Nitric oxide synthase-independent release of nitric oxide induced by KCl in the perfused mesenteric bed of the rat

Mendizábal, Victoria; Poblete, Inés; Lomniczi, Alejandro; Rettori, Valéria; Huidobro‐Toro, J. Pablo; Adler‐Graschinsky, Edda

doi:10.1016/s0014-2999(00)00789-5

Cited by 16 publications

(8 citation statements)

References 13 publications

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“…In the arterial mesenteric bed of the rat, 70 mM KCl releases nitric oxide (32,33). In contrast, in our studies we observed a relaxation sensitive to the nitric oxide synthase inhibitor L-NAME only in the contractile responses induced by 120 mM KCl.…”

Section: Discussioncontrasting

confidence: 91%

High concentrations of KCl release noradrenaline from noradrenergic neurons in the rat anococcygeus muscle

Araújo

Bendhack

2003

Braz J Med Biol Res

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The aim of the present study was to investigate the effects of high concentrations of KCl in releasing noradrenaline from sympathetic nerves and its actions on postsynaptic a-adrenoceptors. We measured the isotonic contractions induced by KCl in the isolated rat anococcygeus muscle under different experimental conditions. The contractile responses induced by KCl were inhibited by a-adrenoceptor antagonists in 2.5 mM Ca 2+ solution. Prazosin reduced the maximum effect from 100 to 53.9 ± 10.2% (P<0.05) while the pD 2 values were not changed. The contractile responses induced by KCl were abolished by prazosin in Ca 2+ -free solution (P<0.05). Treatment of the rats with reserpine reduced the maximum effect induced by KCl as compared to the contractile responses induced by acetylcholine from 339.5 ± 157.8 to 167.3 ± 65.5% (P<0.05), and increased the pD 2 from 1.57 ± 0.01 to 1.65 ± 0.006 (P<0.05), but abolished the inhibitory effect of prazosin (P<0.05). In contrast, L-NAME increased the contractile responses induced by 120 mM KCl by 6.2 ± 2.3% (P<0.05), indicating that KCl could stimulate the neurons that release nitric oxide, an inhibitory component of the contractile response induced by KCl. Our results indicate that high concentrations of KCl induce the release of noradrenaline from noradrenergic neurons, which interacts with a 1 -adrenoceptors in smooth muscle cells, producing a contractile response in 2.5 mM Ca 2+ (100%) and in Ca 2+ -free solution, part of which is due to a direct effect of KCl on the rat anococcygeus muscle.

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Section: Discussioncontrasting

confidence: 91%

High concentrations of KCl release noradrenaline from noradrenergic neurons in the rat anococcygeus muscle

Araújo

Bendhack

2003

Braz J Med Biol Res

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“…There are also several reports of the generation of NO via non‐enzymatic pathways, including reactions between L or D ‐arginine and H 2 O 2 (Nagase et al ., 1997) and the reduction of nitrite to NO (Zweier et al ., 1995). In addition, the basal release of NO from rat mesenteric smooth muscle cells has been detected via chemiluminescence suggesting that vascular smooth muscle can generate NO in the absence of the endothelium (Mendizabal et al ., 2000).…”

Section: Discussionmentioning

confidence: 99%

A photosensitive vascular smooth muscle store of nitric oxide in mouse aorta: no dependence on expression of endothelial nitric oxide synthase

Andrews

McGuire

Triggle

2003

British J Pharmacology

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1 Photorelaxation is the reversible relaxation of vascular smooth muscle (VSM) when irradiated with ultraviolet (UV) light resulting from the release of nitric oxide (NO). In this study we characterize the involvement of endothelial nitric oxide synthase (eNOS) in the photorelaxation response of thoracic aorta from endothelial NOS de®cient (7/7) and control (C57BL/6j) mice. 2 Cirazoline contracted aortae were repeatedly exposed to 30 s of UV light every 3 ± 4 min. Equal levels of photorelaxation (45+2%; n=34) was observed in both strains., 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO), 4-aminopyridine (4-AP) and ethacrynic acid signi®cantly reduced the photorelaxation response. In C57BL/6j mice diethyldithiocarbamate (DETCA) also reduced photorelaxation. 4 Control endothelium-intact and -denuded aorta and L-NAME (100 mM) treated and untreated eNOS (7/7) aortae were repeatedly exposed to UV light for 5 min every 10 min until no photorelaxation response was observed. After 1 h of rest in the dark the vessels showed between 30 ± 70% recovery of the photorelaxation response indicating regeneration of the store in the absence of the endothelium and eNOS. 5 The results of this study suggest that photorelaxation in mouse aorta VSM results from the release of NO from a stable store of RSNOs, which activates soluble guanylate cyclase (sGC), leading to cGMP-dependent relaxation that is partially mediated by an increase in K V channel activation and hyperpolarization. In addition, the eNOS isoform is not essential for the formation of the photorelaxation store and a non-NOS source of NO may be involved in the maintenance of this store.

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“…Series 2: Catecholamine secretion and NO production during non-specific chromaffin cell depolarization A previous study by Mendizabal et al (2000) showed that a depolarizing level of KCl was able to elicit NO production and that this production could be inhibited using a NOS inhibitor. To determine if KCl-induced NO production could be inhibited in the present study, a cocktail containing the NOS inhibitors 7-nitroindazole (7-NI; 10 -4 ·mol·l -1 ) and N-nitro L-arginine methyl ester (L-NAME; 5ϫ10 -3 ·mol·l -1 ) was used.…”

Section: Methodsmentioning

confidence: 99%

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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Nitric oxide synthase-independent release of nitric oxide induced by KCl in the perfused mesenteric bed of the rat

Cited by 16 publications

References 13 publications

High concentrations of KCl release noradrenaline from noradrenergic neurons in the rat anococcygeus muscle

High concentrations of KCl release noradrenaline from noradrenergic neurons in the rat anococcygeus muscle

A photosensitive vascular smooth muscle store of nitric oxide in mouse aorta: no dependence on expression of endothelial nitric oxide synthase

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

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