Addressing the relationship between sympathetic activity and inflammation

Abstract

In this issue of the Journal, Maritta K. Pö yhö nen-Alho and coworkers present an intriguing study on the effects of differential antihypertensive medication (central-sympatholytic agent versus b-blocker) on insulin sensitivity and markers of inflammation in hypertensive overweight postmenopausal women [1].A total of 87 women not taking any medication including hormone-replacement therapy were enrolled into the study. They were randomized to antihypertensive treatment with either atenolol 50 mg per day or moxonidine 0,3 mg twice daily.The authors applied assays for C-reactive protein (CRP), interleukin (IL)-6, tumor necrosis factor-alpha (TNFa), TNFa-RII and adiponectin and measured insulin sensitivity with an oral glucose tolerance test and calculation of the insulin-sensitivity index. The authors observed an increase in TNFa in the atenolol group as opposed to a decrease in TNFa in the moxonidine group. Adiponectine decreased in the atenolol-treated women and did not change significantly in women receiving moxonidine. The other parameters did not change with either treatment. Thus, the authors were able to show that a central sympatholytic agent reduces the level of a proinflammatory cytokine without affecting adiponectin levels in hypertensive overweight postmenopausal women.This study has intriguing findings as it relates pharmacological-central blockade of the sympathetic nervous system to a reduction in inflammatory markers. Peripheral b blockade did not have these beneficial effects. The effects of moxonidine were observed in a population of hypertensive overweight postmenopausal women -thus a population likely to have increased sympathetic tone and increased markers of inflammation [2,3]. The effects of moxonidine were not attributable to a more pronounced decrease in blood pressure with moxonidine.

Multiomics characteristics of neurogenesis-related gene are dysregulated in tumor immune microenvironment

“…Although these drugs have totally different molecular targets, as these results predicted, the potential of these drugs in immune modulation has been supported by an increasing number of recently published articles. For example, histone deacetylase inhibitors (HDACs) are regarded as promising drug candidates by combining them with immunotherapy 30 – 33 , and moxonidine 34 – 37 , β-escin 38 , 39 and AH23848 40 – 46 have shown potential in cytokine signaling modulation and inflammation regulation in published reports. However, whether these drugs can directly affect antitumor immunity in vivo and whether they can enhance the effect of immunotherapy still need to be further explored.…”

Modulation of Voltage-Gated Ca2+ Channels by G Protein-Coupled Receptors in Celiac-Mesenteric Ganglion Neurons of Septic Rats

“…Sepsis compromises the function of both the immune and autonomic nervous systems as well as their interaction [ 2 , 5 , 6 ]. Hemodynamic instability observed during sepsis, including the loss of systemic vascular resistance, may result from an imbalance between sympathetic and parasympathetic activity.…”