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Choline administration reverses hypotension in spinal cord transected rats: the involvement of vasopressin
1Department of Pharmacology, Uludag University Medical Faculty, Bursa, Turkey. vsavci@uu20.bim.uludag.edu.tr
Insights
Choline administration effectively reverses hypotension in rats with spinal cord transection by activating central nicotinic receptors. This process involves increased vasopressin and modulated heart rate via nicotinic and muscarinic pathways.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Pharmacology
Background:
- Spinal cord transection leads to hypotension and cardiovascular dysfunction.
- The role of choline in modulating cardiovascular responses in spinal shock requires further elucidation.
Purpose of the Study:
- To investigate the cardiovascular effects of choline in spinal cord-transected rats.
- To determine the underlying neurochemical mechanisms of choline's action on blood pressure, heart rate, and vasopressin release.
Main Methods:
- Administration of choline intracerebroventricularly (i.c.v.) and intraperitoneally in spinal cord-transected rats.
- Pharmacological blockade of nicotinic, muscarinic, and vasopressin V1 receptors.
- Measurement of blood pressure, heart rate, and plasma vasopressin levels.
Main Results:
- Intracerebroventricular choline increased blood pressure and decreased heart rate, an effect partially mimicked by intraperitoneal administration.
- Choline-induced pressor response was associated with increased plasma vasopressin and mediated by central nicotinic receptors.
- Bradycardia was mediated by both nicotinic and muscarinic receptors, while vasopressin V1 receptor antagonism abolished the pressor response.
Conclusions:
- Choline effectively restores hypotension in spinal shock by activating central nicotinic receptors through presynaptic mechanisms.
- Choline's cardiovascular effects involve a complex interplay of central nicotinic and muscarinic pathways, alongside vasopressin modulation.
Abstract:
Intracerebroventricular (i.c.v.) choline (50-150 microg) increased blood pressure and decreased heart rate in spinal cord transected, hypotensive rats. Choline administered intraperitoneally (60 mg/kg), also, increased blood pressure, but to a lesser extent. The pressor response to i.c.v. choline was associated with an increase in plasma vasopressin. Mecamylamine pretreatment (50 microg; i.c.v.) blocked the pressor, bradycardic and vasopressin responses to choline (150 microg). Atropine pretreatment (10 microg; i.c.v.) abolished the bradycardia but failed to alter pressor and vasopressin responses. Hemicholinium-3 [HC-3 (20 microg; i.c.v.)] pretreatment attenuated both bradycardia and pressor responses to choline. The vasopressin V1 receptor antagonist, (beta-mercapto-beta,beta-cyclopenta-methylenepropionyl1, O-Me-Tyr2, Arg8)-vasopressin (10 microg/kg) administered intravenously 5 min after choline abolished the pressor response and attenuated the bradycardia-induced by choline. These data show that choline restores hypotension effectively by activating central nicotinic receptors via presynaptic mechanisms, in spinal shock. Choline-induced bradycardia is mediated by central nicotinic and muscarinic receptors. Increase in plasma vasopressin is involved in cardiovascular effects of choline.