Baroreflex responses to electrical stimulation of aortic depressor nerve in conscious SHR

Salgado, Hélio César; Barale, Álvaro R.; Castania, Jaci Airton; Machado, Benedito H.; Chapleau, Mark W.; Fazan, Rubens

doi:10.1152/ajpheart.00181.2006

Cited by 49 publications

(64 citation statements)

References 46 publications

(75 reference statements)

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“…In contrast to the total baroreflex transfer function, the transfer function of HR control showed significant depression in dynamic gain in SHR. Although the decreased baroreflex-mediated HR response is primarily attributed to a defect in parasympathetic control (29), the present results obtained in vagotomized rats indicate that the dynamic sympathetic control of HR may also be depressed in SHR. Despite the significant alteration in the sympathetic HR control, the total baroreflex transfer function did not differ between WKY and SHR, suggesting little contribution of HR to the determination of dynamic AP regulation.…”

Section: Discussioncontrasting

confidence: 45%

Dynamic characteristics of baroreflex neural and peripheral arcs are preserved in spontaneously hypertensive rats

Kawada

Shimizu

Kamiya

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Although baroreceptors are known to reset to operate in a higher pressure range in spontaneously hypertensive rats (SHR), the total profile of dynamic arterial pressure (AP) regulation remains to be clarified. We estimated open-loop transfer functions of the carotid sinus baroreflex in SHR and Wistar Kyoto (WKY) rats. Mean input pressures were set at 120 (WKY120 and SHR120) and 160 mmHg (SHR160). The neural arc transfer function from carotid sinus pressure to efferent splanchnic sympathetic nerve activity (SNA) revealed derivative characteristics in both WKY and SHR. The slope of dynamic gain (in decibels per decade) between 0.1 and 1 Hz was not different between WKY120 (10.1 ± 1.0) and SHR120 (10.4 ± 1.1) but was significantly greater in SHR160 (13.2 ± 0.8, P < 0.05 with Bonferroni correction) than in SHR120. The peripheral arc transfer function from SNA to AP showed low-pass characteristics. The slope of dynamic gain (in decibels per decade) did not differ between WKY120 (−34.0 ± 1.2) and SHR120 (−31.4 ± 1.0) or between SHR120 and SHR160 (−32.8 ± 1.3). The total baroreflex showed low-pass characteristics and the dynamic gain at 0.01 Hz did not differ between WKY120 (0.91 ± 0.08) and SHR120 (0.84 ± 0.13) or between SHR120 and SHR160 (0.83 ± 0.11). In both WKY and SHR, the declining slope of dynamic gain was significantly gentler for the total baroreflex than for the peripheral arc, suggesting improved dynamic AP response in the total baroreflex. In conclusion, the dynamic characteristics of AP regulation by the carotid sinus baroreflex were well preserved in SHR despite significantly higher mean AP.

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Section: Discussioncontrasting

confidence: 45%

Dynamic characteristics of baroreflex neural and peripheral arcs are preserved in spontaneously hypertensive rats

Kawada

Shimizu

Kamiya

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Most commonly, baroreflex studies electrically activate all ADN baroreceptors to examine the central control of the baroreflex in several pathological states, such as obesity (2,9,25), hypertension (37), and high sodium intake (14). Such high-intensity shocks may well mask the contributions of the myelinated baroreceptors and reflect primarily the powerful C-fiber baroreflex pathways.…”

Section: Discussionmentioning

confidence: 99%

Diet-induced obesity severely impairs myelinated aortic baroreceptor reflex responses

McCully

Brooks

Andresen

2012

American Journal of Physiology-Heart and Circulatory Physiology

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McCully BH, Brooks VL, Andresen MC. Diet-induced obesity severely impairs myelinated aortic baroreceptor reflex responses. Am J Physiol Heart Circ Physiol 302: H2083-H2091, 2012. First published March 9, 2012; doi:10.1152/ajpheart.01200.2011.-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 ␤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. obesity; autonomic nervous system; arterial baroreflex OBESITY IS ASSOCIATED WITH multisystem morbidity, including endocrine, immune, and autonomic manifestations (3,8,28), such as impairment of the baroreceptor reflex pathways. The depression of baroreceptor reflex sensitivity during weight gain in humans (4, 21) is replicated in animal models of obesity (9,24,25,39,40). Furthermore, the restoration of baroreflex function with weight loss suggests a dynamic interrelationship between diet, metabolic status, and cardiovascular autonomic control (4,21,41,42). Obesity not only increases sympathetic outflow (SNS) to muscle (1, 21) and kidneys (45), but it also decreases cardiac parasympathetic (PNS) drive (6, 36). Because a depressed cardiac PNS baroreflex is an important predictor of cardiac morbidity and mortality (29), independent of blood pressure changes, the mechanisms responsible for baroreflex modification during obesity are critical to understand.Changes in arterial pressure are transmitted via the arterial baroreceptors to the...

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“…16,23,26,27 Similarly, high-frequency STM also becomes saturated in its depressor effect. 28,29 The sigmoidal CSP-AP relationship of the native baroreflex reflects either or both saturations, whereas that of the bionic baroreflex reflects STM saturation.…”

Section: Bionic Pressure Regulation Under Open-loop Conditionsmentioning

confidence: 99%

Bionic Baroreceptor Corrects Postural Hypotension in Rats With Impaired Baroreceptor

et al. 2012

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Background-Impairment of the arterial baroreflex causes orthostatic hypotension. Arterial baroreceptor sensitivity degrades with age. Thus, an impaired baroreceptor plays a pivotal role in orthostatic hypotension in most elderly patients. There is no effective treatment for orthostatic hypotension. The aims of this investigation were to develop a bionic baroreceptor (BBR) and to verify whether it corrects postural hypotension. Methods and Results-The BBR consists of a pressure sensor, a regulator, and a neurostimulator. In 35 Sprague-Dawley rats, we vascularly and neurally isolated the baroreceptor regions and attached electrodes to the aortic depressor nerve for stimulation. To mimic impaired baroreceptors, we maintained intracarotid sinus pressure at 60 mm Hg during activation of the BBR. Native baroreflex was reproduced by matching intracarotid sinus pressure to the instantaneous pulsatile aortic pressure. The encoding rule for translating intracarotid sinus pressure into stimulation of the aortic depressor nerve was identified by a white noise technique and applied to the regulator. The open-loop arterial pressure response to intracarotid sinus pressure (nϭ7) and upright tilt-induced changes in arterial pressure (nϭ7) were compared between native baroreceptor and BBR conditions. The intracarotid sinus pressure-arterial pressure relationships were comparable. Compared with the absence of baroreflex, the BBR corrected tilt-induced hypotension as effectively as under native baroreceptor conditions (native, Ϫ39Ϯ5

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Baroreflex responses to electrical stimulation of aortic depressor nerve in conscious SHR

Cited by 49 publications

References 46 publications

Dynamic characteristics of baroreflex neural and peripheral arcs are preserved in spontaneously hypertensive rats

Dynamic characteristics of baroreflex neural and peripheral arcs are preserved in spontaneously hypertensive rats

Diet-induced obesity severely impairs myelinated aortic baroreceptor reflex responses

Bionic Baroreceptor Corrects Postural Hypotension in Rats With Impaired Baroreceptor

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