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Quantifying Acute Changes in Renal Sympathetic Nerve Activity in Response to Central Nervous System Manipulations in Anesthetized Rats
Published on: September 11, 2018
Central cholinergic modulation of blood pressure short-term variability
Sanja Milutinović1, David Murphy, Nina Japundzić-Zigon
1Laboratory for Cardiovascular Pharmacology, Institute of Pharmacology, Clinical Pharmacology and Toxicology, School of Medicine, University of Belgrade, P.O. Box 840, 11129 Belgrade, Serbia and Montenegro.
Central cholinergic neurons facilitate cardiovascular variability. Physostigmine increased systolic arterial pressure (SAP) and its low-frequency (LF) and high-frequency (HF) components, suggesting central nervous system involvement.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Pharmacology
Background:
- Acetylcholine plays a crucial role in central nervous system functions.
- Understanding the central modulation of cardiovascular short-term variability is vital for managing cardiovascular health.
Purpose of the Study:
- To investigate the role of centrally acting acetylcholine in modulating cardiovascular short-term variability.
- To elucidate the specific pathways involved in cholinergic cardiovascular control.
Main Methods:
- Experiments were conducted on instrumented conscious rats.
- Physostigmine, a cholinesterase inhibitor, was used as a pharmacological probe.
- Spectral analysis of systolic arterial pressure (SAP), diastolic arterial pressure (DAP), and heart rate (HR) was performed.
Main Results:
- Physostigmine increased SAP and its low-frequency (LF) and high-frequency (HF) variability.
- Neostigmine decreased heart rate (HR) but did not affect HR variability.
- Pharmacological antagonists indicated involvement of muscarinic, sympathetic, and vasopressin pathways.
Conclusions:
- Central cholinergic neurons facilitate, but do not solely generate, LF and HF SAP variability.
- Physostigmine's effects on LF SAP involve central muscarinic sites and the peripheral sympathetic system.
- Non-muscarinic central sites and vasopressin pathways contribute to the increase in HF SAP.
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