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Published on: February 14, 2021
Diet-induced obesity severely impairs myelinated aortic baroreceptor reflex responses
Belinda H McCully1, Virginia L Brooks, Michael C Andresen
1Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR 97239, USA. houghtob@ohsu.edu
Abstract:
Diet-induced obesity (DIO) attenuates the arterial cardiac baroreceptor reflex, but the mechanisms and sites of action are unknown. This study tested the hypothesis that DIO impairs central aortic baroreceptor pathways. Normal chow control (CON) and high-fat-chow obesity-resistant (OR) and obesity-prone (OP) rats were anesthetized (inactin, 120 mg/kg) and underwent sinoaortic denervation. The central end of the aortic depressor nerve (ADN) was electrically stimulated to generate frequency-dependent baroreflex curves (5-100 Hz) during selective activation of myelinated (A-fiber) or combined (A- and C-fiber) ADN baroreceptors. A mild stimulus (1 V) that activates only A-fiber ADN baroreceptors induced robust, frequency-dependent depressor and bradycardic responses in CON and OR rats, but these responses were completely abolished in OP rats. Maximal activation of A fibers (3 V) elicited frequency-dependent reflexes in all groups, but a dramatic deficit was still present in OP rats. Activation of all ADN baroreceptors (20 V) evoked even larger reflex responses. Depressor responses were nearly identical among groups, but OP rats still exhibited attenuated bradycardia. In separate groups of rats, the reduced heart rate (HR) response to maximal activation of ADN A fibers (3 V) persisted in OP rats following pharmacological blockade of β(1)-adrenergic or muscarinic receptors, suggesting deficits in both parasympathetic nervous system (PNS) and sympathetic nervous system (SNS) reflex pathways. However, the bradycardic responses to direct efferent vagal stimulation were similar among groups. Taken together, our data suggest that DIO severely impairs the central processing of myelinated aortic baroreceptor control of HR, including both PNS and SNS components.
Insights
Diet-induced obesity impairs the central processing of aortic baroreceptor reflexes. Obesity-prone rats show abolished heart rate responses to aortic depressor nerve stimulation, indicating impaired autonomic control.
Area of Science:
- Cardiovascular Physiology
- Autonomic Nervous System Regulation
- Obesity Pathophysiology
Background:
- Diet-induced obesity (DIO) is known to attenuate arterial baroreflex function.
- The specific mechanisms and central sites of action for this impairment remain largely unknown.
Purpose of the Study:
- To investigate whether DIO impairs central aortic baroreceptor pathways.
- To determine the impact of obesity on the processing of baroreflex signals originating from the aortic depressor nerve (ADN).
Main Methods:
- Utilized Sprague-Dawley rats categorized as obesity-resistant (OR) and obesity-prone (OP) fed either control (CON) or high-fat diets.
- Performed sinoaortic denervation and electrically stimulated the central end of the ADN to activate myelinated (A-fiber) or combined (A- and C-fiber) baroreceptors.
- Assessed frequency-dependent depressor and bradycardic responses, and evaluated heart rate (HR) responses after pharmacological blockade of adrenergic and muscarinic receptors.
Main Results:
- Obesity-prone rats exhibited a complete abolition of depressor and bradycardic responses to low-level A-fiber ADN stimulation, unlike CON and OR rats.
- While maximal A-fiber activation elicited reflexes in all groups, OP rats showed significant deficits in bradycardia, which persisted after receptor blockade.
- OP rats demonstrated attenuated bradycardia even with maximal ADN activation and direct vagal nerve stimulation, suggesting central processing deficits.
Conclusions:
- Diet-induced obesity severely impairs the central processing of myelinated aortic baroreceptor signals controlling heart rate.
- These impairments involve both parasympathetic nervous system (PNS) and sympathetic nervous system (SNS) reflex pathways.
- The findings highlight a critical role for central autonomic pathways in mediating the cardiovascular consequences of obesity.
