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 with 36Cl. 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 microM DIDS, but not by 1 mM furosemide. The Cl- efflux was temperature-dependent (Q10 = 2.3-2.5), and it was not affected on depolarisation by high [K+]o. The [Cl-]i of rabbit aorta determined by uptake studies with 36Cl, decreased slightly (by 15%) below controls in PSS containing 140 microM 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 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 HCO3- 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.