Behavior of left ventricular mechanoreceptors with myelinated and nonmyelinated afferent vagal fibers in cats.

Gupta, B. N.; Thames, Marc D.

doi:10.1161/01.res.52.3.291

Cited by 51 publications

(24 citation statements)

References 23 publications

(54 reference statements)

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“…18 Despite data suggesting that the activation of LV mechanoreceptors correlates linearly with LV end-diastolic pressure 19 and that enhanced contrac- tility may have a synergistic (but not independent) effect on receptor discharge, it has also been shown that acute hemorrhage (unloading of the left ventricle) triggers a paradoxical increase in mechanoreceptor activation. Therefore, one cannot disregard the possibility that the lower end-diastolic volume observed in the tilt-positive patients may have had a role in activating LV mechanoreceptors and triggering reflex bradycardia and hypotension.…”

Section: Discussionmentioning

confidence: 99%

Left Ventricular Geometry and Function Preceding Neurally Mediated Syncope

et al. 2000

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Background-Neurally mediated syncope has been associated with increased left ventricular (LV) fractional shortening (FS) during tilt testing, which is consistent with the hypothesis that the stimulation of LV mechanoreceptors leads to reflex hypotension and/or bradycardia. However, FS does not represent true LV contractility because of its dependence on afterload and preload. Methods and Results-To elucidate the role of increased contractility in the mediation of neurally mediated syncope, we compared echocardiographic measures of LV performance corrected for end-systolic stress (ESS) in 21 patients (13 women and 8 men) with unexplained syncope who had either positive (nϭ10) or negative (nϭ11) responses to a tilt-table test. Two-dimensional echocardiographic LV imaging was performed at baseline and during the initial 5 minutes of upright tilt. In the supine position, both groups had similar LV end-diastolic volume indexes, stroke volumes, FS, circumferential ESS, and afterload-independent measures of LV performance (stress-corrected midwall and FS). However, after 5 minutes of upright tilt, patients who subsequently had a positive test had a lower stroke volume, lower stress-corrected midwall shortening, and endocardial FS. The tilt-positive group also had a greater fall in ESS and FS early during upright tilt. Conclusions-Reduced ESS, LV volume, and chamber function during initial upright tilt are associated with a subsequent positive tilt response in patients with unexplained syncope. These data suggest that if paradoxic activation of LV mechanoreceptors has a role in mediating neurally mediated syncope, it is not triggered by LV hypercontractility or increased systolic wall stress during the initial period of upright tilt. (Circulation. 2000;101:777-783.)

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Section: Discussionmentioning

confidence: 99%

Left Ventricular Geometry and Function Preceding Neurally Mediated Syncope

et al. 2000

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“…Procedures of stimulation and methods for controlling against simultaneous co-activation of other cardiorespiratory receptors are described below. Since cardiac mechanoreceptors are sensitive to changes in left ventricular enddiastolic pressure (LVEDP; Oberg & Thor en, 1972;Gupta & Thames, 1983), this variable only is quoted.…”

Section: Stimulation Of Cardiorespiratory Receptors and Controlling Fmentioning

confidence: 99%

“…Since pulse-modulated activity was only seen in cardiac vagal afferents during high and maintained levels of LVEDP (e.g. Oberg & Thor en, 1972;Gupta & Thames, 1983), this may explain the absence of pulse-modulated discharge in DS NTS neurones. In contrast, the lack of pulse modulation of NTS neurones receiving baroreceptor inputs probably reflects the small amplitude of the pulse pressure in the WHBP (see Methods and Results).…”

Section: Veratridine-driven Nts Neurones In the Mousementioning

confidence: 99%

Convergence properties of solitary tract neurones driven synaptically by cardiac vagal afferents in the mouse

Paton

1998

The Journal of Physiology

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Cardiac vagal receptors are chemically and/or mechanically sensitive but it is unknown if this information is preserved centrally within the nucleus of the solitary tract (NTS). The present study had two aims: first, to investigate qualitatively whether both mechanically and chemically sensitive cardiac vagal encoding were preserved within the NTS, and second, to determine the patterns of convergence from other cardiorespiratory afferents to NTS neurones receiving cardiac vagal inputs. The extracellular activity of single NTS neurones was investigated during stimulation of both chemically and mechanically sensitive cardiac vagal receptors in a working heart‐brainstem preparation of mouse. Chemically sensitive cardiac receptors were stimulated using intra‐left ventricular injections of either veratridine (1‐3 μg kg−1), bradykinin (0.25‐1 μg) or prostaglandin E2 (100‐200 ng), whereas the left ventricle was distended to activate cardiac mechanoreceptors. Forty‐three NTS neurones were activated both synaptically by electrical stimulation of the ipsilateral vagus nerve (latency, 35 ± 3 ms), and by intra‐left ventricular injection of veratridine and also, in some cases, by bradykinin and/or PGE2. These NTS neurones were delineated into two populations based on their response to left ventricular distension and convergence properties. Left ventricular distension‐insensitive neurones (n= 30) were excited by stimulation of carotid body chemoreceptors (81 %) but not arterial baroreceptors (3 %; i.e. n= 1 neurone), whereas distension‐sensitive cells (n= 13) were activated mainly by baroreceptors (86 %) rather than peripheral chemoreceptors (14 %; i.e. n= 1 neurone). The data reveal two distinct populations of NTS neurones receiving cardiac vagal inputs: (a) cells responsive to veratridine stimulation only, and (b) neurones activated by both veratridine and mechanical stimuli. The specific convergence pattern of baroreceptors and chemoreceptors to these cardioreceptive NTS neurones is discussed in relation to a common afferent modality integration within the NTS.

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“…The left ventricle is the site of many cardiac sensory receptors. [25][26][27] Nerve endings in the ventricle, the so called C-fiber of the vagus nerve, may be activated mechanically, either by cardiac stretching or by vigorous forceful contraction, or by other chemical stimuli such as catecholamines, veratridine and nicotine.28) The arterial baroreflex is an important buffer for elevations in arterial pressure. A similar reflex, which originates in the heart, is the cardiac mechanoreflex.29) Under normal circumstances, a reduction of systemic venous return reduces cardiac output and arterial blood pressure, which unloads the arterial baroreceptors and diminishes their inhibitory drive to the vasomotor center, resulting in reflex sympathetic activation.…”

mentioning

confidence: 99%