The role of peripheral catecholamines in mediating the pressor and tremorigenic effects of oxotremorine were investigated in conscious rats. At time of peak tremor intensity induced by oxotremorine, plasma adrenaline and noradrenaline were increased 3--4-fold. Tremor intensity was substantially reduced by either adrenal medullectomy, chemical sympathectomy with 6-hydroxydopamine, or injection of 2.5 mg/kg L-propranolol. The pressor response to oxotremorine was not reduced by adrenal denervation, which however prevented the usual rise in plasma adrenaline but not that of noradrenaline. It is concluded that central cholinergic receptor stimulation activates the sympatho-adrenal system. While both adrenaline and intact sympathetic nerves are necessary for the mediation of the full tremorigenic effect, the pressor response to oxotremorine is mainly due to the effect of noradrenaline on vascular alpha-receptors.

Download full-text PDF

Source
http://dx.doi.org/10.1159/000388821DOI Listing

Publication Analysis

Top Keywords

peripheral catecholamines
8
central cholinergic
8
cholinergic receptor
8
receptor stimulation
8
tremor intensity
8
plasma adrenaline
8
adrenaline noradrenaline
8
reduced adrenal
8
pressor response
8
response oxotremorine
8

Similar Publications

Biomarkers.

Alzheimers Dement

December 2024

Alzheimer's disease and other cognitive disorders unit, Hospital Clínic, IDIBAPS, Barcelona, Spain.

Background: Sleep-wake alterations are common symptoms in Alzheimer's Disease (AD) associated with faster cognitive decline. Noradrenaline dysfunction and neuroinflammation have been proposed as potential driving mechanisms. The ADIS project aims to study the relationship between sleep-wake patterns, immune signatures (peripheral blood cytotoxic lymphocytes), and noradrenergic markers across the AD spectrum.

View Article and Find Full Text PDF

Myxoedema coma is a rare medical emergency, presenting even less commonly without sepsis and with the diagnosis of distributive shock. Reports of catecholamine-refractory shock are scarce. This report describes the case of a 54-year-old male, who presented to the emergency department with altered mental status.

View Article and Find Full Text PDF

Chronic stress is associated with a higher risk for carcinogenesis as well as age-related diseases and immune dysfunction. There is evidence showing that psychological stress can contribute to premature immunosenescence. Therefore, the question arose whether chronic exposure to catecholamine could drive immune cells into senescence.

View Article and Find Full Text PDF

Effect of regional crosstalk between sympathetic nerves and sensory nerves on temporomandibular joint osteoarthritic pain.

Int J Oral Sci

January 2025

Department of Stomatology, Tangdu Hospital & State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, School of Stomatology, The Fourth Military Medical University, Xi'an, China.

Temporomandibular joint osteoarthritis (TMJ-OA) is a common disease often accompanied by pain, seriously affecting physical and mental health of patients. Abnormal innervation at the osteochondral junction has been considered as a predominant origin of arthralgia, while the specific mechanism mediating pain remains unclear. To investigate the underlying mechanism of TMJ-OA pain, an abnormal joint loading model was used to induce TMJ-OA pain.

View Article and Find Full Text PDF

Psychosocial stress has been proposed to induce a redistribution of immune cells, but a comparison with an active placebo-psychosocial stress control condition is lacking so far. We investigated immune cell redistribution due to psychosocial stress compared to that resulting from an active placebo-psychosocial stress but otherwise identical control condition. Moreover, we tested for mediating effects of endocrine parameters and blood volume changes.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!