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  • 1
    Online Resource
    Online Resource
    Cardiac Responsiveness to Chronotropic Agents in the Cobra, Naja naja L.: Effect of Temperature and Thyroid Hormones
    Oxford University Press (OUP) ; 1987
    In:  American Zoologist Vol. 27, No. 1 ( 1987-02), p. 121-131
    Details
    In: American Zoologist, Oxford University Press (OUP), Vol. 27, No. 1 ( 1987-02), p. 121-131
    Type of Medium: Online Resource
    ISSN: 0003-1569
    URL: Article
    DOI: 10.1093/icb/27.1.121
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 1987
    detail.hit.zdb_id: 2159110-6
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Bronchodilator activity of bitter tastants in human tissue
    Springer Science and Business Media LLC ; 2011
    In:  Nature Medicine Vol. 17, No. 7 ( 2011-7), p. 776-778
    Details
    In: Nature Medicine, Springer Science and Business Media LLC, Vol. 17, No. 7 ( 2011-7), p. 776-778
    Type of Medium: Online Resource
    ISSN: 1078-8956 , 1546-170X
    URL: Article
    DOI: 10.1038/nm0711-776b
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2011
    detail.hit.zdb_id: 1484517-9
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  • 3
    Online Resource
    Online Resource
    Bitter taste receptors on airway smooth muscle bronchodilate by localized calcium signaling and reverse obstruction
    Springer Science and Business Media LLC ; 2010
    In:  Nature Medicine Vol. 16, No. 11 ( 2010-11), p. 1299-1304
    Details
    In: Nature Medicine, Springer Science and Business Media LLC, Vol. 16, No. 11 ( 2010-11), p. 1299-1304
    Type of Medium: Online Resource
    ISSN: 1078-8956 , 1546-170X
    URL: Article
    DOI: 10.1038/nm.2237
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2010
    detail.hit.zdb_id: 1484517-9
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  • 4
    Online Resource
    Online Resource
    The isolated polycystin-1 cytoplasmic COOH terminus prolongs ATP-stimulated Cl – conductance through increased Ca 2+ entry
    American Physiological Society ; 2003
    In:  American Journal of Physiology-Renal Physiology Vol. 285, No. 6 ( 2003-12), p. F1168-F1178
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 285, No. 6 ( 2003-12), p. F1168-F1178
    Abstract: The precise steps leading from mutation of the polycystic kidney disease ( PKD1) gene to the autosomal dominant polycystic kidney disease (ADPKD) phenotype remain to be established. Fluid accumulation is a requirement for cyst expansion in ADPKD, suggesting that abnormal fluid secretion into the cyst lumen might play a role in disease. In this study, we sought to establish a link between polycystin-1 (the PKD1 gene product) and ATP-stimulated Cl – secretion in renal tubule cells. To do this, we performed a whole cell patch-clamp analysis of the effects of expression of the isolated cytoplasmic COOH-terminus of polycystin-1 in stably transfected mouse cortical collecting duct cells. The truncated polycystin-1 fusion protein prolonged the duration of ATP-stimulated Cl – conductance and intracellular Ca 2+ responses. Both effects were dependent on extracellular Ca 2+ . It was determined that expression of the truncated polycystin-1 fusion protein introduced, or activated, an ATP-induced Ca 2+ entry pathway that was undetectable in transfection control cell lines. Our findings are concordant with increasing evidence for a role of polycystin-1 in cell Ca 2+ homeostasis and indicate that dysregulated Ca 2+ entry might promote Cl – secretion and cyst expansion in ADPKD.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00171.2003
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1477287-5
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  • 5
    Online Resource
    Online Resource
    Acetylcholine Increases Intracellular Calcium of Arterial Chemoreceptor Cells of Adult Cats
    American Physiological Society ; 1997
    In:  Journal of Neurophysiology Vol. 78, No. 5 ( 1997-11-01), p. 2388-2395
    Details
    In: Journal of Neurophysiology, American Physiological Society, Vol. 78, No. 5 ( 1997-11-01), p. 2388-2395
    Abstract: Shirahata, Machiko, Robert S. Fitzgerald, and James S. K. Sham. Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats. J. Neurophysiol. 78: 2388–2395, 1997. Several neurotransmitters have been reported to play important roles in the chemoreception of the carotid body. Among them acetylcholine (ACh) appears to be involved in excitatory processes in the cat carotid body. As one of the steps to elucidate possible roles of ACh in carotid body chemoreception in the cat, we examined the effect of ACh on intracellular calcium concentration ([Ca 2+ ] i ) of cultured carotid body cells. The carotid body from adult cats was dissociated and cultured for up to 2 wk. [Ca 2+ ] i was measured from clusters of cells with a microfluorometric technique using Indo-1 AM. Experiments were performed at 37°C, and cells were continuously superfused with modified Krebs solutions equilibrated with 5% CO 2 -16% O 2 -79% N 2 . ACh (100 μM) caused a marked increase in [Ca 2+ ] i in ∼70% of clusters, and the responses to 1–300 μM of ACh were concentration dependent. The magnitude and kinetics of the ACh response were mimicked by the application of nicotine, whereas muscarinic agonists, pilocarpine, and muscarine failed to evoke a similar response. ACh-induced increase in [Ca 2+ ] i was dependent on extracellular Ca 2+ : it was greatly reduced or completely abolished by a transient removal of extracellular Ca 2+ . The response was consistently but only partially reduced by caffeine (5 mM) or nifedipine (10 μM). The effect of mecamylamine (100 μM) was inhibitory but small. Moreover, the increase in [Ca 2+ ] i in response to ACh was also observed in some clusters that did not respond to high K (100 mM) Krebs. These results suggest that ACh increases [Ca 2+ ] i of cultured carotid body cells by activating neuronal nicotinic ACh receptors, leading to Ca 2+ influx via nicotinic channels. In addition, other pathways such as Ca 2+ influx through L-type calcium channels, perhaps secondary to membrane depolarization, and Ca 2+ release from intracellular stores may participate in increasing [Ca 2+ ] i in response to ACh. Muscarinic receptors appear to play only a small role, if any.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    URL: Article
    DOI: 10.1152/jn.1997.78.5.2388
    RVK:
    XA 10000 ; XA 552555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1997
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 6
    Online Resource
    Online Resource
    TRPM7 channels regulate breathing during sleep in obesity by acting peripherally in the carotid bodies
    Wiley ; 2022
    In:  The Journal of Physiology Vol. 600, No. 23 ( 2022-12), p. 5145-5162
    Details
    In: The Journal of Physiology, Wiley, Vol. 600, No. 23 ( 2022-12), p. 5145-5162
    Abstract: Sleep‐disordered breathing (SDB) affects over 50% of obese individuals. Exaggerated hypoxic chemoreflex is a cardinal trait of SDB in obesity. We have shown that leptin acts in the carotid bodies (CB) to augment chemoreflex and that leptin activates the transient receptor potential melastatin 7 (TRPM7) channel. However, the effect of leptin‐TRPM7 signalling in CB on breathing and SDB has not been characterized in diet‐induced obesity (DIO). We hypothesized that leptin acts via TRPM7 in the CB to increase chemoreflex leading to SDB in obesity. DIO mice were implanted with EEG/EMG electrodes and transfected with Lepr b short hairpin RNA (shRNA) or Trpm7 shRNA vs . control shRNA in the CB area bilaterally. Mice underwent a full‐polysomnography and metabolic studies at baseline and after transfection. Ventilatory responses to hypoxia and hypercapnia were assessed during wakefulness. Lepr b and Trpm7 were upregulated and their promoters were demethylated in the CB of DIO mice. Lepr b knockdown in the CB did not significantly affect ventilation. Trpm 7 knockdown in the CB stimulated breathing during sleep in normoxia. These effects were not driven by changes in CB chemosensitivity or metabolism. Under sustained hypoxia, Trpm7 shRNA in the CB augmented ventilation during sleep, but decreased oxyhaemoglobin saturation. We conclude that the suppression of TRPM7 in the CB improved sleep‐related hypoventilation and that the respiratory effects of CB TRPM7 channels in obesity are independent of leptin. TRPM7 signalling in the CB could be a therapeutic target for the treatment of obesity‐related SDB. image Key points The leptin‐TRPM7 axis in the carotid bodies may play an important role in the pathogenesis of sleep‐disordered breathing. TRPM7 channels regulate breathing during sleep by acting peripherally in the carotid bodies. Suppression of TRPM7 signalling in the carotid bodies improves the obesity‐induced hypoventilation in mice. Pharmacological blockade of TRPM7 channels in the carotid bodies could be a therapy for sleep‐disordered breathing in obesity.
    Type of Medium: Online Resource
    ISSN: 0022-3751 , 1469-7793
    URL: Issue
    URL: Article
    DOI: 10.1113/tjp.v600.23
    DOI: 10.1113/JP283678
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 1475290-6
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Functional expression of transient receptor potential melastatin- and vanilloid-related channels in pulmonary arterial and aortic smooth muscle
    American Physiological Society ; 2006
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 290, No. 6 ( 2006-06), p. L1267-L1276
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 290, No. 6 ( 2006-06), p. L1267-L1276
    Abstract: Transient receptor potential melastatin- (TRPM) and vanilloid-related (TRPV) channels are nonselective cation channels pertinent to diverse physiological functions. Multiple TRPM and TRPV channel subtypes have been identified and cloned in different tissues. However, their information in vascular tissue is scant. In this study, we sought to identify TRPM and TRPV channel subtypes expressed in rat deendothelialized intralobar pulmonary arteries (PAs) and aorta. With RT-PCR, mRNA of TRPM2, TRPM3, TRPM4, TRPM7, and TRPM8 of TRPM family and TRPV1, TRPV2, TRPV3, and TRPV4 of TRPV family were detected in both PAs and aorta. Quantitative real-time RT-PCR showed that TRPM8 and TRPV4 were the most abundantly expressed TRPM and TRPV subtypes, respectively. Moreover, Western blot analysis verified expression of TRPM2, TRPM8, TRPV1, and TRPV4 proteins in both types of vascular tissue. To examine the functional activities of these channels, we monitored intracellular Ca 2+ transients ([Ca 2+ ] i ) in pulmonary arterial smooth muscle cells (PASMCs) and aortic smooth muscle cells (ASMCs). The TRPM8 agonist menthol (300 μM) and the TRPV4 agonist 4α-phorbol 12,13-didecanoate (1 μM) evoked significant increases in [Ca 2+ ] i in PASMCs and ASMCs. These Ca 2+ responses were abolished in the absence of extracellular Ca 2+ or the presence of 300 μM Ni 2+ but were unaffected by 1 μM nifedipine, suggesting Ca 2+ influx via nonselective cation channels. Hence, for the first time, our results indicate that multiple functional TRPM and TRPV channels are coexpressed in rat intralobar PAs and aorta. These novel Ca 2+ entry pathways may play important roles in the regulation of pulmonary and systemic circulation.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.00515.2005
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2006
    detail.hit.zdb_id: 1477300-4
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Calcium signaling in vasopressin-induced aquaporin-2 trafficking
    Springer Science and Business Media LLC ; 2008
    In:  Pflügers Archiv - European Journal of Physiology Vol. 456, No. 4 ( 2008-7), p. 747-754
    Details
    In: Pflügers Archiv - European Journal of Physiology, Springer Science and Business Media LLC, Vol. 456, No. 4 ( 2008-7), p. 747-754
    Type of Medium: Online Resource
    ISSN: 0031-6768 , 1432-2013
    URL: Article
    DOI: 10.1007/s00424-007-0371-7
    RVK:
    WA 15000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2008
    detail.hit.zdb_id: 1463014-X
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Magnesium attenuates endothelin‐1‐induced vasoreactivity and enhances vasodilatation in mouse pulmonary arteries: Modulation by chronic hypoxic pulmonary hypertension
    Wiley ; 2018
    In:  Experimental Physiology Vol. 103, No. 4 ( 2018-04), p. 604-616
    Details
    In: Experimental Physiology, Wiley, Vol. 103, No. 4 ( 2018-04), p. 604-616
    Abstract: What is the central question of this study? The central goal of this study was to elucidate the role of magnesium in the regulation of pulmonary vascular reactivity in relationship to hypoxic pulmonary hypertension. What is the main finding and its importance? We found that magnesium is essential for normal vasoreactivity of the pulmonary artery. Increasing the magnesium concentration attenuates vasoconstriction and improves vasodilatation via release of nitric oxide. Pulmonary hypertension is associated with endothelial dysfunction resulting in the suppression of magnesium modulation of vasodilatation. These results provide evidence that magnesium is important for the modulation of pulmonary vascular function. Abstract Pulmonary hypertension (PH) is characterized by enhanced vasoreactivity and sustained pulmonary vasoconstriction, arising from aberrant Ca 2+ homeostasis in pulmonary arterial (PA) smooth muscle cells. In addition to Ca 2+ , magnesium, the most abundant intracellular divalent cation, also plays crucial roles in many cellular processes that regulate cardiovascular function. Recent findings suggest that magnesium regulates vascular functions by altering the vascular responses to vasodilator and vasoactive agonists and affects endothelial function by modulating endothelium‐dependent vasodilatation in hypertension. Administration of magnesium also decreased pulmonary arterial pressure and improved cardiac output in animal models of PH. However, the role of magnesium in the regulation of pulmonary vascular function related to PH has not been studied. In this study, we examined the effects of magnesium on endothelin‐1 (ET‐1)‐induced vasoconstriction, ACh‐induced vasodilatation and the generation of NO in PAs of normoxic mice and chronic hypoxia (CH)‐treated mice. Our data showed that removal of extracellular magnesium suppressed vasoreactivity of PAs to both ET‐1 and ACh. A high concentration of magnesium (4.8 m m ) inhibited ET‐1‐induced vasoconstriction in endothelium‐intact or endothelium‐disrupted PAs of normoxic and CH‐treated mice, and enhanced the ACh‐induced production of NO in PAs of normoxic mice. Moreover, magnesium enhanced ACh‐induced vasodilatation in PAs of normoxic mice, and the enhancement was completely abolished after exposure to CH. Hence, in this study we demonstrated that increasing the magnesium concentration can attenuate the ET‐1‐induced contractile response and improve vasodilatation via release of NO from the endothelium. We also demonstrated that chronic exposure to hypoxia can cause endothelial dysfunction resulting in suppression of the magnesium‐dependent modulation of vasodilatation.
    Type of Medium: Online Resource
    ISSN: 0958-0670 , 1469-445X
    URL: Issue
    URL: Article
    DOI: 10.1113/eph.2018.103.issue-4
    DOI: 10.1113/EP086655
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 1493802-9
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  • 10
    Online Resource
    Online Resource
    Mechanisms Underlying the Effects of the Pyrethroid Tefluthrin on Action Potential Duration in Isolated Rat Ventricular Myocytes
    American Society for Pharmacology & Experimental Therapeutics (ASPET) ; 2005
    In:  Journal of Pharmacology and Experimental Therapeutics Vol. 315, No. 1 ( 2005-10), p. 16-23
    Details
    In: Journal of Pharmacology and Experimental Therapeutics, American Society for Pharmacology & Experimental Therapeutics (ASPET), Vol. 315, No. 1 ( 2005-10), p. 16-23
    Type of Medium: Online Resource
    ISSN: 0022-3565 , 1521-0103
    URL: Article
    DOI: 10.1124/jpet.105.084822
    Language: English
    Publisher: American Society for Pharmacology & Experimental Therapeutics (ASPET)
    Publication Date: 2005
    detail.hit.zdb_id: 1475023-5
    SSG: 15,3
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