title: Impaired endothelial function of thoracic aorta in hereditary hypertriglyceridemic rats.
abstract: OBJECTIVE
  Hereditary hypertriglyceridemia (hHTG) in rats was found to be associated with metabolic abnormalities and elevation of blood pressure. There is controversy regarding the relation between hHTG and vascular function. The aim of this study was to determine the reactivity and accompanying structural changes in thoracic aorta from hereditary hypertriglyceridemic rats and hHTG rats that were given, for a long time, N(G)-nitro-l-arginine methyl ester (L-NAME) with and without simultaneous captopril treatment.
  
  
  METHODS
  Isolated rings of thoracic aorta were mounted in organ chambers for isometric tension recording or for measurement of endothelium-dependent relaxation. Morphological changes of thoracic aorta (wall thickness, diameter) were measured using light microscopy.
  
  
  RESULTS
  Endothelium-dependent relaxation (EDR) to acetylcholine (ACh, 10(-5) M) was significantly attenuated in the hHTG group compared to control Wistar rats (59.3 +/- 8.5% vs. 95.8 +/- 6.5%, p < 0.001), but normalized after pretreatment with captopril. EDR to ACh was further inhibited in hHTG rats treated with L-NAME (36.0 +/- 2.3%, p < 0.001). Maximum residual relaxation was only partly restored with captopril treatment (72.4 +/- 5.8%, p < 0.001). Hypertriglyceridemia did not significantly alter the sensitivity of the thoracic aorta to exogenous noradrenaline. The diameter/wall thickness (D/W) ratio in aortas of control Wistar rats averaged 16.25 +/- 0.57. This ratio was significantly lower in hHTG rats (12.52 +/- 0.38, p < 0.01) and was not altered after treatment with captopril. In the hHTG rats treated with L-NAME, the D/W ratio was further significantly decreased (8.25 +/- 0.30, p < 0.001). Simultaneous captopril treatment attenuated the decrement of this ratio (9.80 +/- 0.75, p < 0.05).
  
  
  CONCLUSIONS
  Results showed that hHTG is accompanied by functional and morphological alterations in the rat thoracic aorta. These changes in hHTG and in hHTG rats treated with L-NAME could be, at least in part, protected by captopril treatment.
authors.affiliation: Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic. torok@unpf.savba.sk
authors.forename: J
authors.initials: J
authors.lastname: Török
authors.forename: P
authors.initials: P
authors.lastname: Babál
authors.forename: J
authors.initials: J
authors.lastname: Matusková
authors.forename: I
authors.initials: I
authors.lastname: Lupták
authors.forename: I
authors.initials: I
authors.lastname: Klimes
authors.forename: F
authors.initials: F
authors.lastname: Simko
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000503:physiopathology*; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D015228:Hypertriglyceridemia / Q000503:physiopathology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D002216:Captopril; D019331:NG-Nitroarginine Methyl Ester