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  • American Physiological Society  (5)
  • 1995-1999  (5)
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  • American Physiological Society  (5)
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  • 1995-1999  (5)
Year
  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 276, No. 4 ( 1999-04-01), p. R1118-R1124
    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
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Location Call Number Limitation Availability
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 277, No. 4 ( 1999-10-01), p. R1051-R1056
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 277, No. 4 ( 1999-10-01), p. R1051-R1056
    Abstract: We examined the effects of sarafotoxin 6c (S6c), an endothelin-B (ET B ) receptor agonist, on adrenal catecholamine secretion in response to cholinergic stimuli in pentobarbital sodium-anesthetized dogs. Drugs were administered intra-arterially into the adrenal gland through the phrenicoabdominal artery. Infusion of S6c attenuated increases in adrenal catecholamine output induced by splanchnic nerve stimulation. The inhibitory effect of S6c on the catecholamine secretion response was suppressed with a selective ET B receptor antagonist N- cis2,6-dimethylpiperidinocarbonyl-l-γ-methylleucyl-d-1-methoxycarbonyltryptophanyl-d-norleucine (BQ-788), a nitric oxide synthase (NOS) inhibitor N ω -nitro-l-arginine methyl ester, and a neuronal NOS inhibitor 7-nitroindazole monosodium salt (7-NINA). Similar results were obtained with the catecholamine secretion response induced by injection of ACh. 7-NINA alone did not affect these catecholamine secretion responses. These results suggest that ET B receptors play an inhibitory role in adrenal catecholamine secretion by activating neuronal NOS, whereas neuronal NOS is unlikely to be involved in regulation of adrenal catecholamine secretion in the absence of simultaneous ET B receptor stimulation.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 277, No. 4 ( 1999-10-01), p. R1057-R1062
    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
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 274, No. 4 ( 1998-04-01), p. R1125-R1130
    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
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Location Call Number Limitation Availability
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 275, No. 4 ( 1998-10-01), p. R1075-R1081
    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
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Location Call Number Limitation Availability
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