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Plasma and organ catecholamine levels following stimulation of the rat insular cortex
S M Oppenheimer1, T M Saleh, J X Wilson
1Department of Stroke and Aging, Robarts Research Institute, London, Ont., Canada.
Insights
Stimulating the insular cortex in rats can alter heart rate. Tachycardia results from sympathetic nervous system activation, while bradycardia involves parasympathetic mechanisms, indicating distinct neural pathways.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
Background:
- The posterior insular cortex plays a role in regulating heart rate.
- Cardiac chronotropic representation exists within the insular cortex, with distinct areas for tachycardia and bradycardia.
Purpose of the Study:
- To investigate the neural mechanisms underlying heart rate changes induced by insular cortex stimulation.
- To differentiate the roles of the sympathetic and parasympathetic nervous systems in insular cortex-mediated cardiac chronotropy.
Main Methods:
- Phasic stimulation of the insular cortex in ketamine-anesthetized rats, synchronized with the cardiac cycle.
- Measurement of plasma catecholamine levels (norepinephrine and epinephrine).
- Pharmacological blockade using atenolol (beta-blocker) and atropine (anticholinergic).
Main Results:
- Insular stimulation-induced tachycardia correlated with increased plasma norepinephrine, blocked by atenolol, suggesting sympathetic involvement.
- Insular stimulation-induced bradycardia was unaffected by atenolol but blocked by atropine, indicating parasympathetic mediation.
- Cardiac norepinephrine concentration inversely correlated with heart rate during tachycardia stimulation.
- No significant correlation between catecholamines and heart rate was found for bradycardia or control sites.
Conclusions:
- Insular cortex stimulation-induced tachycardia in rats is mediated by the sympathetic nervous system.
- Insular cortex stimulation-induced bradycardia is mediated by parasympathetic mechanisms.
- Sympathetic effects appear localized to cardiac nerves rather than other visceral beds.
Abstract:
The posterior insular cortex of the rat contains an area of cardiac chronotropic representation within which tachycardia sites occur rostrally to those producing bradycardia. In the current study using ketamine-anesthetized rats, the insular cortex was stimulated for 1 h using a phasic technique synchronized with the cardiac cycle. Tachycardia was associated with an increase in plasma norepinephrine concentration; epinephrine remained unchanged. This indicates a neural origin of the norepinephrine increment. The tachycardia response was completely blocked by atenolol. Plasma catecholamine levels remained unchanged during stimulation of insular bradycardia sites. Atenolol was without effect during stimulation-induced bradycardia which was completely blocked by atropine. Total cardiac norepinephrine concentration inversely correlated with change in heart rate during stimulation of tachycardia sites. No correlation between intracardiac catecholamines and heart rate variables was found for the bradycardia or control sites. These results indicate that in the ketamine-anesthetized rat, whereas insular stimulation-induced tachycardia is dependent on the sympathetic nervous system, bradycardia elicited by insular cortex stimulation is mediated by parasympathetic mechanisms. No correlation was identified between renal or skeletal muscle norepinephrine levels and any heart rate parameter. This implies that the sympathetic effects of phasic insular microstimulation may be exerted mainly on cardiac nerves, and less so in other visceral beds.