1  the tight binding system carbonic anhydrase-chlorothiazide.

2 ism was easily controlled with diazoxide and chlorothiazide.

3 he two patients with GS failed to respond to chlorothiazide.

4 ylchitotriose (NAG3), and carbonic anhydrase-chlorothiazide.

5 he Na(+)-Cl(-) cotransporter (NCC) inhibitor chlorothiazide (10 microM) and the Na(+)-K(+)-2Cl(-) cot

6  natriuresis was additive to that induced by chlorothiazide and amiloride.

7 solutions and in the presence of bumetanide, chlorothiazide and ouabain.

8 Metal chelation, diuresis with furosemide or chlorothiazide, and competitive metal blockade may be us

9 ree sample in the case of carbonic anhydrase-chlorothiazide binding.

10 of thiazide diuretic action (acetazolamide > chlorothiazide > metolazone) differed significantly from

11 e functional significance of these findings, chlorothiazide-inhibitable 22Na uptake was measured in P

12                             In control PBMC, chlorothiazide inhibited 22Na uptake by approximately 9%

13 anced by the combination of DMPS with either chlorothiazide or furosemide (P < 0.0001).

14  100 microM levels of amiloride, bumetanide, chlorothiazide, or stilbene.

15               In the presence of bumetanide, chlorothiazide produced a further dose-dependent fall in

16 were significantly reduced by furosemide and chlorothiazide treatment (P < 0.0001).

17 21, hydroflumethiazide, hydrochlorothiazide, chlorothiazide, trichlormethiazide, and althiazide) for