Nitric oxide modulates evoked catecholamine release from canine adrenal medulla

Barnes, Roxann D.; Ward, L. Emmerson; Frank, Keith; Tyce, Gertrude M.; Hunter, Larry W.; Rorie, Duane K.

doi:10.1016/s0306-4522(01)00146-4

Cited by 28 publications

(19 citation statements)

References 42 publications

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“…However, there is also evidence implicating eNOS (Torres et al, 1994;Barnes et al, 2001). A number of NOS inhibitors have been identified and used as experimental tools to investigate the biological significance of NO (Bland-Ward and Moore, 1995).…”

Section: Nos Isoformsmentioning

confidence: 99%

“…Currently, most inhibitors show a lack of selectivity on isolated enzymes (Moncada et al, 1997;Mayer and Andrew, 1998). Not surprisingly, therefore, 7-NI, a compound often used as a selective nNOS inhibitor (Barnes et al, 2001;Xu et al, 2001), was shown to inhibit the other isoforms with equal potency (Bland-Ward and Moore, 1995;Dick and Lefebvre, 1997;Moncada et al, 1997). For this reason, the use of 'selective' NOS inhibitors may not be an appropriate method to assess the involvement of the different isoforms.…”

Section: Nos Isoformsmentioning

confidence: 99%

“…In rainbow trout Oncorhynchus mykiss, nNOS was localized in the head kidney tissue (Jimenez et al, 2001) but, unlike in mammals, it appears to be only sparsely present in chromaffin cells (Gallo and Civinini, 2001). Several studies have implicated nNOS in catecholamine regulation in mammals (Schwarz et al, 1998;Vicente et al, 2002;Barnes et al, 2001) whereas fewer studies have implicated endothelial NOS (eNOS) (Barnes et al, 2001;Torres et al, 1994); there is no evidence for a role for inducible NOS (iNOS).…”

mentioning

confidence: 99%

“…Results from these studies were obtained using cultured chromaffin cells (Torres et al, 1994;Oset-Gasque et al, 1994;RodriguezPascual et al, 1995;Vicente et al, 2002) or perfused adrenal glands (Marley et al, 1995;Nagayama et al, 1998;Barnes et al, 2001). These prior studies have relied mainly on pharmacological approaches including the use of NO itself (Oset-Gasque et al, 1994), NO donors, SNP and/or SNAP (Marley et al, 1995;Schwarz et al, 1998) and/or NOS inhibitors (Torres et al, 1994;Nagayama et al, 1998;Schwarz et al, 1998;Barnes et al, 2001;Vicente et al, 2002).…”

mentioning

confidence: 99%

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Nitric oxide and the control of catecholamine secretion in rainbow trout Oncorhynchus mykiss

McNeill

Perry

2005

Journal of Experimental Biology

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SUMMARY An in situ saline-perfused posterior cardinal vein preparation was used to assess the role of nitric oxide (NO) in the regulation of basal and stimulus-evoked catecholamine secretion from rainbow trout Oncorhynchus mykiss chromaffin cells. Addition of the NO donor, sodium nitroprusside(SNP) to the inflowing perfusate abolished catecholamine secretion during electrical field stimulation, thereby establishing the potential for NO to act as a potent inhibitor of catecholamine release. A possible role for endogenously produced NO was established by demonstrating that stimulus-evoked(depolarizing levels of KCl or electrical field stimulation) catecholamine secretion was markedly stimulated in the presence of the nitric oxide synthase(NOS) inhibitors l-NAME and 7-NI. Although in vitroexperiments demonstrated that catecholamine degradation was enhanced by NO in a dose-dependent manner, the dominant factor contributing to the reduction in catecholamine appearance in the perfusate was specific inhibition of catecholamine secretion. Subsequent experiments were performed to identify the NOS isoform(s) contributing to the inhibition of stimulus-evoked catecholamine secretion. Inducible NOS (iNOS; an enzyme that can be activated in the absence of Ca2+), although present in the vicinity of the chromaffin cells(based on mRNA measurements), does not appear to play a role because stimulus-evoked NO production was eliminated during perfusion with Ca2+-free saline. The potential involvement of endothelial NOS(eNOS) was revealed by showing that hypoxic perfusate evoked NO production and corresponded with an inhibition of stimulus-evoked catecholamine secretion;chemical removal of the endothelium (using saponin) prevented the production of NO during hypoxia. However, because removal of the endothelium did not affect NO production during electrical field stimulation, it would appear that the neuronal form of NOS (nNOS) is the key isoform modulating catecholamine secretion from trout chromaffin cells.

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Section: Nos Isoformsmentioning

confidence: 99%

Section: Nos Isoformsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Nitric oxide and the control of catecholamine secretion in rainbow trout Oncorhynchus mykiss

McNeill

Perry

2005

Journal of Experimental Biology

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“…A previous study by others, however, suggests that NO both from the neuronal and the endothelial sources inhibits evoked catecholamine release from canine adrenal medulla, while NO from the endothelial source is most likely responsible for inhibiting catecholamine release under basal conditions (39). On the other hand, in a pathological state such as endotoxemia, the endotoxin (bacterial lipopolysacchride) may suppress the adrenal catecholamine secretion by increasing NO production along with an enhanced expression of inducible NOS (40).…”

Section: +mentioning

confidence: 89%

Nitric Oxide Inhibits the Bradykinin B2 Receptor-Mediated Adrenomedullary Catecholamine Release but Has No Effect on Adrenal Blood Flow Response In Vivo

Bouallegue

Yamaguchi

2005

J Pharmacol Sci

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Abstract. The role of nitric oxide (NO) in bradykinin (BK)-induced adrenal catecholamine secretion still remains obscure. The present study was to investigate whether an inhibition of NO synthase with N ω -nitro-L-arginine methyl ester (L-NAME) would modulate BK-induced adrenal catecholamine secretion (ACS) and adrenal vasodilating response (AVR) in anesthetized dogs. Plasma catecholamine concentrations were determined with an HPLC coupled with an electrochemical detector. All drugs were locally administered to the left adrenal gland via intra-arterial infusion. BK dose-dependently increased both ACS and AVR. Hoe-140, a selective B 2 antagonist, significantly blocked the BK-induced increases in both ACS and AVR. In the presence of L-NAME, the BK-induced ACS was significantly enhanced, while the simultaneous AVR remained unaffected. These results suggest that the both BK-induced ACS and AVR are primarily mediated by B 2 receptors in the canine adrenal gland. Our results also suggest that the enhanced ACS in response to BK in the presence of L-NAME may have resulted from a specific inhibition of NO formation in the adrenal gland. It is concluded that the BK-induced NO may play an inhibitory role in the B 2 -receptor-mediated mechanisms regulating ACS, while it may not be implicated in the B 2 -receptor-mediated AVR under in vivo conditions.

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Phylogenesis of constitutively formed nitric oxide in non-mammals

Toda¹,

Ayajiki²

2006

Reviews of Physiology Biochemistry and Pharmacology

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Nitric oxide modulates evoked catecholamine release from canine adrenal medulla

Cited by 28 publications

References 42 publications

Nitric oxide and the control of catecholamine secretion in rainbow trout Oncorhynchus mykiss

Nitric oxide and the control of catecholamine secretion in rainbow trout Oncorhynchus mykiss

Nitric Oxide Inhibits the Bradykinin B2 Receptor-Mediated Adrenomedullary Catecholamine Release but Has No Effect on Adrenal Blood Flow Response In Vivo

Phylogenesis of constitutively formed nitric oxide in non-mammals

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