The aim of this study was to compare the vascular reactivity and morphology of iliac artery (IA) in adult spontaneously hypertensive rats (SHR) and hereditary hypertriglyceridemic (hHTG) rats. The isolated rings of iliac artery (IA) from Wistar rats (controls), SHR and hHTG rats were used for measurement of relaxant responses to acetylcholine (ACh) and contractile responses to noradrenaline (NA). Morphological changes of IA were measured using light microscopy. Systolic blood pressure (BP) measured by plethysmographic method was increased in SHR approximately by 88 % and in hHTG rats by 44 % compared to controls. BP increase was accompanied by cardiac hypertrophy. In both SHR and hHTG groups (experimental groups) reduced relaxation to ACh and enhanced maximal contraction and sensitivity to adrenergic stimuli were observed. The sensitivity to NA in SHR was higher also in comparison with hHTG. Geometry
of IA in both experimental groups revealed increased wall thickness and wall cross-sectional area, in SHR even in comparison with hHTG. Inner diameter was decreased in both experimental groups. Thus, independently of etiology, hypertension in both models was connected with impaired endothelial function accompanied by structural alterations of
IA. A degree of BP elevation was associated with arterial wall hypertrophy and increased contractile sensitivity.
The hypothesis on Fetal and Infant Origins of Adult Disease proposes that an altered in utero environment may impair fetal development and physiological function, increasing susceptibility to disease in adulthood. Previous studies demonstrated that reduced fetal growth predisposes to adult cardiovascular diseases. Maternal smoking and high altitude are also linked to reduced fetal growth and adult disease, and both cause fetal hypoxia. We therefore wanted to determine whether fetal hypoxia produces alterations in the adult pulmonary vasculature. Body and ventricular weight, pulmonary arterial compliance and vasoreactivity to potassium chloride (KCl), prostaglandin F2α (PGF2α), acetylcholine (ACh) and sodium nitroprusside (SNP) were studied in adult rats exposed to 10 % hypoxia throughout the perinatal period, compared to age-matched controls. Rats exposed to perinatal hypoxia had reduced body weight (199±15 vs. 294±10 g, P<0.001), elevated right ventricular weight (70.3±8.8 vs. 51.4±1.2 mg/100 g, P<0.05), elevated left ventricular weight (281±27 vs. 232±5 mg/100 g, P<0.05), reduced pulmonary arterial compliance (35.2±2.0 vs. 46.4±2.4 μm/mN, P<0.05) and reduced maximal pulmonary vasoconstriction to KCl (1.74±0.14 vs. 2.63±0.31 mN/mm, P<0.01), and PGF22α (1.40±0.14 vs. 2.47±0.44 mN/mm, P<0.05). Perinatal exposure to hypoxia had a profound effect upon the adult pulmonary circulation, which could predispose to cardiopulmonary diseases in adulthood.