odeling · mechanismObjective To investigate mechanisms of anti hypertension and anti cardiovascular remodeling by phenylalanine (phe) in spontaneously hypertensive rats (SHRs) Methods The comparison of ...
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odeling · mechanismObjective To investigate mechanisms of anti hypertension and anti cardiovascular remodeling by phenylalanine (phe) in spontaneously hypertensive rats (SHRs) Methods The comparison of blood pressure (BP) increment with the ages and cardiovascular changes of SHRs was made between the 3% phe intervented group (SHR phe) and the control SHRs group Detection of the structural changes with the VIDAS digital vedio frequency processing technique and light and electron microscopy were made The cell growth and proliferation of cultured smooth muscle cells (CSMCs) of the thoracic aortas or myocardial fibroblasts were evaluated by measuring the 3 H thymidine counts per minute (cpm) incorporated into the new synthesized desoxyribonucleic acid (DNA) and determining the cell number with the crystal violet stain technique The Ca 2+ influx was measured in counts/min of 45 CaCl 2 after incubating it with 5 different concentrations of phenylalanine and the intracellular [Ca 2+ ] i by Fura Ⅱ/Am indicator The total messenger ribonucleic acid (mRNA) of the myocardium was extracted and Northern blot analysis was performed with the probe collagen α 2(Ⅰ)cDNA The tyrosine hydroxylase (TH) activity was measured by high performance liquid chromatography (HPLC) with electrochemical detector after having reacted with its substrate tyrosine and other reagents The catecholamine contents in brain homogenat were detected by HPLC method The comparison of pharmacokinetics of phenylalanine among SHR phe, SHRs and control Wistar Kyoto (WKY) rats was made after intravenous injection of 3 H L phe (1?ml/kg) by PK GRAPH Program for kinetic calculation The 3H L phe uptake by CSMCs after incubating for difinite intervals was also detected and compared Results Phenylalanine could prevent the increase of BP with ages and the heart weight (heart/body weight index) The aortic media thickness and the collagen content in
Objective To clarify whether the disturbances in metabolic kinetics of the essential aminoacid, phenylalanine (phe), are implicated in the genetic pathogenesis of essential hypertension (EH).Methods 1. L-(2, 3D3)-le...
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Objective To clarify whether the disturbances in metabolic kinetics of the essential aminoacid, phenylalanine (phe), are implicated in the genetic pathogenesis of essential hypertension (EH).Methods 1. L-(2, 3D3)-leucine, L-(2, 3D3)-isoleucine, L-15N-lysine, L-(2, 3D3)-valine and L-(2, 3D3)-phe were used for simultaneously studying comparative metabolic kinetics using stable isotope tracer methods with a GC-MS system. Study groups were the offspring with both parents suffering EH (n=10, FH+), 2 or more than 2 parents and grand-parents with EH and stroke (n=12, FS+) and those without genetic predisposition of EH and stroke (n=12, F) groups. 2. By comparing the radioactive counts of ［3H］-phe, and their weight transformation in blood after 1.5?Ci/kg i.v. administration at defined intervals and in tissues obtained after being sacrified among spontaneously hypertensive rats (SHR), 2 kidney-1 clip hypertensive rats (2K1C) and their normotensive controls (WKY). 3. The time transport and concentration transport of ［3H］-L-phe in cpm between the cultured vascular smooth muscle cell of 5th generation in SHR and WKY were *** A single and unique disturbance of metabolic kinetics in phe were found in FH+, FS+ and SHR. The plasma pool or apparent volume of distribution was enlarged, and the turnover rate constants between plasma and cell tended to show a decrease. The pharmacokinetics of phe in 2K1C was not changed. Only phe content in heart and aorta, the vital organs for predicting BP, were higher in SHR than in WKY tissues studied. Both the time and concentration transport were higher in SHR, e.g., an increment in the net-uptake of L-phe by vascular *** A unique aberrant of metabolic kinetics of phe might be implicated in the inherited pathogenesis of EH and stroke both from clinical and animal studies.
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