Aromatherapy: Activating olfactory calcium-sensing receptors impairs renal hemodynamics via sympathetic nerve-mediated vasoconstriction

Shih Pin Lee, Wei Yi Wu, Jong Kai Hsiao, Jia Hao Zhou, Hao Hsiang Chang, Chiang Ting Chien

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Aim: This study determines whether the activation of olfactory calcium-sensing receptor initiates a sympathetic activation-dependent neurovascular reflex subsequently contributing to renal hemodynamic depression. Methods: Immunohistochemistry and nose-loading calcium-sensitive dye were used to explore the location and function of calcium-sensing receptor on the olfactory sensory neuron. The renal sympathetic nervous activity, renal hemodynamics and the microcirculation of kidney, liver and intestine were evaluated after liquid-phase intranasal administrations of saline, lidocaine, calcium-sensing receptor agonists and antagonist in sham and bilateral renal denervated rats. Real-time renal glomerular filtration rate was measured by a magnetic resonance renography. Results: Calcium-sensing receptors were expressed on the cilia the olfactory sensory neuron and their activation depolarized olfactory sensory neuron and induced the calcium influx in the terminal side on olfactory glomeruli. Activating olfactory calcium-sensing receptors significantly increased arterial blood pressure and renal sympathetic nervous activities and subsequently decreased renal blood flow, renal, hepatic and enteral microcirculation. Cotreatments with calcium-sensing receptor antagonist or lidocaine inhibited these physiological alterations. The renal hemodynamic depressions by olfactory calcium-sensing receptor activation were significantly blocked by bilateral renal denervation. The intranasal manganese administration decreased the glomerular filtration rate. Conclusion: Calcium-sensing receptor acts as a functional chemosensory receptor on olfactory sensory neuron, and its activation causes the global sympathetic enhancement contributing to systematic vasoconstriction and subsequently depresses renal blood flow and glomerular filtration rate. These data implicate a possibly clinical aspect that several environmental stimuli may activate olfactory calcium-sensing receptors to evoke a sympathetic nervous system-mediated neurovascular reflex to depress renal hemodynamics.

Original languageEnglish
Article numbere13157
JournalActa Physiologica
Volume225
Issue number1
DOIs
Publication statusPublished - 2019 Jan 1

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Aromatherapy
Calcium-Sensing Receptors
Vasoconstriction
Olfactory Receptor Neurons
Hemodynamics
Kidney
Glomerular Filtration Rate
Intranasal Administration
Renal Circulation
Microcirculation
Lidocaine
Reflex
Depression
Radioisotope Renography
Calcium
Cilia
Olfactory Bulb
Liver
Sympathetic Nervous System
Denervation

Keywords

  • calcium-sensing receptor
  • olfactory sensory neuron
  • renal hemodynamics
  • renal sympathetic nerve
  • vasoconstriction

ASJC Scopus subject areas

  • Physiology

Cite this

Aromatherapy : Activating olfactory calcium-sensing receptors impairs renal hemodynamics via sympathetic nerve-mediated vasoconstriction. / Lee, Shih Pin; Wu, Wei Yi; Hsiao, Jong Kai; Zhou, Jia Hao; Chang, Hao Hsiang; Chien, Chiang Ting.

In: Acta Physiologica, Vol. 225, No. 1, e13157, 01.01.2019.

Research output: Contribution to journalArticle

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abstract = "Aim: This study determines whether the activation of olfactory calcium-sensing receptor initiates a sympathetic activation-dependent neurovascular reflex subsequently contributing to renal hemodynamic depression. Methods: Immunohistochemistry and nose-loading calcium-sensitive dye were used to explore the location and function of calcium-sensing receptor on the olfactory sensory neuron. The renal sympathetic nervous activity, renal hemodynamics and the microcirculation of kidney, liver and intestine were evaluated after liquid-phase intranasal administrations of saline, lidocaine, calcium-sensing receptor agonists and antagonist in sham and bilateral renal denervated rats. Real-time renal glomerular filtration rate was measured by a magnetic resonance renography. Results: Calcium-sensing receptors were expressed on the cilia the olfactory sensory neuron and their activation depolarized olfactory sensory neuron and induced the calcium influx in the terminal side on olfactory glomeruli. Activating olfactory calcium-sensing receptors significantly increased arterial blood pressure and renal sympathetic nervous activities and subsequently decreased renal blood flow, renal, hepatic and enteral microcirculation. Cotreatments with calcium-sensing receptor antagonist or lidocaine inhibited these physiological alterations. The renal hemodynamic depressions by olfactory calcium-sensing receptor activation were significantly blocked by bilateral renal denervation. The intranasal manganese administration decreased the glomerular filtration rate. Conclusion: Calcium-sensing receptor acts as a functional chemosensory receptor on olfactory sensory neuron, and its activation causes the global sympathetic enhancement contributing to systematic vasoconstriction and subsequently depresses renal blood flow and glomerular filtration rate. These data implicate a possibly clinical aspect that several environmental stimuli may activate olfactory calcium-sensing receptors to evoke a sympathetic nervous system-mediated neurovascular reflex to depress renal hemodynamics.",
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N2 - Aim: This study determines whether the activation of olfactory calcium-sensing receptor initiates a sympathetic activation-dependent neurovascular reflex subsequently contributing to renal hemodynamic depression. Methods: Immunohistochemistry and nose-loading calcium-sensitive dye were used to explore the location and function of calcium-sensing receptor on the olfactory sensory neuron. The renal sympathetic nervous activity, renal hemodynamics and the microcirculation of kidney, liver and intestine were evaluated after liquid-phase intranasal administrations of saline, lidocaine, calcium-sensing receptor agonists and antagonist in sham and bilateral renal denervated rats. Real-time renal glomerular filtration rate was measured by a magnetic resonance renography. Results: Calcium-sensing receptors were expressed on the cilia the olfactory sensory neuron and their activation depolarized olfactory sensory neuron and induced the calcium influx in the terminal side on olfactory glomeruli. Activating olfactory calcium-sensing receptors significantly increased arterial blood pressure and renal sympathetic nervous activities and subsequently decreased renal blood flow, renal, hepatic and enteral microcirculation. Cotreatments with calcium-sensing receptor antagonist or lidocaine inhibited these physiological alterations. The renal hemodynamic depressions by olfactory calcium-sensing receptor activation were significantly blocked by bilateral renal denervation. The intranasal manganese administration decreased the glomerular filtration rate. Conclusion: Calcium-sensing receptor acts as a functional chemosensory receptor on olfactory sensory neuron, and its activation causes the global sympathetic enhancement contributing to systematic vasoconstriction and subsequently depresses renal blood flow and glomerular filtration rate. These data implicate a possibly clinical aspect that several environmental stimuli may activate olfactory calcium-sensing receptors to evoke a sympathetic nervous system-mediated neurovascular reflex to depress renal hemodynamics.

AB - Aim: This study determines whether the activation of olfactory calcium-sensing receptor initiates a sympathetic activation-dependent neurovascular reflex subsequently contributing to renal hemodynamic depression. Methods: Immunohistochemistry and nose-loading calcium-sensitive dye were used to explore the location and function of calcium-sensing receptor on the olfactory sensory neuron. The renal sympathetic nervous activity, renal hemodynamics and the microcirculation of kidney, liver and intestine were evaluated after liquid-phase intranasal administrations of saline, lidocaine, calcium-sensing receptor agonists and antagonist in sham and bilateral renal denervated rats. Real-time renal glomerular filtration rate was measured by a magnetic resonance renography. Results: Calcium-sensing receptors were expressed on the cilia the olfactory sensory neuron and their activation depolarized olfactory sensory neuron and induced the calcium influx in the terminal side on olfactory glomeruli. Activating olfactory calcium-sensing receptors significantly increased arterial blood pressure and renal sympathetic nervous activities and subsequently decreased renal blood flow, renal, hepatic and enteral microcirculation. Cotreatments with calcium-sensing receptor antagonist or lidocaine inhibited these physiological alterations. The renal hemodynamic depressions by olfactory calcium-sensing receptor activation were significantly blocked by bilateral renal denervation. The intranasal manganese administration decreased the glomerular filtration rate. Conclusion: Calcium-sensing receptor acts as a functional chemosensory receptor on olfactory sensory neuron, and its activation causes the global sympathetic enhancement contributing to systematic vasoconstriction and subsequently depresses renal blood flow and glomerular filtration rate. These data implicate a possibly clinical aspect that several environmental stimuli may activate olfactory calcium-sensing receptors to evoke a sympathetic nervous system-mediated neurovascular reflex to depress renal hemodynamics.

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KW - vasoconstriction

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