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

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Abstract
Cl− efflux into various incubation media (PSS) was studied in pieces of rabbit aortae loaded with36Cl. Replacement of HCO −3 /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 NO −3 -PSS, or Br−-PSS. The stimulant effect of HCO −3 withdrawal on Cl− efflux was reduced by 140 μM 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 μM DIDS, but drastically (from 32.6 to 13.5 mM, i.e. by 59%) in PSS containing 1 mM furosemide. — Withdrawal of HCO −3 /CO2 depolarized rabbit pulmonary artery in standard PSS and in Br−-PSS or NO −3 -PSS, but not in benzenesulfonate-PSS. — The pHi 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 HCO −3 across the cell membrane. This mechanism seems to be involved in the regulation of pHi. 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.