title: Differential regulations of blood pressure and perturbed metabolism by total ginsenosides and conventional antihypertensive agents in spontaneously hypertensive rats.
abstract: OBJECTIVE
  To investigate the regulatory effects of total ginsenosides and the conventional antihypertensive agents (captopril, amlodipine, terazosin and hydrochlorothiazide) on the blood pressure and perturbed metabolism in spontaneously hypertensive rats (SHRs) and to analyze the cause-effect relationships between high blood pressure and the metabolic disorders of hypertension.
  
  
  METHODS
  SHRs were administrated with total ginsenosides or the antihypertensive agents for eight weeks. Systolic blood pressure (SP) was measured every week and low-molecular-weight compounds in blood plasma were quantitatively analyzed using a nontargeted high-throughput metabolomic tool: gas chromatography/time of flight mass spectrometry (GC/TOFMS) . The metabolic patterns were evaluated using principal components analysis and potential markers of hypertension were identified.
  
  
  RESULTS
  Total ginsenosides and the antihypertensive agents differentially regulated SP and the metabolic pattern in SHRs. Total ginsenosides caused a progressive and prolonged reduction of SP and markedly normalized the perturbed metabolism with 14 of 27 (51.8%) markers of hypertension which were regulated toward normal. Total ginsenosides also reduced free fatty acids' level toward normal levels. In contrast, captopril, amlodipine and terazosin efficiently depressed SP, but had little effect on metabolic perturbation with only 8 (29.6%), 4 (14.8%), and 4 (14.8%) markers, respectively, which were regulated.
  
  
  CONCLUSIONS
  The metabolic changes persisted when the blood pressure was lowered by the conventional antihypertensive agents, suggesting that hypertension may not be the cause of the metabolic perturbation in SHRs.
authors.affiliation: China Pharmaceutical University, Nanjing, China.
authors.forename: Ji-ye
authors.initials: JY
authors.lastname: Aa
authors.forename: Guang-ji
authors.initials: GJ
authors.lastname: Wang
authors.forename: Hai-ping
authors.initials: HP
authors.lastname: Hao
authors.forename: Qing
authors.initials: Q
authors.lastname: Huang
authors.forename: Yi-hong
authors.initials: YH
authors.lastname: Lu
authors.forename: Bei
authors.initials: B
authors.lastname: Yan
authors.forename: Wei-bin
authors.initials: WB
authors.lastname: Zha
authors.forename: Lin-sheng
authors.initials: LS
authors.lastname: Liu
authors.forename: An
authors.initials: A
authors.lastname: Kang
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects*; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D008401:Gas Chromatography-Mass Spectrometry / Q000379:methods; D036145:Ginsenosides / Q000494:pharmacology*; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR
chemical_list: D000959:Antihypertensive Agents; D005230:Fatty Acids, Nonesterified; D036145:Ginsenosides