A chloride-bicarbonate exchanging anion carrier in vascular smooth muscle of the rabbit

Cl^– efflux into various incubation media (PSS) was studied in pieces of rabbit aortae loaded with³⁶Cl. Replacement of HCO₃^–/CO₂ by HEPES/O₂ in the PSS increased the rate of Cl^– efflux by a factor of 2.4. This effect was suppressed in Cl^–-free PSS containing isethionate, propionate, or benzenesulfonate, but not in NO₃^–-PSS, or Br^–-PSS. The stimulant effect of HCO₃^– withdrawal on Cl^– efflux was reduced by 140 M DIDS, but not by 1 mM furosemide. The Cl^– effux was temperature-dependent (Q₁₀=2.3–2.5), and it was not affected on depolarisation by high [K⁺]₀. — The [Cl^–]_i of rabbit aorta determined by uptake studies with³⁶Cl, decreased slightly (by 15%) below controls in PSS containing 140 M DIDS, but drastically (from 32.6 to 13.5 mM, i.e. by 59%) in PSS containing 1 mM furosemide. — Withdrawal of HCO₃^–/CO₂ depolarized rabbit pulmonary artery in standard PSS and in Br^–-PSS or NO₃^–-PSS, but not in benzenesulfonate-PSS. — The pH_i of rabbit aorta determined by the distribution of (¹⁴C)-DMO, increased in Cl^–-free PSS containing isethionate or glucuronate. — It is concluded that transport mechanisms play a major role in the distribution of Cl^– in vascular smooth muscle, and that a membrane anion carrier operates in this tissue which can transport Cl^– and HCO₃^– across the cell membrane. This mechanism seems to be involved in the regulation of pH_i. However, the known high [Cl^–]_i of vascular smooth muscle is rather mediated by the furosemide-sensitive Na–K–Cl cotransport than by this anion carrier.Supported by the Deutsche Forschungsgemeinschaft. Parts of this study have been reported to the German Physiological and Pharmacological Societies (Kreye and Gertheimer 1982; Kreye et al. 1984a, b), and at the First International Congress on Diuretics, Miami/USA (Kreye et al. 1984c)