Dominant role of aortic baroreceptors in the cardiac baroreflex of the rat in situ

Pickering, Anthony E.; Simms, Annabel E.; Paton, Julian F. R.

doi:10.1016/j.autneu.2008.03.009

Cited by 32 publications

(36 citation statements)

References 30 publications

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“…This may have contributed to the difference between this study and our previous study examining sSNA, in which we demonstrated comparatively normal gain in the LPK rats [20]. However, baroreceptor afferent input is also communicated via the carotid sinus nerve [36,37], and significant disruption to sympathetic baroreflex function is only seen after the ADN and both carotid sinus nerves are sectioned [38]. With regards to the peripheral chemoreflex responses, the rat ADN does not carry functional chemoreceptor fibres [39], with chemoreceptor afferent nerves located in the carotid sinus nerve as a branch of the glossopharyngeal nerve [38].…”

Section: Discussioncontrasting

confidence: 76%

“…However, baroreceptor afferent input is also communicated via the carotid sinus nerve [36,37], and significant disruption to sympathetic baroreflex function is only seen after the ADN and both carotid sinus nerves are sectioned [38]. With regards to the peripheral chemoreflex responses, the rat ADN does not carry functional chemoreceptor fibres [39], with chemoreceptor afferent nerves located in the carotid sinus nerve as a branch of the glossopharyngeal nerve [38]. As we observed robust responses to activation of the baroreceptor and peripheral chemoreceptor reflexes in the vagotomized Lewis controls, comparable to our previous studies in vagotomized Sprague Dawley rats [40], we consider it unlikely the vagotomized preparation had any significant impact upon our assessment of baroreflex and peripheral chemoreflex function in this study.…”

Section: Discussionmentioning

confidence: 99%

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The effect of losartan on differential reflex control of sympathetic nerve activity in chronic kidney disease

Yao

Hildreth

Farnham³

et al. 2015

Journal of Hypertension

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Section: Discussioncontrasting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

The effect of losartan on differential reflex control of sympathetic nerve activity in chronic kidney disease

Yao

Hildreth

Farnham³

et al. 2015

Journal of Hypertension

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“…If constriction loops located directly over the heart transmitted external pressures to the thoracic cavity and ultimately to the aorta, this increased pressure could have stimulated the aortic arch baroreceptors to induce bradycardia. Interestingly, our results are consistent with recent work in rats showing that the baroreceptors found in the aortic arch play a dominant role in controlling the cardiac (f H ) component of the baroreflex while the carotid baroreceptors tend to drive inhibition of sympathetic outflow to the vasculature (Pickering et al, 2008). Although our results are limited in this regard, two of the three rats that responded with an increased f H (tachycardia rather than bradycardia) were constricted around the neck, not the thorax.…”

Section: Effect Of Constriction On Cardiac Electrical Functionsupporting

confidence: 80%

Snake constriction rapidly induces circulatory arrest in rats

Boback

McCann

Wood

et al. 2015

Journal of Experimental Biology

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As legless predators, snakes are unique in their ability to immobilize and kill their prey through the process of constriction, and yet how this pressure incapacitates and ultimately kills the prey remains unknown. In this study, we examined the cardiovascular function of anesthetized rats before, during and after being constricted by boas (Boa constrictor) to examine the effect of constriction on the prey's circulatory function. The results demonstrate that within 6 s of being constricted, peripheral arterial blood pressure (PBP) at the femoral artery dropped to 1/2 of baseline values while central venous pressure (CVP) increased 6-fold from baseline during the same time. Electrocardiographic recordings from the anesthetized rat's heart revealed profound bradycardia as heart rate (f H ) dropped to nearly half of baseline within 60 s of being constricted, and QRS duration nearly doubled over the same time period. By the end of constriction (mean 6.5±1 min), rat PBP dropped 2.9-fold, f H dropped 3.9-fold, systemic perfusion pressure (SPP=PBP−CVP) dropped 5.7-fold, and 91% of rats (10 of 11) had evidence of cardiac electrical dysfunction. Blood drawn immediately after constriction revealed that, relative to baseline, rats were hyperkalemic (serum potassium levels nearly doubled) and acidotic (blood pH dropped from 7.4 to 7.0). These results are the first to document the physiological response of prey to constriction and support the hypothesis that snake constriction induces rapid prey death due to circulatory arrest.

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“…In support, Sanders et al (1988) showed that stimulation of the aortic baroreflexes, but not carotid sinus reflexes, produced a substantial and sustained inhibition of muscle sympathetic nervous activity in humans. Prior studies (Dampney et al 1971;Donald and Edis 1971;Pelletier et al 1972;Pickering et al 2008;Sanders et al 1988) have also shown that the cardiac baroreflex is critically dependent upon the aortic afferents with relatively little contribution from the carotid sinus. All together, these results indicate that the aortic baroreflex has a more dominant role than the carotid baroreflex in overall blood pressure regulation.…”

Section: The Cns Is a Major Source Of Post-sad Apvmentioning

confidence: 93%

Neural control of arterial pressure variability in the neuromuscularly blocked rat

Tang

2011

Eur J Appl Physiol

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The baroreflexes stabilize moment-to-moment arterial pressure. Sinoaortic denervation (SAD) of the baroreflexes results in a large increase in arterial pressure variability (APV) across various species. Due to an incomplete understanding of the nonlinear interactions between central and peripheral systems, the major source of APV remains controversial. While some studies suggested that the variability is endogenous to the central nervous system (CNS), others argued that peripheral influences may be the main source. For decades, abnormal cardiovascular variability has been associated with a number of cardiovascular diseases including hypertension, heart failure, and stroke. Delineating mechanisms of the APV is critical for the improvement of current strategies that use APV as a clinical tool for the diagnosis and prognosis of cardiovascular diseases. In this study, with a unique chronic neuromuscularly blocked (NMB) rat preparation that largely constrains peripheral influences, we determined the CNS contribution to the post-SAD APV. First, we confirmed that SAD significantly increased APV in the NMB rat, then demonstrated that post-SAD ganglionic blockade substantially reduced APV, and subsequent intravenous infusions of phenylephrine and epinephrine (in presence of ganglionic blockade) only slightly increased APV. These data suggest that the CNS is an important source, and skeletal activity, thermal challenges or other forms of peripherally generated cardiovascular stress are not required for the post-SAD APV. In addition, we showed that bilateral aortic denervation produced a larger increase in APV than bilateral carotid sinus denervation, suggesting that the aortic baroreflex plays a more dominant role in the control of APV than the carotid sinus.

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Dominant role of aortic baroreceptors in the cardiac baroreflex of the rat in situ

Cited by 32 publications

References 30 publications

The effect of losartan on differential reflex control of sympathetic nerve activity in chronic kidney disease

The effect of losartan on differential reflex control of sympathetic nerve activity in chronic kidney disease

Snake constriction rapidly induces circulatory arrest in rats

Neural control of arterial pressure variability in the neuromuscularly blocked rat

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