title: Activation of two inward chloride transport systems in rat femoral arterial smooth muscle in deoxycorticosterone acetate/salt hypertension.
abstract: 1. Intracellular [Cl-] ([Cl-]i) was measured with ion-selective microelectrodes in rat femoral arterial smooth muscle in normotensive controls and after the induction of deoxycorticosterone acetate/salt hypertension. 2. Linear regression of [Cl-]i and time after the induction of hypertension showed good correlation (r = 0.96) for 5-6 weeks, as [Cl-]i increased from 30 +/- 1 mmol/l (mean +/- SD, n = 16), to 49 +/- 2 mmol/l (n = 9, P < 0.0001). 3. Arterial systolic blood pressure also increased linearly (r = 0.97) for 5-6 weeks as hypertension developed from 122 +/- 1 mmHg (n = 20) to 187 +/- 7 mmHg (n = 14): there was consequently a linear relationship between [Cl-]i and arterial systolic blood pressure (r = 0.96). 4. The increase in [Cl-]i was partly because Na(+)-K(+)-Cl- co-transport activity, estimated from the fall in [Cl-]i caused by bumetanide, was greater in hypertension (18 mmol/l) than in normotension (10 mmol/l). This finding, and the depolarization of the membrane potential in hypertension (-56 +/- 3 mV compared with -64 +/- 4 mV in normotension; P < 0.0001), confirms previous studies. 5. The increase in [Cl-]i was also partly due to greater activity of an Na(+)- and HCO3(-)-independent, acetazolamide-sensitive inward Cl- transport system; thus acetazolamide reduced [Cl-]i by 7 mmol/l in normotension and by 16 mmol/l in hypertension. 6. In Cl(-)-free media, the membrane potential in normotension (-59 +/- 5 mV) was not significantly different from that in hypertension (-60 +/- 4 mV). 7. The role of [Cl-]i in the depolarization of the membrane potential in hypertension is discussed.
authors.affiliation: Department of Anatomy and Physiology, University of Dundee, U.K.
authors.forename: A A
authors.initials: AA
authors.lastname: Harper
authors.forename: J P
authors.initials: JP
authors.lastname: Davis
authors.forename: A R
authors.initials: AR
authors.lastname: Chipperfield
mesh_terms: D000086:Acetazolamide / Q000494:pharmacology; D000818:Animals; D000838:Anions; D002034:Bumetanide / Q000494:pharmacology; D018118:Chloride Channels / Q000187:drug effects / Q000378:metabolism*; D003900:Desoxycorticosterone; D004232:Diuretics / Q000494:pharmacology; D006973:Hypertension / Q000378:metabolism*; D008297:Male; D008564:Membrane Potentials; D008839:Microelectrodes; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012965:Sodium Chloride; D018709:Statistics, Nonparametric
chemical_list: D000838:Anions; D018118:Chloride Channels; D004232:Diuretics; D002034:Bumetanide; D003900:Desoxycorticosterone; D012965:Sodium Chloride; D000086:Acetazolamide