ライフサイエンスコーパス: thiazide

1 lcium channel blockers; 1.00 [0.90-1.10] for thiazides).

2 and exhibited a severely blunted response to thiazide.

3 ith an increase in the natriuretic effect of thiazide.

4 orming cells may be an additional target for thiazides.

5 First, eel NCCbeta is resistant to thiazides.

6 nts; or 1.5% of the overall percentage using thiazides [33.4%], P = .01).

7 with diuretic agents (loop diuretic agents, thiazides, acetazolamide) or mechanical devices.

8 rinol combined with thiazide was superior to thiazide alone.

9 s lithium-NDI development in mice similar to thiazide/amiloride but with fewer adverse effects.

10 nt of lithium-NDI mice with acetazolamide or thiazide/amiloride induced similar antidiuresis and incr

11 Thiazide/amiloride-treated mice showed hyponatremia, hyp

12 a slight differential increase in the use of thiazides among beneficiaries with hypertension in the 2

13 ients with bipolar disorder are treated with thiazide and amiloride, which are thought to induce anti

14 erventions and more among those who received thiazide and citrate than among control patients.

15 Thiazide and loop diuretics were associated with higher

16 Thiazide and loop diuretics were associated with increas

17 Hypersensitivity to thiazide and loop diuretics, angiotensin-converting enzy

18 Use of diuretics (both thiazide and nonthiazide), activity levels and muscle st

19 e-affirms the initial ALLHAT conclusion that thiazide and similar diuretics (at evidence-based doses)

20 ronic kidney disease, selection and doses of thiazide and similar diuretics, and the association of a

21 Thiazide and thiazide-like diuretic agents are being inc

22 the genetic underpinnings of BP response of thiazide and thiazide-like diuretics and help identify t

23 help identify the patients better suited for thiazide and thiazide-like diuretics compared to beta-bl

24 beta blockers) was significantly better than thiazides and thiazide-like diuretics as a first-line th

25 escribing combinations of potassium citrate, thiazides, and bisphosphonates, and correcting bone and

26 nsin-receptor blocker], hydrochlorothiazide [thiazide], and amlodipine [calcium channel blocker]), wi

27 Our study reveals that thiazides attenuate insulin secretion through inhibition

28 Previous studies demonstrated that thiazides attenuate insulin secretion, but the molecular

29 Thiazide-based treatment gives less cardiovascular prote

30 people similar to that in outcome trials of thiazide-based treatment.

31 2 different BP lowering-regimens (atenolol+/-thiazide-based versus amlodipine+/-perindopril-based the

32 nt classes of blood pressure-lowering drugs (thiazides, beta-blockers, ACE inhibitors, and angiotensi

33 However, the thiazide-binding site in NCC is unknown.

34 ing diuretic, amiloride, to treatment with a thiazide can prevent glucose intolerance and improve blo

35 showed markedly increased natriuresis after thiazide challenge.

36 th multiple past calcium stones, addition of thiazide, citrate, or allopurinol further reduced risk.

37 Its inhibition with thiazides constitutes the primary baseline therapy for a

38 tems, coexpression of NCC with I-1 increased thiazide-dependent Na(+) uptake, whereas RNAi-mediated k

39 Thiazides did not affect osteoblast proliferation, but d

40 to thiazide-induced glucose intolerance, and thiazides did not alter insulin secretion in CA5b KO isl

41 New-onset diabetes associated with thiazides did not increase cardiovascular outcomes.

42 Overall, our study demonstrates that thiazides directly stimulate osteoblast differentiation

43 ihypertensive drug than in those receiving a thiazide diuretic (-2.38 mm Hg [-6.16 to 1.40]).

44 ny diuretic (HR 1.48 [95% CI 1.11, 1.98]), a thiazide diuretic (HR 1.44 [95% CI 1.00, 2.10]), or a lo

45 drug (NSAID; P = .03), statin (P = .01), and thiazide diuretic (P = .025) intake was inversely relate

46 The potency series of thiazide diuretic action (acetazolamide > chlorothiazide

47 pyridine CCBs (hazard ratio 1.49 considering thiazide diuretic agents as a comparator; 95% CI, 1.04-2

48 should be given to medical treatment with a thiazide diuretic and/or citrate therapy.

49 ts were used to test the hypothesis that the thiazide diuretic chlorthalidone would decrease urine ca

50 Thiazide diuretic drugs act in the distal convoluted tub

51 However, although thiazide diuretic drugs have been advocated as first-lin

52 eabsorption mechanisms provides insight into thiazide diuretic efficacy.

53 The intact hypocalciuric response to a thiazide diuretic indicates that inactivation of the ClC

54 Between 1990-2018, we compared thiazide diuretic initiators with dCCB initiators and es

55 trol, and drug therapy emphasized the use of thiazide diuretic intensification and addition of spiron

56 , continuous infusions, or the addition of a thiazide diuretic or aldosterone antagonist.

57 nd unravel a complex mechanism that explains thiazide diuretic resistance.

58 reasing diuretic dosage, concurrent use of a thiazide diuretic to inhibit downstream NaCl reabsorptio

59 pediatric patients indicate that citrate or thiazide diuretic treatment may improve BMD.

60 Five years of NSAID, statin, and thiazide diuretic use was associated with PSA levels low

61 CC alone and in complex with a commonly used thiazide diuretic using cryo-electron microscopy.

62 ceptor blocker, calcium channel blocker, and thiazide diuretic) with estimated glomerular filtration

63 ARB), calcium channel blocker, beta-blocker, thiazide diuretic, and other antihypertensive medication

64 nts with normal plasma K+ and aldosterone, a thiazide diuretic, bendroflumethiazide, would be as effe

65 recommends pharmacologic monotherapy with a thiazide diuretic, citrate, or allopurinol to prevent re

66 i-drug combination, particularly including a thiazide diuretic, is very often necessary and should be

67 red with not using any diuretic, not using a thiazide diuretic, or not using a loop diuretic, respect

68 than treatment with an ACE inhibitor plus a thiazide diuretic.

69 cker, an angiotensin receptor blocker, and a thiazide diuretic.

70 use of B blockers (RR 1.48 [1.27-1.72]) and thiazide diuretics (RR 1.20 [1.07-1.35]) increased this

71 Thiazide diuretics (TD) are commonly prescribed anti-hyp

72 onstrating the efficacy of very low doses of thiazide diuretics added to other antihypertensive agent

73 Previous research has suggested that thiazide diuretics and beta-blockers may promote the dev

74 rvational studies on the association between thiazide diuretics and colorectal cancer risk is conflic

75 The studies most strongly support the use of thiazide diuretics and long-acting calcium channel block

76 , genetic disorders, and medications such as thiazide diuretics and supplements such as calcium, vita

77 beta-blockers, calcium-channel blockers, or thiazide diuretics and the likelihood of a positive or n

78 n mechanisms and sites of action of loop and thiazide diuretics and the similarity of their chronic e

79 Thiazide diuretics are among the most commonly prescribe

80 As thiazide diuretics are among the most efficacious agents

81 Thiazide diuretics are among the most widely used treatm

82 essential hypertension remains unknown, but thiazide diuretics are frequently recommended as first-l

83 Thiazide diuretics are frequently used in these patients

84 the major conclusion of this trial was that thiazide diuretics are superior in preventing 1 or more

85 The initial ALLHAT conclusion, that thiazide diuretics are superior to angiotensin-convertin

86 Thiazide diuretics are used to treat hypertension; howev

87 Thiazide diuretics are used worldwide as a first-choice

88 In this large pragmatic trial of thiazide diuretics at doses commonly used in clinical pr

89 scriptomics) to identify novel biomarkers of thiazide diuretics BP response.

90 suggests VASP as a potential determinant of thiazide diuretics BP response.

91 How specific thiazide diuretics compare in regard to safety and clini

92 on and potentially severe adverse event, and thiazide diuretics constitute a leading cause of drug-in

93 e in the CLOROTIC trial (Combining Loop with Thiazide Diuretics for Decompensated Heart Failure).

94 ta have called into question the efficacy of thiazide diuretics for the prevention of kidney stones.

95 It is unclear whether different thiazide diuretics have a differential impact on kidney

96 Thiazide diuretics have proven themselves effective agai

97 We found that men using NSAIDs, statins, and thiazide diuretics have reduced PSA levels by clinically

98 ciuric stones, sodium restriction along with thiazide diuretics helps to reduce urinary calcium.

99 ature evaluating the combination of loop and thiazide diuretics in patients with heart failure in ord

100 Potassium depletion by thiazide diuretics is associated with a rise in blood gl

101 suggest that inexpensive and well-tolerated thiazide diuretics may be especially effective in preven

102 directly in cells expressing NCC, indicating thiazide diuretics may be particularly effective for low

103 apy with beta-receptor blockers, digoxin and thiazide diuretics may worsen sexual dysfunction owing t

104 er exclusion of participants who were taking thiazide diuretics or those with diabetes.

105 The combination of statins and thiazide diuretics showed the greatest reduction in PSA

106 d not discourage physicians from prescribing thiazide diuretics to nondiabetic adults who have hypert

107 nce has been available to support the use of thiazide diuretics to treat hypertension in patients wit

108 Thiazide diuretics treat the disease, fostering the view

109 with blood pressure less than 140/90 mm Hg; thiazide diuretics used in multidrug hypertensive regime

110 -analysis of all cohorts, genetic proxies of thiazide diuretics were associated with a lower odds of

111 Genetic proxies of thiazide diuretics were associated with higher serum cal

112 enetic association study, genetic proxies of thiazide diuretics were associated with reduced kidney s

113 Genetic proxies of thiazide diuretics were derived from the International C

114 Genetic proxies of thiazide diuretics were genetic variants in the thiazide

115 Compared with dCCBs, thiazide diuretics were not associated with an overall i

116 Compared with dCCBs, thiazide diuretics were not associated with colorectal c

117 , subjects with hypertension who were taking thiazide diuretics were not at greater risk for the subs

118 Loop or thiazide diuretics were used in all 14 patients, and ang

119 open-label antihypertensive therapy (mostly thiazide diuretics) added as needed to control blood pre

120 serotonin reuptake inhibitors, statins, and thiazide diuretics), with evaluation of how often drugs

121 Thiazide diuretics, ACE-inhibitors or angiotensin recept

122 46.6%) calcium channel blockers, 180 (16.7%) thiazide diuretics, and 277 (25.7%) other antihypertensi

123 ce of PHAII phenotypes, their sensitivity to thiazide diuretics, and the observation that they consti

124 Thiazide diuretics, angiotensin II receptor blockers, an

125 However, it is reasonable to conclude that thiazide diuretics, angiotensin-II receptor blockers, an

126 Overall, the use of thiazide diuretics, beta-blockers, angiotensin-convertin

127 otensin II receptor blockers, beta-blockers, thiazide diuretics, calcium channel blockers, and metfor

128 Thiazide diuretics, niacin, and beta-adrenergic blockers

129 patients with truly resistant hypertension, thiazide diuretics, particularly chlorthalidone, should

130 blockers, putting them on equal footing with thiazide diuretics, renin-angiotensin system blockers (e

131 ent with alternate mechanism of actions (eg, thiazide diuretics, such as metolazone), or need for ult

132 safety and clinical outcomes associated with thiazide diuretics, these results suggest that there is

133 l nephron of the kidney and is the target of thiazide diuretics, which are commonly prescribed to tre

134 egulates blood pressure and is the target of thiazide diuretics, which have been widely prescribed as

135 Disease features are reversed by thiazide diuretics, which inhibit the Na-Cl cotransporte

136 ients except for NSAIDs, ACE inhibitors, and thiazide diuretics, which were more prevalent in black p

137 nts receiving dialysis and 847 discharged on thiazide diuretics.

138 al features of GS with a blunted response to thiazide diuretics.

139 ive classes of antihypertensive medications, thiazide diuretics.

140 f action of SPIRO and a potential target for thiazide diuretics.

141 ressure 137/75 mm Hg [17/9]) who were not on thiazide diuretics.

142 1.43 to 3.91) compared with those prescribed thiazide diuretics.

143 d correction of physiologic abnormalities by thiazide diuretics.

144 o-structures individually complexed with the thiazide drug hydrochlorothiazide, and two thiazide-like

145 onic anhydrases (CAs) confers the beneficial thiazide effect.

146 f the current study was to determine whether thiazides exert a direct bone-forming effect independent

147 Rats on high-fructose diets that are given thiazides exhibit potassium depletion and hyperuricemia.

148 eveloped for plasma sodium concentration and thiazide exposure on sodium concentration and hyponatrem

149 ere found for the risk of hyponatremia after thiazide exposure.

150 As evidenced by the dictum to "use thiazides for most patients with uncomplicated hypertens

151 ion in risk for hip fracture associated with thiazide in many epidemiologic studies.

152 The density of receptors for thiazides in the rat DCT is known to be increased by adr

153 n addition to their antihypertensive effect, thiazides increase bone mineral density and reduce the p

154 s in fetal rat calvarial cells, we show that thiazides increase the formation of mineralized nodules,

155 However, thiazides induced antidiuresis and alkalinized the urine

156 CA5b KO mice were resistant to thiazide-induced glucose intolerance, and thiazides did

157 NCC and the NDCBE/pendrin system may explain thiazide-induced hypokalemia in some patients.

158 widely used treatments for hypertension, but thiazide-induced hyponatremia (TIH), a clinically signif

159 ide-induced sodium concentration decrease or thiazide-induced hyponatremia.

160 and total NCC and had significantly blunted thiazide-induced natriuresis as well as renal potassium

161 um intake inhibited and low intake augmented thiazide-induced natriuresis in wild-type but not in Kcn

162 pression of phosphorylated NCC/total NCC and thiazide-induced natriuresis were significantly increase

163 C (pNCC) and total NCC (tNCC), and augmented thiazide-induced natriuresis.

164 genome-wide significant loci were found for thiazide-induced sodium concentration decrease or thiazi

165 int mutagenesis supports that the absence of thiazide inhibition is, at least in part, due to the sub

166 (NCC), which is the target of inhibition by thiazides, is located in close proximity to the chloride

167 rential effects on the potencies of specific thiazide-like and thiazide-type diuretics.

168 ecision medicine to manage hypertension with thiazide-like and thiazide-type diuretics.

169 s and distinctions between NCC-inhibition by thiazide-like and thiazide-type diuretics.

170 lisinopril, or doxazosin was not superior to thiazide-like diuretic (chlorthalidone) in preventing co

171 Thiazide and thiazide-like diuretic agents are being increasingly use

172 f different classes, including a long-acting thiazide-like diuretic and an MR (mineralocorticoid rece

173 Chlorthalidone is a potent, long-acting thiazide-like diuretic and should be used preferentially

174 underpinnings of BP response of thiazide and thiazide-like diuretics and help identify the patients b

175 was significantly better than thiazides and thiazide-like diuretics as a first-line therapy for any

176 the patients better suited for thiazide and thiazide-like diuretics compared to beta-blockers for im

177 Safety profiles also favoured thiazide or thiazide-like diuretics over angiotensin-converting enzy

178 rences between classes; however, thiazide or thiazide-like diuretics showed better primary effectiven

179 uidelines, with the exception of thiazide or thiazide-like diuretics superiority to angiotensin-conve

180 mong the first-line drug classes thiazide or thiazide-like diuretics, angiotensin-converting enzyme i

181 e thiazide drug hydrochlorothiazide, and two thiazide-like drugs chlorthalidone and indapamide, revea

182 erent classes, including a diuretic, usually thiazide-like, a long-acting calcium channel blocker, an

183 Thiazide may have beneficial effects on bone mineral den

184 hypertensive drugs, our results suggest that thiazides may find a role in the prevention and treatmen

185 However, thiazide-mediated inhibition of NCC and consequent resto

186 f potassium supplements and allopurinol with thiazides might be helpful in the management of metaboli

187 However, <40% of patients treated with thiazide monotherapy achieve BP control.

188 Safety profiles also favoured thiazide or thiazide-like diuretics over angiotensin-con

189 veness differences between classes; however, thiazide or thiazide-like diuretics showed better primar

190 th current guidelines, with the exception of thiazide or thiazide-like diuretics superiority to angio

191 mary agent among the first-line drug classes thiazide or thiazide-like diuretics, angiotensin-convert

192 drug therapy for hypertension consists of a thiazide or thiazidelike diuretic such as hydrochlorothi

193 ue-Dawley rats on (1) the density of the rat thiazide receptor (TZR), as quantitated by binding of (3

194 te solid phase may be the mechanism by which thiazides reduce CaOx stone formation.

195 The findings suggest that thiazide-related incident diabetes has less adverse long

196 n the upper normal to hypermagnesemic range, thiazide responsiveness was not blunted, and genetic ana

197 take, moderate-strength evidence showed that thiazides (RR, 0.52 [CI, 0.39 to 0.69]), citrates (RR, 0

198 (+) secretion via variable inhibition of the thiazide-sensistive NaCl cotransporter and the K(+) chan

199 ressing HEK293 cells to assess the effect on thiazide-sensitive (22)Na(+) transport.

200 Functional assessment of NCC by using thiazide-sensitive (22)Na(+) uptakes revealed that TPA c

201 studies implicate WNK4 in inhibition of both thiazide-sensitive co-transporter-mediated Na+ reabsorpt

202 A human homolog of rat thiazide-sensitive cotransporter was cloned and mapped t

203 rstanding of the molecular physiology of the thiazide-sensitive cotransporter, are strong evidence th

204 We recently described a novel thiazide-sensitive electroneutral NaCl transport mechani

205 However, aldosterone may also stimulate the thiazide-sensitive Na(+)-Cl(-) cotransporter (NCC).

206 The thiazide-sensitive Na(+)/Cl(-) cotransporter (NCC) is ac

207 ges include increases in the activity of the thiazide-sensitive Na(+)/Cl(-)-cotransporter (NCC).

208 Mutations in the gene encoding the thiazide-sensitive Na+-Cl- cotransporter (NCC) of the di

209 The Na+-H+ exchanger NHE3 and the thiazide-sensitive Na+-Cl- cotransporter NCC are the maj

210 e-sensitive Na+-K+-2Cl- cotransporters and a thiazide-sensitive Na+-Cl- cotransporter.

211 channel (ROMK), and total and phosphorylated thiazide-sensitive Na+Cl- cotransporter (NCC) levels wer

212 orylation sites, including serine-811 in the thiazide-sensitive Na-Cl co-transporter, NCC.

213 in increased whole-kidney abundances of the thiazide-sensitive Na-Cl co-transporter, the alpha-subun

214 " diuretic-sensitive Na-K-Cl cotransport and thiazide-sensitive Na-Cl cotransport.

215 Na-K-Cl cotransporter (NKCC or BSC) and the thiazide-sensitive Na-Cl cotransporter (NCC or TSC).

216 one increases expression and activity of the thiazide-sensitive Na-Cl cotransporter (NCC) and the epi

217 ) was shown to result from activation of the thiazide-sensitive Na-Cl cotransporter (NCC) by mutation

218 Dietary sodium intake regulates the thiazide-sensitive Na-Cl cotransporter (NCC) in the dist

219 The thiazide-sensitive Na-Cl cotransporter (NCC) is the majo

220 sis revealed that the renal abundance of the thiazide-sensitive Na-Cl cotransporter (NCC) was profoun

221 esis that WNK kinases regulate the mammalian thiazide-sensitive Na-Cl cotransporter (NCC).

222 lting from loss of function mutations in the thiazide-sensitive Na-Cl cotransporter (NCCT) suggest th

223 alocorticoids regulate the expression of the thiazide-sensitive Na-Cl cotransporter (TSC), the chief

224 elationship between dietary Mg and the renal thiazide-sensitive Na-Cl cotransporter (TZR, measured by

225 CC2]), and the distal convoluted tubule (the thiazide-sensitive Na-Cl cotransporter [NCC]) in immunob

226 mRNA levels for the thiazide-sensitive Na-Cl cotransporter decreased by 57 a

227 Thus, the thiazide-sensitive Na-Cl cotransporter of the distal con

228 n's syndrome to the locus encoding the renal thiazide-sensitive Na-Cl cotransporter, and identify a w

229 rome, a disease caused by dysfunction of the thiazide-sensitive Na-Cl cotransporter.

230 ransporters in the distal nephron, including thiazide-sensitive Na-Cl cotransporters and ROMK channel

231 We showed previously that WNK4 downregulates thiazide-sensitive NaCl cotransporter (NCC) activity, an

232 renal distal convoluted tubule (DCT) by the thiazide-sensitive NaCl cotransporter (NCC) is a major d

233 The thiazide-sensitive NaCl cotransporter (NCC) is important

234 The thiazide-sensitive NaCl cotransporter (NCC) is the prima

235 The thiazide-sensitive NaCl cotransporter (NCC) of the renal

236 s an important role in the regulation of the thiazide-sensitive NaCl cotransporter (NCC).

237 tenuating the cell surface expression of the thiazide-sensitive NaCl cotransporter (NCC).

238 he effect of dietary potassium intake on the thiazide-sensitive NaCl cotransporter (NCC).

239 The thiazide-sensitive NaCl cotransporter (NCC, SLC12A3) med

240 nt data suggest that sex hormones affect the thiazide-sensitive NaCl cotransporter (TSC) density or b

241 study the possible involvement of the renal thiazide-sensitive NaCl cotransporter gene in the syndro

242 ced urinary flow and reduced activity of the thiazide-sensitive NaCl cotransporter may support renal

243 Phosphorylation of the thiazide-sensitive NaCl cotransporter was consistently l

244 was no difference in the mRNA expressions of thiazide-sensitive NaCl cotransporter, epithelial Na cha

245 ulate the furosemide-sensitive NKCC2 and the thiazide-sensitive NCC, kidney-specific CCCs.

246 the two main sodium transport proteins, the thiazide-sensitive sodium chloride cotransporter (NCC) a

247 A T60M mutation in the thiazide-sensitive sodium chloride cotransporter (NCC) i

248 at occurs secondary to the inhibition of the thiazide-sensitive sodium chloride cotransporter (NCC) i

249 mon with ultraprocessed foods, activates the thiazide-sensitive sodium chloride cotransporter (NCC) v

250 eported that tacrolimus stimulates the renal thiazide-sensitive sodium chloride cotransporter (NCC),

251 nal phosphorylation (encoded by WNK4) of the thiazide-sensitive sodium chloride cotransporter encoded

252 onstrated complete linkage between the human thiazide-sensitive sodium chloride cotransporter gene (N

253 azide diuretics were genetic variants in the thiazide-sensitive sodium chloride cotransporter gene as

254 t genes, Scnn1a, Scnn1b, and Scnn1g, and the thiazide-sensitive sodium chloride cotransporter gene, S

255 cient mice, which are unable to activate the thiazide-sensitive sodium chloride cotransporter NCC (en

256 The thiazide-sensitive sodium chloride cotransporter, NCC, i

257 is a potent driver of hypertension, and the thiazide-sensitive sodium-chloride cotransporter (NCC) h

258 stering the view that hyperactivation of the thiazide-sensitive sodium-chloride cotransporter (NCC) i

259 t sodium-chloride co-transporter, NKCC2, and thiazide-sensitive sodium-chloride cotransporter, NCC, i

260 tions in the SLC12A3 gene, which encodes the thiazide-sensitive sodium-chloride cotransporter.

261 expression and NCC activity, as measured by thiazide-sensitive, chloride-dependent (22)Na uptake, we

262 CA5b in beta -cell function and in mediating thiazide sensitivity in vitro and in vivo .

263 distal convoluted tubule and indicates that thiazides should be useful in reducing the risk of kidne

264 In support of these findings, thiazides significantly attenuated Krebs cycle anapleros

265 then used to assess the role of the putative thiazide target CA5b in beta -cell function and in media

266 n islets of mice lacking the known molecular thiazide targets NCC or NDCBE.

267 Because NCC and NDCBE are both thiazide targets, the combined inhibition of NCC and the

268 For calcium channel blockers and thiazides, the matched odds ratios were 4.21 (95% CI, 1.

269 CA-SPAK mice displayed thiazide-treatable hypertension and hyperkalemia, concur

270 However, <50% of thiazide-treated patients achieve blood pressure (BP) co

271 in children may be improved with citrate or thiazide treatment.

272 eased blood pressure, which were reversed by thiazide treatment.

273 icipants were randomly assigned to receive a thiazide-type diuretic (n = 15 002), a CCB (n = 8898), o

274 tic agents that impair this mechanism (e.g., thiazide-type diuretic agents and mineralocorticoid rece

275 eceptor blocker irbesartan, but not with the thiazide-type diuretic chlorthalidone, restored sympatho

276 eceptor blocker, calcium channel blocker, or thiazide-type diuretic in the nonblack hypertensive popu

277 with diabetes, a calcium channel blocker or thiazide-type diuretic is recommended as initial therapy

278 oop diuretic resistance is the addition of a thiazide-type diuretic to produce diuretic synergy via "

279 ith 2 agents, 1 of which usually should be a thiazide-type diuretic; and (7) The most effective thera

280 Thiazide-type diuretics are associated with an increased

281 nation diuretic therapy using any of several thiazide-type diuretics can more than double daily urine

282 lifestyle modifications to prevent CVD; (4) Thiazide-type diuretics should be used in drug treatment

283 the investigators' original conclusion that thiazide-type diuretics should remain the preferred firs

284 the potencies of specific thiazide-like and thiazide-type diuretics.

285 o manage hypertension with thiazide-like and thiazide-type diuretics.

286 between NCC-inhibition by thiazide-like and thiazide-type diuretics.

287 a calcium channel blocker, and a long acting thiazide-type/like diuretic; if a fourth drug is needed,

288 ctivity and causes insulin resistance during thiazide usage.

289 n 140/90 mm Hg (OR, 1.0 [95% CI, 0.92-1.2]); thiazide use (OR, 1.0 [95% CI, 0.8-1.3]); atheroscleroti

290 l/L lower plasma sodium per SD decrease, and thiazide use was associated with 0.80 (95% confidence in

291 The prevalence of thiazide use was higher among the glaucoma cases than am

292 A protective effect for current thiazide use was observed (OR = 0.53, CI = 0.31-0.90), a

293 was used to adjust for age, body mass index, thiazide use, and dietary factors.

294 ke of calcium, animal protein and potassium, thiazide use, geographic region, profession, and total f

295 for body mass index; hypertension; diabetes; thiazide use; and intake of potassium, animal protein, o

296 either citrate nor allopurinol combined with thiazide was superior to thiazide alone.

297 Inhibition of insulin secretion by thiazides was CO 2 /HCO 3- -dependent, not additive to u

298 nd controls for calcium channel blockers and thiazides was noted.

299 9-1.07] for B blockers; 1.01 [0.95-1.07] for thiazides), with the exception of calcium channel blocke

300 tion of calcium channel blockers, as well as thiazides, with CEEA in the United States.