Role of potassium channels in the nitrergic nerve stimulation‐induced vasodilatation in the guinea‐pig isolated basilar artery

Jiang, Fan; Li, Chun Guang; Rand, M. J.

doi:10.1038/sj.bjp.0701552

Cited by 13 publications

(8 citation statements)

References 36 publications

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“…To confirm the involvement of K + channels, the preparations were pretreated with TEA (3 mM), a nonselective K + channel blocker [23]. In the presence of this pharmacological tool, the vasorelaxant response induced by increasing concentrations of VPR was significantly attenuated, corroborating our previous observation that VPR appears to have a significant effect on the open probability of K + channels in mesenteric artery rings.…”

Section: Discussionsupporting

confidence: 77%

Involvement of Potassium Channels in Vasorelaxant Effect Induced byValeriana prionophyllaStandl. in Rat Mesenteric Artery

Reis

Filho

Rodrigues

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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Assays in vitro and in vivo were performed on extract from roots and leaves from the Valeriana prionophylla Standl. (VPR and VPF, resp.). In phenylephrine (1 μM) precontracted rings, VPR (0.01–300 μg/mL) induced a concentration-dependent relaxation (maximum response (MR) = 75.4 ± 4.0%, EC50 = 5.97 (3.8–9.3) μg/mL, n = 6]); this effect was significantly modified after removal of the endothelium (EC50 = 39.6 (27.2–57.6) μg/mL, P < 0.05). However, VPF-induced vasorelaxation was less effective compared to VPR. When rings were preincubated with L-NAME (100 μM) or indomethacin (10 μM), the endothelium-dependent relaxation induced by VPR was significantly attenuated (MR = 20.9 ± 2.3%, 34.2 ± 2.9%, resp., P < 0.001). In rings denuded endothelium, precontracted with KCl (80 mM), or in preparations pretreated with KCl (20 mM) or tetraethylammonium (1 or 3 mM), the vasorelaxant activity of VPR was significantly attenuated (MR = 40.0 ± 8.2, n = 5; 50.5 ± 6.0%; 49.3 ± 6.4%; 46.8 ± 6.2%; resp., P < 0.01). In contrast, neither glibenclamide (10 μM), barium chloride (30 μM), nor 4-aminopyridine (1 mM) affected VPR-induced relaxation. Taken together, these results demonstrate that hypotension induced by VPR seems to involve, at least in part, a vascular component. Furthermore, endothelium-independent relaxation induced by VPR involves K+ channels activation, most likely due to BKCa channels, in the rat superior mesenteric artery.

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Section: Discussionsupporting

confidence: 77%

Involvement of Potassium Channels in Vasorelaxant Effect Induced byValeriana prionophyllaStandl. in Rat Mesenteric Artery

Reis

Filho

Rodrigues

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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“…In addition, opening K + channels in smooth muscle cell membranes increases K + efflux, hence resulting in membrane hyperpolarization, closure of voltage-dependent Ca 2+ channels and decreases in the cytosolic Ca 2+ concentration, thus leading to relaxation of the smooth muscle cells (Nelson and Quayle 1995). Activation of K + channels via cGMP-dependent or independent mechanisms may be involved in the relaxations induced by nitrergic nerve stimulation, NO and NO donors (Bolotina et al 1994;Jiang et al 1998). However, this role of K + channels does not seem to be common to all tissues and species and, where present, differences related to the K + channel types involved also exist.…”

Section: Introductionmentioning

confidence: 97%

Nitrergic relaxation in urethral smooth muscle: involvement of potassium channels and alternative redox forms of NO

Costa

Labadía²,

Triguero³

et al. 2001

Naunyn-Schmied Arch Pharmacol

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We examined the contribution of K+ channels to the relaxation responses induced by different redox forms of nitric oxide (NO., NO- and NO+) in comparison with those evoked by electrical field stimulation (EFS) of nitrergic nerves in the sheep urethra. K+ channel blockers with different selectivity profile were used. Sodium nitroprusside (SNP) and different S-nitrosothiols were used as NO+ donors, Angeli's salt as an NO- donor and nitroglycerin (GTN) was chosen as a representative compound known to require metabolic activation in the target tissue. Pure NO gas was used to prepare NO. solutions. Relaxation evoked by EFS of nitrergic nerves or by exogenous NO was not inhibited by any of the K+ channel blockers, but was enhanced by 4-aminopyridine [inhibitor of voltage-dependent K+ (KV) channels]. This suggests that, whereas K+ channel activation and hyperpolarization of the postsynaptic membrane do not contribute to relaxation, prejunctional modulation of the nitrergic neurotransmission by Kv channels may be relevant. Relaxation induced by NO+ or NO- donors was not affected by K+ channel blockade with the following exceptions: glybenclamide, a blocker of ATP-sensitive K+ channels (KATP), enhanced responses to SNP and Angeli's salt, 4-aminopyridine inhibited relaxation evoked by Angeli's salt and GTN, and charybdotoxin, a blocker of large-conductance, Ca2+-activated K+ channels (BKCa) inhibited those induced by the S-nitrosothiol S-nitrosoglutathione. These results do not suggest the existence of a general mechanism of action on K+ channels for compounds releasing either NO+ or NO- in the sheep urethra. None of the K+ channel blockers affected relaxation induced by the membrane-permeable analogue of cGMP, 8-bromo-cGMP. However, the fact that the addition of the phosphodiesterase inhibitor zaprinast (0.1 mM) enhanced the relaxation to Angeli's salt, while preventing the inhibition induced by 4-aminopyridine, suggests that involvement of guanylate cyclase activation in the action of NO donors on K+ channels can not be excluded. Accordingly, the guanylate cyclase inhibitors 1H-[1,2,4]-oxadiazole-[4,3-a]-quinoxalin-1-one (ODQ, 10 microM) and 4H-8-bromo-1,2,4-oxadiazolo(3,4-d)benz(b)(1,4)oxazin-1-one (NS 2028, 10 microM) almost abolished relaxations to EFS and Angeli's salt. In contrast, ODQ only moderately inhibited relaxations to NO.. In addition, the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl imidazoline-1-oxyl 3-oxide (carboxy-PTIO) effectively inhibited responses to NO. whilst not affecting those to EFS or NO-, suggesting a close similarity between the nitrergic transmitter and nitroxyl ion. We conclude that nitrergic relaxation induced either by the endogenous transmitter or by exogenous NO donors in the ovine urethra is not mediated by postsynaptic alterations in the K+ conductance; only a prejunctional modulation through Kv channels seems to be significant. In addition, the production and/or release of alternative redox forms of NO, such as NO-, may be involved in neurotransmission processes in the urethra.

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“…This mechanism occurs in cerebral blood vessels as well, where NO and NO donors produce marked in creases in cGMP levels and vasorelaxation (Brian et aI., 1994;Homayoun et aI., 1989;Katusic et aI., 1989;Kim et a!., 1992;Onoue and Katusic, 1997, 1998a, 1998bPearce et aI., 1994;Yang et a!., 1991a). Several lines of evidence, including studies using inhibitors of soluble guanylate cyclase, suggest that relaxation of cerebral blood vessels (large arteries and microvessels) in re sponse to NO is mediated predominantly by soluble gua nylate cyclase (Dong et aI., 1998;Jiang et a!., 1998;Meng et aI., 1998;Onoue and Katusic, 1998b;Sobey and Cocks, 1998;Sobey and Faraci, 1997 a;Yang and Iadecola, 1998) (Fig. 3).…”

Section: Vasoactive Stimuli Nitric Oxidementioning

confidence: 99%

Role of Potassium Channels in Regulation of Cerebral Vascular Tone

Faraci

Sobey

1998

J Cereb Blood Flow Metab

129

108

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Role of potassium channels in the nitrergic nerve stimulation‐induced vasodilatation in the guinea‐pig isolated basilar artery

Cited by 13 publications

References 36 publications

Involvement of Potassium Channels in Vasorelaxant Effect Induced byValeriana prionophyllaStandl. in Rat Mesenteric Artery

Involvement of Potassium Channels in Vasorelaxant Effect Induced byValeriana prionophyllaStandl. in Rat Mesenteric Artery

Nitrergic relaxation in urethral smooth muscle: involvement of potassium channels and alternative redox forms of NO

Role of Potassium Channels in Regulation of Cerebral Vascular Tone

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