenergic blockers. During week 1 of diabetes, plasma renin activity (PRA) increased and then returned to control levels in D rats. PRA increased progressively in D+L rats, and chronic adrenergic receptor blockade restored the biphasic renin response in D+LB rats. These results suggest that the sympathetic nervous system may be involved in the hypertensive response to onset of diabetes inl-NAME-treated rats, possibly through control of renin secretion.

Sign in / Sign up

Export Citation Format

Share Document