title: 45Ca2+ movements induced by Ca2+ chloride in isolated rat aorta under K(+)-free conditions.
abstract: Increasing the extracellular Ca2+ concentration induced a dihydropyridine-insensitive contraction in the isolated rat aorta bathed in K(+)-free solution. To obtain further insight into the mechanism of this contraction 45Ca2+ uptake measurements were carried out with isolated rat aorta. Increasing the extracellular Ca2+ concentration from 0.63 to 5.0 mM enhanced the 45Ca2+ uptake from 186 +/- 3 to 359 +/- 12 dpm/mg ww (n = 8). Under K(+)-free conditions increasing the extracellular Ca2+ concentration from 0.63 to 5.0 mM enhanced the 45Ca2+ uptake from 184 +/- 4 to 541 +/- 6 dpm/mg ww (n = 12) and elicited an increase in tension of 10.0 +/- 0.4 mN (n = 9). The Ca2(+)-induced 45Ca2+ uptake was not affected by the Ca2% channel antagonists, nifedipine (L-type), flunarizine (L- and T-type) and omega-conotoxin (N-type). Amiloride, a blocker of the Na+/Ca2+ exchange, indomethacin, a blocker of prostaglandin synthesis, the local anaesthetic, lidocaine, and the Ca2+ overload blocker. R 56865, had no effect on Ca2(+)-induced 45Ca2+ uptake. Additionally, R 56865 did not affect the Ca2(+)-induced contractile response. The inorganic Ca2+ entry blocker, lanthanum, reduced both the non-stimulated and stimulated 45Ca2+ uptake and inhibited the Ca2(+)-induced contractile response. We would like to suggest that the 45Ca2+ uptake induced by Ca2+ under K(+)-free conditions enters the cell via the leakage Ca2+ channel, because lanthanum was an effective antagonist and a significant contribution of any other Ca2+ pathway could not be demonstrated.
authors.affiliation: Janssen Research Foundation, Neuss, F.R.G.
authors.forename: D
authors.initials: D
authors.lastname: Wermelskirchen
authors.forename: U
authors.initials: U
authors.lastname: Nebel
authors.forename: A
authors.initials: A
authors.lastname: Wirth
authors.forename: B
authors.initials: B
authors.lastname: Wilffert
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects* / Q000378:metabolism; D052160:Benzothiazoles; D002118:Calcium / Q000378:metabolism*; D002122:Calcium Chloride / Q000494:pharmacology; D002132:Calcium Radioisotopes; D005444:Flunarizine / Q000494:pharmacology; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D007811:Lanthanum / Q000494:pharmacology; D008012:Lidocaine / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D010456:Peptides, Cyclic / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D011188:Potassium / Q000502:physiology; D051381:Rats; D013844:Thiazoles / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects; D020960:omega-Conotoxins
chemical_list: D052160:Benzothiazoles; D002132:Calcium Radioisotopes; D010456:Peptides, Cyclic; D010880:Piperidines; D013844:Thiazoles; D020960:omega-Conotoxins; C053423:Conus magus toxin; D007811:Lanthanum; D000584:Amiloride; C054551:R 56865; D008012:Lidocaine; D009543:Nifedipine; D002122:Calcium Chloride; D005444:Flunarizine; D011188:Potassium; D002118:Calcium; D007213:Indomethacin