title: The in vivo effects of Tulbhagia violacea on blood pressure in a salt-sensitive rat model.
abstract: OBJECTIVE
  The in vivo effects of Tulbhagia violacea on systemic arterial blood pressure and on the renin-angiotensin system in a Dahl salt-sensitive rat model were investigated.
  
  
  METHODS
  Animals were treated for 14 days intraperitoneally as follows: Tulbhagia violacea (Tvl) (50mg/kg b.w.), captopril (Cap) (10mg/kg b.w.) or DMSO (Con). Baseline blood pressures were recorded prior to the commencement of the study and biweekly during the experimental period. Urine volume and sodium concentration were measured during the experimental period. On day 15, animals were anaesthetized (sodium thiopentane, 50mg/kg, i.p.), blood samples for aldosterone levels were taken and the kidneys removed for determining AT1a mRNA expression.
  
  
  RESULTS
  Cap and Tvl groups showed significantly reduced AT1a mRNA expressions by 3.11- and 5.03-fold, respectively, when compared to the Con group (p<0.05). When compared to baseline blood pressures (day 0); Cap and Tvl showed reductions in systolic blood pressure (SBP) of 7.76+/-0.41% and 9.12+/-0.31%, respectively (mean% decrease from day 0 to day 14). In contrast, in the Con group the systolic blood pressure increased from day 0 to day 14 by 4.66+/-0.56%. Blood pressure changes in all treated groups differed from Con significantly. Systolic blood pressure decreased with the decrease in AT1a mRNA expressions in these groups. When comparing day 0 to day 14, urine output increased in the Cap and Tvl groups. In the Con group, urinary volume was reduced by day 14 as compared to day 0. Urinary sodium excretion was increased in the treated groups by day 14.
  
  
  CONCLUSIONS
  It can be concluded that Tulbhagia violacea reduces systemic arterial blood pressure in the Dahl rat by decreasing renal AT1 receptor gene expression and hence modulating sodium and water homeostasis.
authors.affiliation: Pfizer Molecular Biology Research Facility, University of KwaZulu-Natal, Durban 4000, South Africa. mackraji@ukzn.ac.za
authors.forename: Irene
authors.initials: I
authors.lastname: Mackraj
authors.forename: S
authors.initials: S
authors.lastname: Ramesar
authors.forename: M
authors.initials: M
authors.lastname: Singh
authors.forename: T
authors.initials: T
authors.lastname: Govender
authors.forename: H
authors.initials: H
authors.lastname: Baijnath
authors.forename: R
authors.initials: R
authors.lastname: Singh
authors.forename: P
authors.initials: P
authors.lastname: Gathiram
mesh_terms: D000450:Aldosterone / Q000097:blood; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D006973:Hypertension / Q000139:chemically induced / Q000188:drug therapy*; D019668:Liliaceae / Q000737:chemistry* / Q000633:toxicity; D008297:Male; D008517:Phytotherapy; D010936:Plant Extracts / Q000627:therapeutic use / Q000633:toxicity; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D020303:Rats, Inbred Dahl; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics; D012084:Renin-Angiotensin System / Q000187:drug effects; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012964:Sodium / Q000652:urine; D012982:Sodium, Dietary / Q000494:pharmacology*; D014563:Urodynamics / Q000187:drug effects
chemical_list: D010936:Plant Extracts; D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D012982:Sodium, Dietary; D000450:Aldosterone; D012964:Sodium