Effects of Ba2+ on F&F 96365-sensitive sustained contraction of rat pulmonary artery.
The effects of Ba2+ on receptor-mediated sustained contraction of rat pulmonary artery and guinea-pig oesophageal muscularis mucosae were studied in-vitro. In rat isolated pulmonary artery, sustained contraction induced by noradrenaline (1 microM) was resistant to nicardipine (1 microM), but this same sustained contraction was completely inhibited by SK&F 96365 (30 microM), a blocker of voltage-dependent L-type Ca2+ channels and receptor-activated Ca2+ influx. The SK&F 96365-sensitive sustained contraction induced by noradrenaline (1 microM) may be due primarily to Ca2+ influx through receptor-activated Ca)+ channels resistant to nicardipine. Cumulatively applied BaCl2 (0.1 - 10 mM) increased the noradrenaline (1 microM)-induced sustained contraction of the pulmonary arterial preparation in the absence of nicardipine, but in the presence of nicardipine (1 microM), BaCl2 (0.1 - 3 mM) did not affect this contraction. A higher concentration of BaCl22 (10 mM), however, weakly inhibited the noradrenaline (1 microM)-induced tone. In addition, BaCl2 (3-10 mM) increased the tone induced by KCl (60 mM), and the BaCl2-elevated KCl tone was markedly inhibited by nicardipine (1 microM) treatment. In the guinea-pig isolated oesophageal muscularis mucosae, sustained contraction induced by acetylcholine (3 microM) was resistant to nicardipine (1 microM) but was returned to its basal level by SK&F 96365 (30-60 microM). The SK&F 96365-sensitive, acetylcholine-induced sustained contraction of the oesophageal muscularis mucosae is also likely to link with receptor-activated Ca2+ channels resistant to nicardipine. In contrast to the rat pulmonary artery, cumulatively applied BaC12 (0.3 - 10 mM) inhibited the acetylcholine (3 microM)-induced sustained contraction of the oesophageal muscularis mucosae in a concentration-dependent manner in the presence of nicardipine (1 microM). In conclusion, Ba2+ presumably activates voltage-dependent Ca2+ channels by depolarizing plasma membrane and also passes through voltage-dependent Ca2+ channels to contract the pulmonary artery in the absence of nicardipine, and Ba2+ also has a minor effect on the nicardipine-resistant, SK&F 96365-sensitive sustained contraction induced by noradrenaline in rat isolated pulmonary artery.
Uchida
K
K
Department of Pharmacology, Dokkyo University School of Medicine, Tochigi, Japan. k-uchida@dokkyomed.ac.jp
Saito
K
K
Kitajima
T
T
Kamikawa
Y
Y
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001464:Barium / Q000494:pharmacology*; D017609:Barium Compounds / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002712:Chlorides / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004947:Esophagus / Q000187:drug effects / Q000502:physiology; D006168:Guinea Pigs; D007093:Imidazoles / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D009092:Mucous Membrane / Q000187:drug effects / Q000502:physiology; D009529:Nicardipine / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011651:Pulmonary Artery / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014661:Vasoconstriction / Q000187:drug effects*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
D017609:Barium Compounds; D002121:Calcium Channel Blockers; D002712:Chlorides; D007093:Imidazoles; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; C024986:barium chloride; D001464:Barium; D009529:Nicardipine; C063159:1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole; D000109:Acetylcholine; D009638:Norepinephrine