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• W2124784666 abstract "The effects of NO donors on Ca 2+ ‐dependent Cl − currents ( I Cl(Ca) ) were investigated in freshly isolated cat tracheal myocytes using the whole‐cell patch clamp technique. With nystatin‐perforated whole‐cell recording, carbachol (CCh, ≥ 1 μ m ) induced a transient inward current ( I CCh ) with a reversal potential of about ‐20 mV. Activation of I CCh probably occurred through the M 3 muscarinic receptor, since nanomolar concentrations of 4‐diphenylacetoxy‐ N ‐methylpiperidine methobromide (4‐DAMP) greatly inhibited this current, while 11‐(2‐(diethylamino)methyl)‐1‐piperidinylacetyl)‐5,11‐dihydro‐6H‐pyrido (2,3β) (1,4)benzodiazepine‐6‐one (AF‐DX 116) or pirenzepine at concentrations of up to 1 μ m were almost ineffective. Chloride channel/transporter blockers such as DIDS (100 μ m ), anthracene‐9‐carboxylic acid (9‐AC, 100 μ m ) and niflumic acid (100 μ m ) greatly inhibited I CCh , but cation channel blockers, such as nifedipine (10 μ m ), Zn 2+ (500 μ m ) or Gd 3+ (500 μ m ), were without effect. Activation of I CCh was strongly attenuated by pretreatment with ryanodine (4 μ m ) plus caffeine (10 mM). Addition of neomycin (1 mM) into the bath or inclusion of heparin (3 mg ml −1 ) in the pipette abolished a substantial part of I CCh . These results suggest that I CCh is I Cl(Ca) , which is activated by inositol 1,4,5‐trisphosphate (IP 3 )‐mediated Ca 2+ release. The nitric oxide donor S‐ nitroso‐ N‐ acetyl penicillamine (SNAP) reduced the amplitude of I CCh dose dependently (IC 50 , ≈10 μ m ). Similar inhibition was also exerted by other types of NO donor such as glyceryl trinitrate (GTN) and (±)‐ E‐ methyl‐2‐( E‐ hydroxyimitol)‐5‐nitro‐6‐methoxy‐3‐hexeneamide (NO‐R). SNAP‐induced I CCh inhibition was effectively antagonized by Methylene Blue (1‐100 nM), and mimicked by dibutyryl cGMP (db‐cGMP) (0.5‐1 mM), whereas two structurally distinct types of cGMP‐dependent (G)‐kinase inhibitor, N ‐(2‐aminoethyl)‐5‐isoquinilinesulphonamide (H‐8, 2.5 μ m ) and KT5823 (1 μ m ), failed to counteract the inhibitory effects of SNAP or db‐cGMP. Another G‐kinase‐specific inhibitor R p ‐8‐( para‐ chlorophenylthio)guanosine‐3′,5′‐cyclic monophosphorothioate (Rp‐8‐pCPT‐cGMPS; 1 μ m ) itself caused a marked reduction in I CCh . SNAP (100 μ m ) or db‐cGMP (100 μ m ) exhibited no inhibitory actions, when caffeine (10 mM) or photolytically released IP 3 were used instead of CCh to activate the inward current. These results suggest that inhibition of I CCh by NO donors involves a cGMP‐dependent but G‐kinase‐independent mechanism, which may operate at a site(s) between the muscarinic (M 3 ) and IP 3 receptors." @default.
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• W2124784666 date "1998-09-01" @default.
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• W2124784666 title "Cyclic GMP-dependent but G-kinase-independent inhibition of Ca²⁺-dependent Cl⁻currents by NO donors in cat tracheal smooth muscle" @default.
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• W2124784666 doi "https://doi.org/10.1111/j.1469-7793.1998.719bg.x" @default.
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