title: Role of calcium and potassium channels in effects of hydrogen sulfide on frog myocardial contractility.
abstract: The effects of sodium hydrosulfide NaHS, a donor of hydrogen sulfide H2S, on the force of muscle contraction were examined on isolated myocardial strips from frog ventricles. NaHS decreased the amplitude of muscle contractions in a dose-dependent manner under normal conditions and during inhibition of Ca channels with nifedipine. In contrast, under conditions of blockade of ATP-dependent potassium channels with glibenclamide, NaHS exerted a positive inotropic effect from the first minute of application. Neither blockade, nor activation of ATP-dependent K-channels with glibenclamide modulated the negative inotropic effect of NaHS. Inhibition of K-channels with tetraethylammonium (TEA) (3, 5, 10 mM) or 4-aminopyridine increased the amplitude of myocardial contractions. Preliminary application of 4-aminopyridine or TEA (3 mM) did not eliminate NaHS-induced negative inotropic effect, although higher TEA concentrations (5 or 10 mM) prevented it. The data indicate that the targets of H(2)S in frog myocardium are ATP-dependent, Ca-activated, and voltage-dependent K-channels.
authors.affiliation: Department of Human and Animal Physiology, Kazan (Privolzhskii) Federal University, Russia. Guzel.Sitdikova@ksu.ru
authors.forename: G F
authors.initials: GF
authors.lastname: Sitdikova
authors.forename: N N
authors.initials: NN
authors.lastname: Khaertdinov
authors.forename: A L
authors.initials: AL
authors.lastname: Zefirov
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000378:metabolism*; D004558:Electric Stimulation; D005905:Glyburide / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D066298:In Vitro Techniques; D054086:KATP Channels / Q000819:agonists / Q000378:metabolism; D008914:Minoxidil / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism*; D009543:Nifedipine / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D024681:Potassium Channels, Calcium-Activated / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011895:Rana ridibunda; D019789:Tetraethylammonium / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D054086:KATP Channels; D026902:Potassium Channel Blockers; D024681:Potassium Channels, Calcium-Activated; D008914:Minoxidil; D019789:Tetraethylammonium; D015761:4-Aminopyridine; D009543:Nifedipine; D005905:Glyburide; D006862:Hydrogen Sulfide