Mechanosensory transduction of vagal and baroreceptor afferents revealed by study of isolated nodose neurons in culture

Snitsarev, Vladislav; Whiteis, Carol A.; Abboud, François M.; Chapleau, Mark W.

doi:10.1016/s1566-0702(02)00033-4

Cited by 39 publications

(37 citation statements)

References 22 publications

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“…ENaC subunits are also expressed in the nodose ganglia which receive inputs from arterial baroreceptors and it has thus been suggested that they are directly involved in sensing pressure changes transmitted from the aortic arch (107,358), although amiloride did not block mechanosensitive currents evoked from nodose ganglia elicited by hypotonic solutions (102). ENaC may additionally play a role in the central control of blood pressure.…”

Section: Other Roles For Enac In Vascular-cardio-renal Diseasementioning

confidence: 99%

ENaCs and ASICs as therapeutic targets

Qadri

Rooj

Fuller

2012

American Journal of Physiology-Cell Physiology

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The epithelial Na+channel (ENaC) and acid-sensitive ion channel (ASIC) branches of the ENaC/degenerin superfamily of cation channels have drawn increasing attention as potential therapeutic targets in a variety of diseases and conditions. Originally thought to be solely expressed in fluid absorptive epithelia and in neurons, it has become apparent that members of this family exhibit nearly ubiquitous expression. Therapeutic opportunities range from hypertension, due to the role of ENaC in maintaining whole body salt and water homeostasis, to anxiety disorders and pain associated with ASIC activity. As a physiologist intrigued by the fundamental mechanics of salt and water transport, it was natural that Dale Benos, to whom this series of reviews is dedicated, should have been at the forefront of research into the amiloride-sensitive sodium channel. The cloning of ENaC and subsequently the ASIC channels has revealed a far wider role for this channel family than was previously imagined. In this review, we will discuss the known and potential roles of ENaC and ASIC subunits in the wide variety of pathologies in which these channels have been implicated. Some of these, such as the role of ENaC in Liddle's syndrome are well established, others less so; however, all are related in that the fundamental defect is due to inappropriate channel activity.

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Section: Other Roles For Enac In Vascular-cardio-renal Diseasementioning

confidence: 99%

ENaCs and ASICs as therapeutic targets

Qadri

Rooj

Fuller

2012

American Journal of Physiology-Cell Physiology

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“…21,23,24 The tip of the pipette was placed 10 m from the cell surface. Depolarizing potential (⌬MP) was measured as the difference between the MP reached during the last 100 ms of a 3-s puff and the MP during 100 ms before the puff.…”

Section: Mechanical Stimulationmentioning

confidence: 99%

Neuronal Prostacyclin Is an Autocrine Regulator of Arterial Baroreceptor Activity

et al. 2005

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Abstract-We tested the hypothesis that neuronal prostacyclin is an autocrine regulator of arterial baroreceptor neuronal activity. In isolated rat aortic nodose baroreceptor neurons, mechanical stimulation depolarized 12 neurons by 13.1Ϯ3.4 mV and triggered action potentials in 5 of them, averaging 18.2Ϯ9.5 spikes. Current injections depolarized 21 neurons by 29.9Ϯ8.0 mV and triggered action potentials averaging 17.0Ϯ2.4 spikes. After a period of prolonged neuronal activation with pulses of 1 nA at 20 Hz for 1 minute, the action potential responses to mechanical stimulation and to current injections were first markedly suppressed (0.2Ϯ0.2 and 2.1Ϯ0.7 spikes, respectively) and then enhanced, reaching levels above control (29.0Ϯ8.0 and 21.7Ϯ2.6 spikes, respectively) over the subsequent 15 minutes. In contrast, there was no inhibition of the depolarizations caused by mechanical stimulation or current injections. The recovery and enhancement of action potentials, which reached 150Ϯ5.4% of control values at 15 minutes (nϭ13), were abrogated by 10 mol/L of indomethacin and replaced by sustained inhibition for over 15 minutes. Carbacyclin (10 mol/L) reversed the inhibition and restored action potential responses. Prostacyclin production by cultured nodose neurons was enhanced by arachidonic acid and electrical field stimulation and inhibited by indomethacin. We conclude that prostacyclin provides an autocrine feedback that restores and enhances the responsiveness of arterial baroreceptor neurons after their inhibition from excessive neuronal activation. We speculate that reduced synthesis of neuronal prostacyclin contributes to the resetting phenomenon and the suppressed activity of arterial baroreceptors in hypertension. Key Words: neurons Ⅲ membranes Ⅲ ion channels Ⅲ baroreflex Ⅲ prostacyclin B aroreceptor neurons (BRNs) innervate the aortic arch and both carotid sinus regions and sense changes in arterial blood pressure. Sustained periods of increased arterial pressure and baroreceptor activity (BRA) often lead to upward "resetting" of the pressure-activity relation to higher pressures, with possible decreases in BRA in vivo, 1-4 which provide a detrimental positive feedback for hypertension. The current view is that postexcitatory inhibition of BRA may be mediated through a hyperpolarizing effect of activated Na ϩ -K ϩ -ATPase. 5,6 In addition, inhibition of voltage-gated Na ϩ channels by NO, 7 which may be generated during baroreceptor stimulation through the activation of Ca 2ϩ -dependent NO synthase, 8,9 may also contribute to postexcitatory inhibition.Several studies indicate that prostaglandins, and prostacyclin (PGI 2 ) in particular, excite BRNs, as well as cardiac vagal afferents. 10 -13 Decreased synthesis of PGI 2 may play a role in acute and chronic baroreceptor resetting and the decreased baroreceptor sensitivity in hypertension. 13,14 PGI 2 released by ischemic myocardium activates cardiac vagal afferents and suppresses the baroreflex. 15 Although a major source of PGI 2 is believed to be vascular end...

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“…Recent physiological studies (Carr et al, 2001;Harper, 1991;Paton and Kasparov, 2000;Resstel et al, 2004;Snitsarev et al, 2002) revealed a critical role for other mechanisms in baroreflex control. With a primary effect on central functional unbalance, these mechanisms suggest an additional etiological factor for cardiac risk in mood disorders.…”

Section: Introductionmentioning

confidence: 99%