Evidence in the human of a hypotensive and a bradycardic effect after mouth opening maintained for 10 min

Seppia, Cristina Del; Ghione, S; Foresi, Paola; Lapi, Dominga; Fommei, Enza; Colantuoni, Antonio; Scuri, Rossana

doi:10.1007/s00421-017-3643-8

Cited by 8 publications

(13 citation statements)

References 27 publications

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“…Another possibility is that the effect is mediated by nitric oxide (NO). Previous studies have demonstrated that a mandibular extension very similar to that applied in our subjects, was able to substantially lower the systemic blood pressure in humans, and lead to an increase in the NO plasma levels in the rat ( Brunelli et al, 2012 ; Lapi et al, 2013 , 2014 , 2016 , 2017 ; Del Seppia et al, 2016 , 2017 ). Notably, NO has been implicated in pain transmission ( Rosenthal et al, 2015 ), and in some cases NO donors have been shown to produce antinociceptive effects, while NO synthase inhibitors lead to pain ( Yeo, 2002 ; da Silva et al, 2008 ; Fan et al, 2009 ).…”

Section: Discussionmentioning

confidence: 55%

Pain Control by Proprioceptive and Exteroceptive Stimulation at the Trigeminal Level

et al. 2018

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The Gate Control Theory of pain, published more than half a century ago to explain nociceptive modulation of peripheral sensory input, assumes inhibition of incoming nociceptive (pain) information produced by mechanical stimulation. To verify the presence of such a gate control mechanism at the level of the human trigeminal system, we evaluated the effects on pain sensation of a proprioceptive trigeminal stimulation induced by mandibular extension. We found that such a stimulation, applied for 7 min, was effective in increasing both the threshold and tolerance of tooth pain induced by electrical activation of dental nociceptors. Moreover the antinociceptive effect lasted for several minutes after the proprioceptive stimulus had ceased. We also tested whether an exteroceptive palatal stimulation superimposed on the proprioceptive stimulation would increase the effects on tooth pain perception of human volunteers. We observed that the exteroceptive stimulation significantly increased the antinociceptive effect induced by the sole proprioceptive stimulation. The physiological mechanisms and the possible implications of these observations are discussed.

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Section: Discussionmentioning

confidence: 55%

Pain Control by Proprioceptive and Exteroceptive Stimulation at the Trigeminal Level

et al. 2018

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“…Previous studies in normotensive rats, investigating arteriolar tone modifications, have shown that the stimulation of trigeminal nerve by ME procedure determines a prolonged hypotensive effect accompanied by initial rapid vasoconstriction, followed by a prolonged vasodilation y in the pial microcirculation ( Lapi et al, 2017 ). Furthermore, our studies on humans demonstrated that the submaximal mouth opening for a relatively brief time (10 min) was followed by a prolonged hypotensive and bradycardic effect on normotensive volunteers ( Del Seppia et al, 2016 , 2017 ). Due to the important role of RAS in the pathophysiology of hypertension, we focused on the gene expression and protein levels of RAS components during ME protocol at cortex level in SHRs and in NT rats.…”

Section: Discussionmentioning

confidence: 79%

“…Therefore, stimulation of specific facial regions may induce reflex with certain important implications ( Brunelli et al, 2012 ). Recently, we showed that, in normotensive anesthetized rats and in normotensive humans, a mandibular extension (ME) induced a reduction in blood pressure (BP) ( Lapi et al, 2013 , 2014 ; Del Seppia et al, 2016 , 2017 ). Moreover, in normotensive rats, this effect was abolished by bilateral peripheral trigeminal section, thus indicating a fundamental role of trigeminal nerve in the hypotensive ME-induced response ( Lapi et al, 2013 ).…”

Section: Introductionmentioning

confidence: 99%

Renin-Angiotensin System Responds to Prolonged Hypotensive Effect Induced by Mandibular Extension in Spontaneously Hypertensive Rats

et al. 2018

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There is an ongoing interest in the renin-angiotensin system (RAS) contribution either to pathological mechanisms leading to hypertension (mainly regarding the ACE/AngII/AT1R axis), or, to RAS protective and pro-regenerative actions, primarily ascribed to the mediation of the AT2R and the MAS1 receptor. In the present study, we evaluated the modulation of gene expression and protein levels of “deleterious” (ACE/AngII/AT1R) and “protective” [ACE/AngII/AT2R and ACE2/Ang(1-7)/MAS1 arms] RAS components in parietal and frontal areas of cerebral cortex of spontaneously hypertensive rats (SHRs), after two periods of mandibular extensions (MEs). Blood pressure, BP and heart rate, HR were also measured. While no significant changes in BP and HR were present in the sham operated (SO) group, in rats after two MEs (2-ME rats), BP displayed a marked decrease (p < 0.001) at ME2, and remained then stably low for the subsequent observation period. In gene expression analysis, in SHRs undergoing two MEs, either in parietal or frontal cortex, we did not observe any significant variation of AT2R and ACE2 with respect to SO rats. In contrast, we observed a decrease in Mas1 gene expression in parietal area (p < 0.01) and an increase in frontal region (p < 0.01). AT1R and ACE gene expression was significantly higher in 2-ME rats than SO in parietal cortex (p < 0.05) but no difference was observed in the frontal area. Concerning protein levels, in parietal area, AT1R and AT2R did not change whereas MAS1 significantly decreased in 2-ME rats (p < 0.05). In frontal area, both AT1R and AT2R significantly decreased in 2-ME rats (p < 0.05), whereas MAS1 did not significantly change. Gene expression analysis in normotensive (NT) rats revealed the non-detectability of AT1R in both parietal and frontal zone. In parietal area, AT2R (p < 0.0001) and Mas1 (p < 0.01) were significantly decreased in 2-ME NT rats, when compared to SO, and ACE and ACE2 resulted not detectable whereas there was some expression of these genes after 2-ME procedure. In conclusion, our data in rat models indicated that a 2-ME procedure induced a hypotensive response and that a modulation of gene expression and protein levels of RAS components occurred in different cerebral cortex areas.

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“…), and another with a fixed mouth opener, defined static extension (Del Seppia et al. ), however, a similar study by other authors using dynamic extension failed to confirm these results (De Innocentiis et al. ).…”

Section: Introductionmentioning

confidence: 91%

Evidence in hypertensive rats of hypotensive effect after mandibular extension

et al. 2018

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Previous studies in anesthetized normotensive rats demonstrated that a single mouth opening for 10 min obtained by an ad hoc dilator (mandibular extension [ME]) produced a blood pressure reduction by about 20 mmHg lasting for about 2 h and that once‐repeated ME prolonged this effect. We here describe these effects in hypertensive rats. Mean (intra) arterial blood pressure (MABP) and heart rate (HR) was followed for up to a maximum of 470 min after single or repeated 10 min‐lasting ME in two groups of anesthetized, male, 6–9 months old hypertensive rats. In one group, hypertension was induced by dexamethasone (20 μg/kg/day, subcutaneously for 7 days; Dex‐HT); the other group was spontaneously hypertensive rats (SHR). Studies were done, in Dex‐HT rats, after only surgical procedures (no ME, sham‐operated rats), single ME, early repeated (after 10 min) ME (ER‐ME) and late repeated (after 160 min) ME (LR‐ME) and, in SHR, after only surgical procedures and ER‐ME. One‐way ANOVA for repeated measures revealed no significant effect on MABP and HR in sham‐operated groups. In Dex‐HT rats, single ME was followed by a significant MABP decline by 25 mmHg, lasting for 100 min; ER‐ME and LR‐ME were followed by an even greater significant MABP decline by 40 mmHg, which outlasted the experimental observation period. In SHR, ER‐ME gave similar results as in Dex‐HT rats. HR significantly declined in all, except sham‐operated groups. In conclusions, ME is followed by a prolonged MABP decline also in hypertensive rats. This effect is even more pronounced, in length and magnitude, after repeated ME.

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Evidence in the human of a hypotensive and a bradycardic effect after mouth opening maintained for 10 min

Abstract: This study shows that, in normotensives, a single fixed submaximal mouth opening for 10 min is followed by prolonged albeit small reductions of blood pressure and heart rate.

Cited by 8 publications

References 27 publications

Pain Control by Proprioceptive and Exteroceptive Stimulation at the Trigeminal Level

Pain Control by Proprioceptive and Exteroceptive Stimulation at the Trigeminal Level

Renin-Angiotensin System Responds to Prolonged Hypotensive Effect Induced by Mandibular Extension in Spontaneously Hypertensive Rats

Evidence in hypertensive rats of hypotensive effect after mandibular extension

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