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Vijay Lyall - One of the best experts on this subject based on the ideXlab platform.

  • Selective Activation of hTRPV1 by N-Geranyl Cyclopropylcarboxamide, an Amiloride-Insensitive Salt Taste Enhancer
    2016
    Co-Authors: Min Jung Kim, Vijay Lyall, Hee Jin Son, Yiseul Kim, Hae-jin Kweon, Byung-chang Suh, Ra Rhyu
    Abstract:

    TRPV1t, a variant of the transient receptor potential vanilloid-1 (TRPV1) has been proposed as a constitutively active, non-selective cation channel as a putative amiloride-insensitive salt taste receptor and shares many properties with TRPV1. Based on our previous chorda tympani taste nerve recordings in rodents and human sensory evaluations, we proposed that N-geranylcyclopropylcarboxamide (NGCC), a novel synthetic compound, acts as a salt taste enhancer by modulating the amiloride/Benzamil-insensitive Na+ entry pathways. As an extension of this work, we investigated NGCC-induced human TRPV1 (hTRPV1) activation using a Ca2+-flux signaling assay in cultured cells. NGCC enhanced Ca2+ influx in hTRPV1-expressing cells in a dose-dependent manner (EC50 = 115 mM). NGCC-induced Ca2+ influx was significantly attenuated by ruthenium red (RR; 30 mM), a non-specific blocker of TRP channels and capsazepine (CZP; 5 mM), a specific antagonist of TRPV1, implying that NGCC directly activates hTRPV1. TRPA1 is often co-expressed with TRPV1 in sensory neurons. Therefore, we also investigated the effects of NGCC on hTRPA1-expressing cells. Similar to hTRPV1, NGCC enhanced Ca2+ influx in hTRPA1-expressing cells (EC50 = 83.65 mM). The NGCC-induced Ca2+ influx in hTRPA1-expressing cells was blocked by RR (30 mM) and HC-030031 (100 mM), a specific antagonist of TRPA1. These results suggested that NGCC selectively activates TRPV1 and TRPA1 in cultured cells. These data may provide additional support for our previous hypothesis that NGCC interacts with TRPV1 variant cation channel, a putative amiloride/Benzamil-insensitive salt taste pathway in th

  • Chem. Senses doi:10.1093/chemse/bjn033 Effect of Maillard Reacted Peptides on Human Salt Taste and the Amiloride-Insensitive Salt Taste Receptor (TRPV1t)
    2014
    Co-Authors: Tadayoshi Katsumata, John A. Desimone, Tam-hao T. Phan, Shobha Mummalaneni, Hiroko Nakakuki, Chikara Tokunaga, Noboru Fujii, Makoto Egi, Vijay Lyall
    Abstract:

    Maillard reacted peptides (MRPs) were synthesized by conjugating a peptide fraction (1000–5000 Da) purified from soy protein hydrolyzate with galacturonic acid, glucosamine, xylose, fructose, or glucose. The effect of MRPs was investigated on human salt taste and on the chorda tympani (CT) taste nerve responses to NaCl in Sprague–Dawley rats, wild-type, and transient receptor potential vanilloid 1 (TRPV1) knockout mice. MRPs produced a biphasic effect on human salt taste perception and on the CT responses in rats and wild-type mice in the presence of NaCl + Benzamil (Bz, a blocker of epithelial Na+ channels), enhancing the NaCl response at low concentrations and suppressing it at high concentrations. The effectiveness of MRPs as salt taste enhancers varied with the conjugated sugar moiety: galacturonic acid = glucosamine> xylose> fructose> glucose. The concentrations atwhichMRPs enhanced human salt tastewere significantly lower than the concentrations ofMRPs that produced increase in the NaCl CT response. Elevated temperature, resiniferatoxin, capsaicin, and ethanol produced additive effects on the NaCl CT responses in the presence of MRPs. Elevated temperature and ethanol also enhanced human salt taste perception. N-(3-methoxyphenyl)-4-chlorocinnamid (a blocker of TRPV1t) inhibited the Bz-insensitive NaCl CT responses in the absence and presence of MRPs. TRPV1 knockout mice demonstrated no Bz-insensitive NaCl CT response in the absence or presence of MRPs. The results suggest that MRPs modulate human salt taste and the NaCl + Bz CT responses by interacting with TRPV1t. Key words: Benzamil, chorda tympani, ENaC, SB-366791, umami tast

  • Selective activation of hTRPV1 by N-geranyl cyclopropylcarboxamide, an amiloride-insensitive salt taste enhancer.
    PLOS ONE, 2014
    Co-Authors: Hae-jin Kweon, Vijay Lyall, Mee-ra Rhyu
    Abstract:

    : TRPV1t, a variant of the transient receptor potential vanilloid-1 (TRPV1) has been proposed as a constitutively active, non-selective cation channel as a putative amiloride-insensitive salt taste receptor and shares many properties with TRPV1. Based on our previous chorda tympani taste nerve recordings in rodents and human sensory evaluations, we proposed that N-geranylcyclopropylcarboxamide (NGCC), a novel synthetic compound, acts as a salt taste enhancer by modulating the amiloride/Benzamil-insensitive Na(+) entry pathways. As an extension of this work, we investigated NGCC-induced human TRPV1 (hTRPV1) activation using a Ca(2+)-flux signaling assay in cultured cells. NGCC enhanced Ca(2+) influx in hTRPV1-expressing cells in a dose-dependent manner (EC50 = 115 µM). NGCC-induced Ca(2+) influx was significantly attenuated by ruthenium red (RR; 30 µM), a non-specific blocker of TRP channels and capsazepine (CZP; 5 µM), a specific antagonist of TRPV1, implying that NGCC directly activates hTRPV1. TRPA1 is often co-expressed with TRPV1 in sensory neurons. Therefore, we also investigated the effects of NGCC on hTRPA1-expressing cells. Similar to hTRPV1, NGCC enhanced Ca(2+) influx in hTRPA1-expressing cells (EC50 = 83.65 µM). The NGCC-induced Ca(2+) influx in hTRPA1-expressing cells was blocked by RR (30 µM) and HC-030031 (100 µM), a specific antagonist of TRPA1. These results suggested that NGCC selectively activates TRPV1 and TRPA1 in cultured cells. These data may provide additional support for our previous hypothesis that NGCC interacts with TRPV1 variant cation channel, a putative amiloride/Benzamil-insensitive salt taste pathway in the anterior taste receptive field.

  • Effects of S3969 or NGCC on αβγ hENaC-expressing cells.
    2014
    Co-Authors: Min Jung Kim, Vijay Lyall, Hee Jin Son, Yiseul Kim, Hae-jin Kweon, Byung-chang Suh, Mee-ra Rhyu
    Abstract:

    Cells expressing αβγ-hENaC were loaded with FMP blue-dye and the effects of S3969 or NGCC were quantitatively evaluated using membrane potential assay. S3969 depolarized membrane potential on αβγ hENaC-expressing cells and Benzamil (Bz) effectively inhibited S3969 activity. NGCC showed no effect on αβγhENaC-expressing cells. Experiments were repeated in triplicate and data points represent the means ± SEM (n = 3–4).

  • trpm5 dependent amiloride and Benzamil insensitive nacl chorda tympani taste nerve response
    American Journal of Physiology-gastrointestinal and Liver Physiology, 2013
    Co-Authors: Zuojun Ren, John A. Desimone, Tam-hao T. Phan, Shobha Mummalaneni, Mee-ra Rhyu, Karnam S Murthy, John R Grider, Vijay Lyall
    Abstract:

    Transient receptor potential (TRP) subfamily M member 5 (TRPM5) cation channel is involved in sensing sweet, bitter, umami, and fat taste stimuli, complex-tasting divalent salts, and temperature-in...

Oscar A Carretero - One of the best experts on this subject based on the ideXlab platform.

  • abstract p325 enhanced afferent arteriole dilatation in dahl salt sensitive rats dahlss role of connecting tubule glomerular feedback ctgf
    Hypertension, 2016
    Co-Authors: Hong Wang, Branislava Janic, Cesar A Romero, Edwards Peterson, Oscar A Carretero
    Abstract:

    Afferent arteriole (Af-Art) resistance is modulated by 2 intrinsic nephron feedbacks: the vasoconstrictor tubuloglomerular feedback (TGF) and the vasodilator CTGF. TGF is mediated by NKCC2 channel in the macula densa and blocked by furosemide; and CTGF is mediated by ENaC in the connecting tubule and blocked by Benzamil. Previously we measured CTGF indirectly, by differences between TGF response with and without CTGF blocker Benzamil. Thus, using this indirect measurement we reported that Dahl SS have greater CTGF than Dahl salt-resistant rats (Dahl SR). We have recently developed a new method to measure CTGF more directly and we found that when we simultaneously blocked TGF with furosemide and CTGF with Benzamil, the increasing tubular perfusion caused Af-Art constriction (TGF-like) that is mediated by the NHE. W e hypothesize that in vivo during simultaneous inhibition of NKCC2 and the NHE, CTGF causes an Af-Art dilatation revealed by an increase in stop-flow pressure (P SF ) and that is greater in Dahl SS than in Dahl SR in a high salt diet. In the presence of furosemide alone, increasing nephron perfusion did not change the P SF in neither Dahl SS nor Dahl SR. When we blocked both, NKCC2 with furosemide and NHE with DMA, increase in tubular flow caused Af-Art dilation that was demonstrated by an increase in P SF . This increase was greater in Dahl SS (5.1±0.4 mmHg) than in Dahl SR (2.9±0.3 mmHg; P

  • abstract 520 na h exchanger participates in tubuloglomerular feedback
    Hypertension, 2014
    Co-Authors: Hong Wang, Kristopher Kutskill, Martin A Dambrosio, Pablo Leung, Sumit R. Monu, Edward L. Peterson, Jeffrey L. Garvin, Yilin Ren, Oscar A Carretero
    Abstract:

    The afferent arteriole (Af-Art) accounts for most renal vasculature resistance, thus controlling glomerular filtration and renal function. The nephron regulates Af-Art resistance via two mechanisms, the vasoconstrictor tubuloglomerular feedback (TGF), initiated in the macula densa via Na/K/2Cl cotransporters (NKCC2), and the vasodilator connecting tubule glomerular feedback (CTGF), initiated in the connecting tubule via the epithelial Na channels (ENaC). However, when TGF and CTGF are inhibited by furosemide and Benzamil, a novel form of TGF is observed. We hypothesize that in addition to NKCC2, TGF can be initiated by Na/H exchangers (NHE). Furthermore, we hypothesize that when NKCC2 and NHE are blocked, CTGF causes Af-Art dilation. In vivo, using the nephron micropuncture technique, we performed two consecutive stop-flow pressure (PSF) curves (an index of glomerular capillary pressure) by increasing the perfusion of the nephron from 0 to 40 nL/min while adding drugs to the tubular perfusate. TGF was blocked by furosemide (vehicle -7.9±0.2 mmHg at 40 nL/min, furosemide -0.4±0.2; P We conclude that NHE in the nephron causes TGF when NKCC2 and ENaC are inhibited and that CTGF causes dilation of the Af-Art when TGF is completely blocked with NKCC2 and NHE inhibitors.

  • connecting tubule glomerular feedback in hypertension
    Hypertension, 2013
    Co-Authors: Hong Wang, Martin A Dambrosio, Jeffrey L. Garvin, Oscar A Carretero
    Abstract:

    In Dahl salt-sensitive rats (Dahl SS), glomerular capillary pressure increases in response to high salt intake and this is accompanied by significant glomerular injury compared with spontaneously hypertensive rats with similar blood pressure. Glomerular capillary pressure is controlled mainly by afferent arteriolar resistance, which is regulated by the vasoconstrictor tubule glomerular feedback (TGF) and the vasodilator connecting TGF (CTGF). We hypothesized that Dahl SS have a decreased TGF response and enhanced TGF resetting compared with spontaneously hypertensive rats, and that these differences are attributable in part to an increase in CTGF. In vivo, using micropuncture we measured stop-flow pressure (a surrogate of glomerular capillary pressure). TGF was calculated as the maximal decrease in stop-flow pressure caused by increasing nephron perfusion, TGF resetting as the attenuation in TGF induced by high salt diet, and CTGF as the difference in TGF response before and during CTGF inhibition with Benzamil. Compared with spontaneously hypertensive rats, Dahl SS had (1) lower TGF responses in normal (6.6±0.1 versus 11.0±0.2 mm Hg; P P P P

  • connecting tubule glomerular feedback antagonizes tubuloglomerular feedback in vivo
    American Journal of Physiology-renal Physiology, 2010
    Co-Authors: Hong Wang, Martin A Dambrosio, Jeffrey L. Garvin, Oscar A Carretero
    Abstract:

    In vitro experiments showed that the connecting tubule (CNT) sends a signal that dilates the afferent arteriole (Af-Art) when Na+ reabsorption in the CNT lumen increases. We call this process CNT glomerular feedback (CTGF) to differentiate it from tubuloglomerular feedback (TGF), which is a cross talk between the macula densa (MD) and the Af-Art. In TGF, the MD signals the Af-Art to constrict when NaCl transport by the MD is enhanced by increased luminal NaCl. CTGF is mediated by CNT Na+ transport via epithelial Na+ channels (ENaC). However, we do not know whether CTGF occurs in vivo or whether it opposes the increase in Af-Art resistance caused by TGF. We hypothesized that CTGF occurs in vivo and opposes TGF. To test our hypothesis, we conducted in vivo micropuncture of individual rat nephrons, measuring stop-flow pressure (PSF) as an index of glomerular filtration pressure. To test whether activation of CTGF opposes TGF, we used Benzamil to block CNT Na+ transport and thus CTGF. CTGF inhibition with the ENaC blocker Benzamil (1 μM) potentiated the decrease in PSF at 40 and 80 nl/min. Next, we tested whether we could augment CTGF by inhibiting NaCl reabsorption in the distal convoluted tubule with hydrochlorothiazide (HCTZ, 1 mM) to enhance NaCl delivery to the CNT. In the presence of HCTZ, Benzamil potentiated the decrease in PSF at 20, 40, and 80 nl/min. We concluded that in vivo CTGF occurs and opposes the vasoconstrictor effect of TGF.

Armando Carpaneto - One of the best experts on this subject based on the ideXlab platform.

  • beyond the patch clamp resolution functional activity of nonelectrogenic vacuolar nhx proton potassium antiporters and inhibition by phosphoinositides
    New Phytologist, 2021
    Co-Authors: Antonella Gradogna, Joachim Scholzstarke, Jose M Pardo, Armando Carpaneto
    Abstract:

    We combined the patch-clamp technique with ratiometric fluorescence imaging using the proton-responsive dye BCECF as a luminal probe. Upon application of a steep cytosol-directed potassium ion (K+ ) gradient in Arabidopsis mesophyll vacuoles, a strong and reversible acidification of the vacuolar lumen was detected, whereas no associated electrical currents were observed, in agreement with electroneutral cation/H+ exchange. Our data show that this acidification was generated by NHX antiport activity, because: it did not distinguish between K+ and sodium (Na+ ) ions; it was sensitive to the NHX inhibitor Benzamil; and it was completely absent in vacuoles from nhx1 nhx2 double knockout plants. Our data further show that NHX activity could be reversed, was voltage-independent and specifically impaired by the low-abundance signaling lipid PI(3,5)P2 , which may regulate salt accumulation in plants by acting as a common messenger to coordinately shut down secondary active carriers responsible for cation and anion uptake inside the vacuole. Finally, we developed a theory based on thermodynamics, which supports the data obtained by our novel experimental approach. This work, therefore, represents a proof-of-principle that can be applied to the study of proton-dependent exchangers from plants and animals, which are barely detectable using conventional techniques.

Hong Wang - One of the best experts on this subject based on the ideXlab platform.

  • abstract p325 enhanced afferent arteriole dilatation in dahl salt sensitive rats dahlss role of connecting tubule glomerular feedback ctgf
    Hypertension, 2016
    Co-Authors: Hong Wang, Branislava Janic, Cesar A Romero, Edwards Peterson, Oscar A Carretero
    Abstract:

    Afferent arteriole (Af-Art) resistance is modulated by 2 intrinsic nephron feedbacks: the vasoconstrictor tubuloglomerular feedback (TGF) and the vasodilator CTGF. TGF is mediated by NKCC2 channel in the macula densa and blocked by furosemide; and CTGF is mediated by ENaC in the connecting tubule and blocked by Benzamil. Previously we measured CTGF indirectly, by differences between TGF response with and without CTGF blocker Benzamil. Thus, using this indirect measurement we reported that Dahl SS have greater CTGF than Dahl salt-resistant rats (Dahl SR). We have recently developed a new method to measure CTGF more directly and we found that when we simultaneously blocked TGF with furosemide and CTGF with Benzamil, the increasing tubular perfusion caused Af-Art constriction (TGF-like) that is mediated by the NHE. W e hypothesize that in vivo during simultaneous inhibition of NKCC2 and the NHE, CTGF causes an Af-Art dilatation revealed by an increase in stop-flow pressure (P SF ) and that is greater in Dahl SS than in Dahl SR in a high salt diet. In the presence of furosemide alone, increasing nephron perfusion did not change the P SF in neither Dahl SS nor Dahl SR. When we blocked both, NKCC2 with furosemide and NHE with DMA, increase in tubular flow caused Af-Art dilation that was demonstrated by an increase in P SF . This increase was greater in Dahl SS (5.1±0.4 mmHg) than in Dahl SR (2.9±0.3 mmHg; P

  • abstract 520 na h exchanger participates in tubuloglomerular feedback
    Hypertension, 2014
    Co-Authors: Hong Wang, Kristopher Kutskill, Martin A Dambrosio, Pablo Leung, Sumit R. Monu, Edward L. Peterson, Jeffrey L. Garvin, Yilin Ren, Oscar A Carretero
    Abstract:

    The afferent arteriole (Af-Art) accounts for most renal vasculature resistance, thus controlling glomerular filtration and renal function. The nephron regulates Af-Art resistance via two mechanisms, the vasoconstrictor tubuloglomerular feedback (TGF), initiated in the macula densa via Na/K/2Cl cotransporters (NKCC2), and the vasodilator connecting tubule glomerular feedback (CTGF), initiated in the connecting tubule via the epithelial Na channels (ENaC). However, when TGF and CTGF are inhibited by furosemide and Benzamil, a novel form of TGF is observed. We hypothesize that in addition to NKCC2, TGF can be initiated by Na/H exchangers (NHE). Furthermore, we hypothesize that when NKCC2 and NHE are blocked, CTGF causes Af-Art dilation. In vivo, using the nephron micropuncture technique, we performed two consecutive stop-flow pressure (PSF) curves (an index of glomerular capillary pressure) by increasing the perfusion of the nephron from 0 to 40 nL/min while adding drugs to the tubular perfusate. TGF was blocked by furosemide (vehicle -7.9±0.2 mmHg at 40 nL/min, furosemide -0.4±0.2; P We conclude that NHE in the nephron causes TGF when NKCC2 and ENaC are inhibited and that CTGF causes dilation of the Af-Art when TGF is completely blocked with NKCC2 and NHE inhibitors.

  • connecting tubule glomerular feedback in hypertension
    Hypertension, 2013
    Co-Authors: Hong Wang, Martin A Dambrosio, Jeffrey L. Garvin, Oscar A Carretero
    Abstract:

    In Dahl salt-sensitive rats (Dahl SS), glomerular capillary pressure increases in response to high salt intake and this is accompanied by significant glomerular injury compared with spontaneously hypertensive rats with similar blood pressure. Glomerular capillary pressure is controlled mainly by afferent arteriolar resistance, which is regulated by the vasoconstrictor tubule glomerular feedback (TGF) and the vasodilator connecting TGF (CTGF). We hypothesized that Dahl SS have a decreased TGF response and enhanced TGF resetting compared with spontaneously hypertensive rats, and that these differences are attributable in part to an increase in CTGF. In vivo, using micropuncture we measured stop-flow pressure (a surrogate of glomerular capillary pressure). TGF was calculated as the maximal decrease in stop-flow pressure caused by increasing nephron perfusion, TGF resetting as the attenuation in TGF induced by high salt diet, and CTGF as the difference in TGF response before and during CTGF inhibition with Benzamil. Compared with spontaneously hypertensive rats, Dahl SS had (1) lower TGF responses in normal (6.6±0.1 versus 11.0±0.2 mm Hg; P P P P

  • connecting tubule glomerular feedback antagonizes tubuloglomerular feedback in vivo
    American Journal of Physiology-renal Physiology, 2010
    Co-Authors: Hong Wang, Martin A Dambrosio, Jeffrey L. Garvin, Oscar A Carretero
    Abstract:

    In vitro experiments showed that the connecting tubule (CNT) sends a signal that dilates the afferent arteriole (Af-Art) when Na+ reabsorption in the CNT lumen increases. We call this process CNT glomerular feedback (CTGF) to differentiate it from tubuloglomerular feedback (TGF), which is a cross talk between the macula densa (MD) and the Af-Art. In TGF, the MD signals the Af-Art to constrict when NaCl transport by the MD is enhanced by increased luminal NaCl. CTGF is mediated by CNT Na+ transport via epithelial Na+ channels (ENaC). However, we do not know whether CTGF occurs in vivo or whether it opposes the increase in Af-Art resistance caused by TGF. We hypothesized that CTGF occurs in vivo and opposes TGF. To test our hypothesis, we conducted in vivo micropuncture of individual rat nephrons, measuring stop-flow pressure (PSF) as an index of glomerular filtration pressure. To test whether activation of CTGF opposes TGF, we used Benzamil to block CNT Na+ transport and thus CTGF. CTGF inhibition with the ENaC blocker Benzamil (1 μM) potentiated the decrease in PSF at 40 and 80 nl/min. Next, we tested whether we could augment CTGF by inhibiting NaCl reabsorption in the distal convoluted tubule with hydrochlorothiazide (HCTZ, 1 mM) to enhance NaCl delivery to the CNT. In the presence of HCTZ, Benzamil potentiated the decrease in PSF at 20, 40, and 80 nl/min. We concluded that in vivo CTGF occurs and opposes the vasoconstrictor effect of TGF.

John A. Desimone - One of the best experts on this subject based on the ideXlab platform.

  • Chem. Senses doi:10.1093/chemse/bjn033 Effect of Maillard Reacted Peptides on Human Salt Taste and the Amiloride-Insensitive Salt Taste Receptor (TRPV1t)
    2014
    Co-Authors: Tadayoshi Katsumata, John A. Desimone, Tam-hao T. Phan, Shobha Mummalaneni, Hiroko Nakakuki, Chikara Tokunaga, Noboru Fujii, Makoto Egi, Vijay Lyall
    Abstract:

    Maillard reacted peptides (MRPs) were synthesized by conjugating a peptide fraction (1000–5000 Da) purified from soy protein hydrolyzate with galacturonic acid, glucosamine, xylose, fructose, or glucose. The effect of MRPs was investigated on human salt taste and on the chorda tympani (CT) taste nerve responses to NaCl in Sprague–Dawley rats, wild-type, and transient receptor potential vanilloid 1 (TRPV1) knockout mice. MRPs produced a biphasic effect on human salt taste perception and on the CT responses in rats and wild-type mice in the presence of NaCl + Benzamil (Bz, a blocker of epithelial Na+ channels), enhancing the NaCl response at low concentrations and suppressing it at high concentrations. The effectiveness of MRPs as salt taste enhancers varied with the conjugated sugar moiety: galacturonic acid = glucosamine> xylose> fructose> glucose. The concentrations atwhichMRPs enhanced human salt tastewere significantly lower than the concentrations ofMRPs that produced increase in the NaCl CT response. Elevated temperature, resiniferatoxin, capsaicin, and ethanol produced additive effects on the NaCl CT responses in the presence of MRPs. Elevated temperature and ethanol also enhanced human salt taste perception. N-(3-methoxyphenyl)-4-chlorocinnamid (a blocker of TRPV1t) inhibited the Bz-insensitive NaCl CT responses in the absence and presence of MRPs. TRPV1 knockout mice demonstrated no Bz-insensitive NaCl CT response in the absence or presence of MRPs. The results suggest that MRPs modulate human salt taste and the NaCl + Bz CT responses by interacting with TRPV1t. Key words: Benzamil, chorda tympani, ENaC, SB-366791, umami tast

  • trpm5 dependent amiloride and Benzamil insensitive nacl chorda tympani taste nerve response
    American Journal of Physiology-gastrointestinal and Liver Physiology, 2013
    Co-Authors: Zuojun Ren, John A. Desimone, Tam-hao T. Phan, Shobha Mummalaneni, Mee-ra Rhyu, Karnam S Murthy, John R Grider, Vijay Lyall
    Abstract:

    Transient receptor potential (TRP) subfamily M member 5 (TRPM5) cation channel is involved in sensing sweet, bitter, umami, and fat taste stimuli, complex-tasting divalent salts, and temperature-in...

  • changes in taste receptor cell ca2 i modulate chorda tympani responses to salty and sour taste stimuli
    Journal of Neurophysiology, 2012
    Co-Authors: John A. Desimone, Tam-hao T. Phan, Zuojun Ren, Shobha Mummalaneni, Gerard L Heck, Vijay Lyall
    Abstract:

    The relationship between taste receptor cell (TRC) Ca2+ concentration ([Ca2+]i) and rat chorda tympani (CT) nerve responses to salty [NaCl and NaCl+Benzamil (Bz)] and sour (HCl, CO2, and acetic aci...

  • effect of nicotine on chorda tympani responses to salty and sour stimuli
    Journal of Neurophysiology, 2007
    Co-Authors: Vijay Lyall, Tam-hao T. Phan, Shobha Mummalaneni, Gerard L Heck, Mahdis Mansouri, Gerd Kobal, John A. Desimone
    Abstract:

    The effect of nicotine on the Benzamil (Bz)-insensitive (transient receptor potential vanilloid-1 variant cation channel, TRPV1t) and the Bz-sensitive (epithelial Na+ channel, ENaC) salt taste rece...

  • modulation of rat chorda tympani nacl responses and intracellular na activity in polarized taste receptor cells by ph
    The Journal of General Physiology, 2002
    Co-Authors: Vijay Lyall, Tam-hao T. Phan, Gerard L Heck, Rammy I Alam, Oneal F Russell, Shahbaz A Malik, John A. Desimone
    Abstract:

    Mixture interactions between sour and salt taste modalities were investigated in rats by direct measurement of intracellular pH (pHi) and Na+ activity ([Na+]i) in polarized fungiform taste receptor cells (TRCs) and by chorda tympani (CT) nerve recordings. Stimulating the lingual surface with NaCl solutions adjusted to pHs ranging between 2.0 and 10.3 increased the magnitude of NaCl CT responses linearly with increasing external pH (pHo). At pH 7.0, the epithelial sodium channel (ENaC) blocker, Benzamil, decreased NaCl CT responses and inhibited further changes in CT responses induced by varying pHo to 2.0 or 10.3. At constant pHo, buffering NaCl solutions with potassium acetate/acetic acid (KA/AA) or HCO3−/CO2 inhibited NaCl CT responses relative to CT responses obtained with NaCl solutions buffered with HEPES. The carbonic anhydrase blockers, MK-507 and MK-417, attenuated the inhibition of NaCl CT responses in HCO3−/CO2 buffer, suggesting a regulatory role for pHi. In polarized TRCs step changes in apical pHo from 10.3 to 2.0 induced a linear decrease in pHi that remained within the physiological range (slope = 0.035; r2 = 0.98). At constant pHo, perfusing the apical membrane with Ringer's solutions buffered with KA/AA or HCO3−/CO2 decreased resting TRC pHi, and MK-507 or MK-417 attenuated the decrease in pHi in TRCs perfused with HCO3−/CO2 buffer. In parallel experiments, TRC [Na+]i decreased with (a) a decrease in apical pH, (b) exposing the apical membrane to amiloride or Benzamil, (c) removal of apical Na+, and (d) acid loading the cells with NH4Cl or sodium acetate at constant pHo. Diethylpyrocarbonate and Zn2+, modification reagents for histidine residues in proteins, attenuated the CO2-induced inhibition of NaCl CT responses and the pHi-induced inhibition of apical Na+ influx in TRCs. We conclude that TRC pHi regulates Na+-influx through amiloride-sensitive apical ENaCs and hence modulates NaCl CT responses in acid/salt mixtures.