Interactions of magnesium and chloride ions on tone and contractility of vascular muscle.
Replacement of extracellular chloride ions ([Cl-]o) by other anions, on contractility and the effects of extracellular magnesium ions ([Mg2+]o) on spontaneous mechanical activity, as well as on agonist-induced responses of rat aorta and portal vein, were studied. Replacement of [Cl-]o with acetate (Ac-) or isethionate (Ise-) ions resulted in an increase and decrease, respectively, of the spontaneous mechanical activity frequency in portal vein; the amplitudes of the spontaneous mechanical activity were attenuated by Ac- and Ise- substitution. Withdrawal of [Mg2+]o in Cl(-)-containing media resulted in elevation of tension development in rat aortas, whereas a similar maneuver in media with Ac- or Ise-, substituted for [Cl-]o, resulted in abrogation of this tension development. Use of disulfonic stilbene anion-channel blockers, DIDS (4,4'-diisothiocyano-2,2'-stilbene disulfonate, 400-600 microM) and SITS (4,4'-acetamido-4'-isothiocyano-2,2'-stilbene disulfonic acid, 400-600 microM), failed to influence either spontaneous mechanical activity or basal tone of rat portal portal vein or aortas. Incubation of DIDS or SITS in Mg(2+)-free media also failed to influence mechanical responses to withdrawal of [Mg2+]o. Use of the Cl- cation transport inhibitor bumetanide (30-80 microM) also failed to alter spontaneous mechanical activity or basal tone in either the presence or absence of [Mg2+]o. Ac- and Ise- substitution attenuated norepinephrine- and K(+)-induced contractile responses in portal vein and aorta, Caffeine-induced contractions of aortas were potentiated by withdrawal of [Mg2+]o in Cl(-)-containing media but inhibited in Ac(-)- or Ise(-)-substituted solutions. In the presence of [Mg2+]o, substitution of foreign anions resulted in alterations in the agonist contractile dose-response curves; EC50s were increased whereas maximum tensions were depressed. Withdrawal of [Mg2+]o amplified these effects. Substitution of Ac- or Ise- for [Cl-]o in the presence or absence of [Mg2+]o depressed contractions induced by Ca acetate in aortas and portal vein. These results suggest that: (1) Cl- plays an important role in regulating spontaneous mechanical activity, basal tone, and contractility in rat aorta and portal vein; and (2) Cl- probably physiologically mediates some of the effects and actions of [Mg2+]o on intracellular release of and influx of Ca2+ in these smooth muscles.
Zhang
A
A
Department of Physiology, State University of New York, Brooklyn, 11203.
Carella
A
A
Altura
B T
BT
Altura
B M
BM
D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D000085:Acetates / Q000494:pharmacology; D019342:Acetic Acid; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000502:physiology; D002034:Bumetanide / Q000494:pharmacology; D002110:Caffeine / Q000494:pharmacology; D002712:Chlorides / Q000502:physiology*; D005110:Extracellular Space / Q000378:metabolism; D008274:Magnesium / Q000502:physiology*; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D011169:Portal Vein / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains
D000085:Acetates; D002712:Chlorides; D002034:Bumetanide; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D002110:Caffeine; D008274:Magnesium; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; D019342:Acetic Acid; D011188:Potassium; D009638:Norepinephrine