title: [Insulin resistance and effects of intravenous acute saline load on renal production of prostaglandin I2 and thromboxane A2 in salt-sensitive hypertensive patients].
abstract: OBJECTIVE
  To investigate insulin resistance and the effects of intravenous acute saline load on renal production of prostaglandin I(2) (PGI(2)) and thromboxane A(2) (TXA(2)) in salt-sensitive hypertensive patients.
  
  
  METHODS
  The 24-hour excretion of urinary 6-keto-prostaglandin F (PGF) 1alpha and thromboxane B(2) were measured before and after intravenous acute saline load in 53 hypertensive patients whose salt sensitivity had been determined. Oral glucose tolerance test and insulin release test were performed in all the subjects.
  
  
  RESULTS
  after intravenous acute saline load, the 24-hour excretions of urinary 6-keto PGF 1alpha were significantly lower in salt-sensitive (SS) hypertensive patients than that in non-salt-sensitive (NSS) ones (316+/-57 pg/min vs 371+/-68 pg/min, P<0.01), and the decrease from baseline was much greater in SS group than that in NSS group (197+/-99 pg/min vs 136+/-101 pg/min, P<0.01). Both 24 hour urinary excretion of TXA(2) and the increase in urinary excretion of TXA(2) were significantly greater in SS hypertensive patients than those in NSS ones after salt loading (394+/-32 pg/min vs 359+/-44 pg/min, P<0.01, and 80+/-47 pg/min vs 47+/-45 pg/min, P<0.01, respectively). The plasma glucose and insulin concentrations in every time point were much higher in SS hypertensive subjects than that in NSS ones, and the former group had lower insulin sensitivity index than the latter (0.013+/-0.003 vs 0.018+/-0.004, P<0.01)
  
  
  CONCLUSIONS
  Saline load produces significantly different effects on renal production of PGI(2) and TXA(2) in SS and NSS hypertensive patients, and these changes may be related to the pathophysiology of SS hypertensive patients after acute salt loading. Insulin resistance is greater in SS hypertensive patients than in NSS ones.
authors.affiliation: Department of Cardiology, First Hospital of Xi'an Jiaotong University, Xi'an 710061, China. Yetao8@sina.com
authors.forename: Tao
authors.initials: T
authors.lastname: Ye
authors.forename: Zhi-quan
authors.initials: ZQ
authors.lastname: Liu
authors.forename: Jie
authors.initials: J
authors.lastname: Liu
authors.forename: Dan-jun
authors.initials: DJ
authors.lastname: Zhu
authors.forename: Yong
authors.initials: Y
authors.lastname: Zheng
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000652:urine; D000328:Adult; D011464:Epoprostenol / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D007275:Injections, Intravenous; D007333:Insulin Resistance; D007668:Kidney / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D012965:Sodium Chloride / Q000008:administration & dosage*; D013928:Thromboxane A2 / Q000096:biosynthesis*; D013929:Thromboxane B2 / Q000652:urine
chemical_list: D012965:Sodium Chloride; D013929:Thromboxane B2; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol