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  • American Physiological Society  (11)
  • Yoshida, Makoto  (11)
  • 1
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    Role of cholinergic receptors in adrenal catecholamine secretion in spontaneously hypertensive rats
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 277, No. 4 ( 1999-10-01), p. R1057-R1062
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 277, No. 4 ( 1999-10-01), p. R1057-R1062
    Abstract: We investigated the role of nicotinic and muscarinic receptors in secretion of catecholamines induced by transmural electrical stimulation (ES) from isolated perfused adrenal glands of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats. ES (1–10 Hz) produced frequency-dependent increases in epinephrine (Epi) and norepinephrine (NE) output as measured in perfusate. The ES-induced increases in NE output, but not Epi output, were significantly greater in adrenal glands of SHRs than in those of WKY rats. Hexamethonium (10–100 μM) markedly inhibited the ES-induced increases in Epi and NE output from adrenal glands of SHRs and WKY rats. Atropine (0.3–3 μM) inhibited the ES-induced increases in Epi and NE output from adrenal glands of SHRs, but not from those of WKY rats. These results suggest that endogenous acetylcholine-induced secretion of adrenal catecholamines is predominantly mediated by nicotinic receptors in SHRs and WKY rats and that the contribution of muscarinic receptors may be different between these two strains.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.1999.277.4.R1057
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477297-8
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  • 2
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    Role of endogenous PACAP in catecholamine secretion from the rat adrenal gland
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 281, No. 5 ( 2001-11-01), p. R1562-R1567
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 281, No. 5 ( 2001-11-01), p. R1562-R1567
    Abstract: We elucidated the contribution of endogenous pituitary adenylate cyclase-activating polypeptide (PACAP) to neurally evoked catecholamine secretion from the isolated perfused rat adrenal gland. Infusion of PACAP (100 nM) increased adrenal epinephrine and norepinephrine output. The PACAP-induced catecholamine output responses were inhibited by the PACAP type I receptor antagonist PACAP- (6-38) (30–3,000 nM) but were resistant to the PACAP type II receptor antagonist [Lys 1 ,Pro 2,5 ,Ara 3,4 ,Tyr 6 ]-vasoactive intestinal peptide (LPAT-VIP; 30–3,000 nM). Transmural electrical stimulation (ES; 1–10 Hz) or infusion of ACh (6–200 nM) increased adrenal epinephrine and norepinephrine output. PACAP-(6–38) (3,000 nM), but not LPAT-VIP, also inhibited the ES-induced catecholamine output responses. However, PACAP-(6–38) did not affect the ACh-induced catecholamine output responses. PACAP at low concentrations (0.3–3 nM), which had no influence on catecholamine output, enhanced the ACh-induced catecholamine output responses, but not the ES-induced catecholamine output responses. These results suggest that PACAP is released from the nerve endings to facilitate the neurally evoked catecholamine secretion through PACAP type I receptors in the rat adrenal gland.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.2001.281.5.R1562
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477297-8
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  • 3
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    Role of potassium channels in catecholamine secretion in the rat adrenal gland
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 279, No. 2 ( 2000-08-01), p. R448-R454
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 279, No. 2 ( 2000-08-01), p. R448-R454
    Abstract: We elucidated the functional contribution of K + channels to cholinergic control of catecholamine secretion in the perfused rat adrenal gland. The small-conductance Ca 2+ -activated K + (SK Ca )-channel blocker apamin (10–100 nM) enhanced the transmural electrical stimulation (ES; 1–10 Hz)- and 1,1-dimethyl-4-phenyl-piperazinium (DMPP; 5–40 μM)-induced increases in norepinephrine (NE) output, whereas it did not affect the epinephrine (Epi) responses. Apamin enhanced the catecholamine responses induced by acetylcholine (6–200 μM) and methacholine (10–300 μM). The putative large-conductance Ca 2+ -activated K + channel blocker charybdotoxin (10–100 nM) enhanced the catecholamine responses induced by ES, but not the responses induced by cholinergic agonists. Neither the K A channel blocker mast cell degranulating peptide (100–1000 nM) nor the K V channel blocker margatoxin (10–100 nM) affected the catecholamine responses. These results suggest that SK Ca channels play an inhibitory role in adrenal catecholamine secretion mediated by muscarinic receptors and also in the nicotinic receptor-mediated secretion of NE, but not of Epi. Charybdotoxin-sensitive Ca 2+ -activated K + channels may control the secretion at the presynaptic site.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.2000.279.2.R448
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477297-8
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  • 4
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    E-cigarette aerosols of propylene glycol impair BK channel activity and parameters of mucociliary function
    American Physiological Society ; 2023
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 324, No. 4 ( 2023-04-01), p. L468-L479
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 324, No. 4 ( 2023-04-01), p. L468-L479
    Abstract: Propylene glycol (PG) is a common delivery vehicle for nicotine and flavorings in e-cigarette (e-cig) liquids and is largely considered safe for ingestion. However, little is known about its effects as an e-cig aerosol on the airway. Here, we investigated whether pure PG e-cig aerosols in realistic daily amounts impact parameters of mucociliary function and airway inflammation in a large animal model (sheep) in vivo and primary human bronchial epithelial cells (HBECs) in vitro. Five-day exposure of sheep to e-cig aerosols of 100% PG increased mucus concentrations (% mucus solids) of tracheal secretions. PG e-cig aerosols further increased the activity of matrix metalloproteinase-9 (MMP-9) in tracheal secretions. In vitro exposure of HBECs to e-cig aerosols of 100% PG decreased ciliary beating and increased mucus concentrations. PG e-cig aerosols further reduced the activity of large conductance, Ca 2+ -activated, and voltage-dependent K + (BK) channels. We show here for the first time that PG can be metabolized to methylglyoxal (MGO) in airway epithelia. PG e-cig aerosols increased levels of MGO and MGO alone reduced BK activity. Patch-clamp experiments suggest that MGO can disrupt the interaction between the major pore-forming BK subunit human Slo1 (hSlo1) and the gamma regulatory subunit LRRC26. PG exposures also caused a significant increase in mRNA expression levels of MMP9 and interleukin 1 beta ( IL1B). Taken together, these data show that PG e-cig aerosols cause mucus hyperconcentration in sheep in vivo and HBECs in vitro, likely by disrupting the function of BK channels important for airway hydration.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.00157.2022
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 1477300-4
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  • 5
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    Role of K + channels in adrenal catecholamine secretion in anesthetized dogs
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 274, No. 4 ( 1998-04-01), p. R1125-R1130
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 274, No. 4 ( 1998-04-01), p. R1125-R1130
    Abstract: We examined the role of K + channels in the secretion of adrenal catecholamine (CA) in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. K + channel blockers and the cholinergic agonists were infused and injected, respectively, into the adrenal gland. The voltage-dependent K + channel (K A type) blocker mast cell degranulating (MCD) peptide infusion (10–100 ng/min) enhanced increases in CA output induced by SNS (1–3 Hz), but it did not affect increases in CA output induced by ACh (0.75–3 μg), DMPP (0.1–0.4 μg), or muscarine (0.5–2 μg). The small-conductance Ca 2+ -activated K + (SK Ca ) channel blocker scyllatoxin infusion (10–100 ng/min) enhanced the ACh-, DMPP-, and muscarine-induced increases in CA output, but it did not affect the SNS-induced increases in CA output. These results suggest that K A channels may play an inhibitory role in the regulation of adrenal CA secretion in response to SNS and that SK Ca channels may play the same role in the secretion in response to exogenously applied cholinergic agonists.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.1998.274.4.R1125
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
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  • 6
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    Facilitatory role of NO in neural norepinephrine release in the rat kidney
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 282, No. 5 ( 2002-05-01), p. R1436-R1442
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 282, No. 5 ( 2002-05-01), p. R1436-R1442
    Abstract: We examined modulation by nitric oxide (NO) of sympathetic neurotransmitter release and vasoconstriction in the isolated pump-perfused rat kidney. Electrical renal nerve stimulation (RNS; 1 and 2 Hz) increased renal perfusion pressure and renal norepinephrine (NE) efflux. Nonselective NO synthase (NOS) inhibitors [ N ω -nitro-l-arginine methyl ester (l-NAME) or N ω -nitro-l-arginine], but not a selective neuronal NO synthase inhibitor (7-n itroindazole sodium salt), suppressed the NE efflux response and enhanced the perfusion pressure response. Pretreatment with l-arginine prevented the effects of l-NAME on the RNS-induced responses. 2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), which eliminates NO by oxidizing it to NO 2 , suppressed the NE efflux response, whereas the perfusion pressure response was less susceptible to carboxy-PTIO. 8-Bromoguanosine cGMP suppressed and a guanylate cyclase inhibitor [4 H-8-bromo-1,2,4-oxadiazolo(3,4-d)benz(b)(1,4)oxazin-1-one] enhanced the RNS-induced perfusion pressure response, but neither of these drugs affected the NE efflux response. These results suggest that endogenous NO facilitates the NE release through cGMP-independent mechanisms, NO metabolites formed after NO 2 rather than NO itself counteract the vasoconstriction, and neuronal NOS does not contribute to these modulatory mechanisms in the sympathetic nervous system of the rat kidney.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00697.2001
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
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  • 7
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    Interaction of SK Ca channels and L-type Ca 2+ channels in catecholamine secretion in the rat adrenal gland
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 279, No. 5 ( 2000-11-01), p. R1731-R1736
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 279, No. 5 ( 2000-11-01), p. R1731-R1736
    Abstract: We elucidated the interaction of small-conductance Ca 2+ -activated K + (SK Ca ) channels and L-type Ca 2+ channels in muscarinic receptor-mediated control of catecholamine secretion in the isolated perfused rat adrenal gland. The muscarinic agonist methacholine (10–300 μM) produced concentration-dependent increases in adrenal output of epinephrine and norepinephrine. The SK Ca channel blocker apamin (1 μM) enhanced the methacholine-induced catecholamine responses. The facilitatory effect of apamin on the methacholine-induced catecholamine responses was not observed during treatment with the L-type Ca 2+ channel blocker nifedipine (3 μM) or Ca 2+ -free solution. Nifedipine did not affect the methacholine-induced catecholamine responses, but it inhibited the responses during treatment with apamin. The L-type Ca 2+ channel activator Bay k 8644 (1 μM) enhanced the methacholine-induced catecholamine responses, whereas the enhancement of the methacholine-induced epinephrine and norepinephrine responses were prevented and attenuated by apamin, respectively. These results suggest that SK Ca channels are activated by muscarinic receptor stimulation, which inhibits the opening of L-type Ca 2+ channels and thereby attenuates adrenal catecholamine secretion.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.2000.279.5.R1731
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477297-8
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  • 8
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    Role of nitric oxide in adrenal catecholamine secretion in anesthetized dogs
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 275, No. 4 ( 1998-10-01), p. R1075-R1081
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 275, No. 4 ( 1998-10-01), p. R1075-R1081
    Abstract: We examined the role of nitric oxide (NO) in adrenal catecholamine secretion in response to splanchnic nerve stimulation (SNS) and exogenous acetylcholine (ACh) in anesthetized dogs. The NO synthase inhibitor N ω -nitro-l-arginine methyl ester (l-NAME), NO donor 3-(2-hydroxy-1-methyl-2-nitrosohydrazino)- N-methyl-1-propanamine (NOC 7), and ACh were administered intra-arterially into the adrenal gland. The increases in catecholamine output induced by ACh (0.75–3 μg) were enhanced byl-NAME (0.1–1 mg/min) and inhibited by NOC 7 (0.2–2 μg/min). Inhibition by NOC 7 (2 μg/min) was observed during treatment withl-NAME (1 mg/min). The increases in catecholamine output induced by SNS (1–2 Hz) were inhibited byl-NAME and by NOC 7. No inhibitory effect of NOC 7 was observed during treatment withl-NAME. These results suggest that NO may play an inhibitory role in the regulation of adrenal catecholamine secretion in response to exogenous ACh.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.1998.275.4.R1075
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
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  • 9
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    Role of calcium channels and adenylate cyclase in the PACAP-induced adrenal catecholamine secretion
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 281, No. 2 ( 2001-08-01), p. R495-R501
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 281, No. 2 ( 2001-08-01), p. R495-R501
    Abstract: We elucidated the functional contribution of voltage-dependent calcium channels (VDCCs) and adenylate cyclase to epinephrine (Epi) and norepinephrine (NE) secretion induced by pituitary adenylate cyclase-activating polypeptide (PACAP) in the isolated perfused rat adrenal gland. PACAP increased Epi and NE output, which was inhibited by perfusion with calcium-free solution or by nifedipine, an L-type VDCC blocker. However, the PACAP-induced responses were resistant to ω-conotoxin GVIA, an N-type VDCC blocker, or ω-conotoxin MVIIC, a P/Q-type VDCC blocker. MDL-12330A, an adenylate cyclase inhibitor, inhibited the PACAP-induced increase in Epi, but not NE, output. Treatment with nifedipine and MDL-12330A caused additive inhibition of the PACAP-induced catecholamine responses. These results suggest that opening of L-type VDCCs is responsible for adrenal catecholamine secretion induced by PACAP and that activation of adenylate cyclase is involved in the PACAP-induced Epi, but not NE, secretion. These pathways may act independently of each other.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.2001.281.2.R495
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477297-8
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  • 10
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    Effects of adrenomedullin and PAMP on adrenal catecholamine release in dogs
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 276, No. 4 ( 1999-04-01), p. R1118-R1124
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 276, No. 4 ( 1999-04-01), p. R1118-R1124
    Abstract: We examined the effects of proadrenomedullin-derived peptides on the release of adrenal catecholamines in response to cholinergic stimuli in pentobarbital sodium-anesthetized dogs. Drugs were administered into the adrenal gland through the phrenicoabdominal artery. Splanchnic nerve stimulation (1, 2, and 3 Hz) and ACh injection (0.75, 1.5, and 3 μg) produced frequency- or dose-dependent increases in adrenal catecholamine output. These responses were unaffected by infusion of adrenomedullin (1, 3, and 10 ng ⋅ kg −1 ⋅ min −1 ) or its selective antagonist adrenomedullin-(22—52) (5, 15, and 50 ng ⋅ kg −1 ⋅ min −1 ). Proadrenomedullin NH 2 -terminal 20 peptide (PAMP; 5, 15, and 50 ng ⋅ kg −1 ⋅ min −1 ) suppressed both the splanchnic nerve stimulation- and ACh-induced increases in catecholamine output in a dose-dependent manner. PAMP also suppressed the catecholamine release responses to the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (0.5, 1, and 2 μg) and to muscarine (0.5, 1, and 2 μg), although the muscarine-induced response was relatively resistant to PAMP. These results suggest that PAMP, but not adrenomedullin, can act as an inhibitory regulator of adrenal catecholamine release in vivo.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.1999.276.4.R1118
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
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