1. Plasma catecholamine, haemodynamic and metabolic responses to sustained isometric exercise were studied in eight healthy subjects, who maintained handgrip at the 30% level of maximal voluntary contraction (MVC) for as long as possible.2. The sustained handgrip was accompanied by a significant increase in plasma noradrenaline (NA) and adrenaline (A) concentrations.3. The increase in plasma NA during handgrip was greater than that associated with heavy dynamic work involving large muscle groups.4. The results suggest that the known haemodynamic responses to static effort are related to a powerful activation of the adrenergic system, which may result from a reflex mechanism initiated in the exercising muscles.Key words : static efforts, plasma catecholamines, activation of adrenergic system, haemodynamic responses to sustained handgrip.Sustained, static muscular efforts are known to produce significant haemodynamic responses. These responses occur even with exercise performed by small muscle groups provided that the isometric contraction is sufficiently strong. Sustained isometric handgrip exercise lasting 5-6 min causes significant increases in systolic, diastolic and mean arterial blood pressure, skin blood flow, heart rate and cardiac output with a small decrease in stroke volume (
In humans, hypercholesterolemia and hypertension are associated with endothelial dysfunction. Here, we assess whether hypercholesterolemia induces endothelial dysfunction in rats with pre-existing hypertension. Spontaneously hypertensive rats (SHR) and normotensive controls (WKY) were fed with a high-cholesterol diet for 12 weeks, and endothelial function was assessed in isolated thoracic aortic rings. In SHR and WKY rats, the hypercholesterolemic diet resulted in the elevation of total cholesterol and low-density lipoprotein levels by approximately 2.5-and 4.5-fold, respectively. However, in aorta, the basal nitric oxide (NO) production-as assessed by the magnitude of L-N G -nitroarginine methyl ester-induced vasoconstriction as well as the NO-dependent relaxation induced by acetylcholine or histamine-were not diminished either in SHR or in WKY rats fed with the hypercholesterolemic diet. Interestingly, prostacyclin (PGI 2 ) production in aortic rings from SHR rats was higher than in the aorta from WKY rats. However, the hypercholesterolemic diet had no further effects on PGI 2 production in the aorta either of SHR or WKY rats. The monocyte chemoattractant protein 1 level in plasma was slightly elevated in SHR and WKY rats fed with the hypercholesterolemic diet compared with their normocholesterolemic counterparts. In summary, even in the presence of pre-existing hypertension, hypercholesterolemia fails to modify NO-dependent and PGI 2 -dependent endothelial function in SHR rats; it also does not induce a robust inflammatory response. Both are prerequisites for the development of atherosclerosis.
The objective of the present study was to re-evaluate critically the potential of spontaneously hypertensive rats (SHR) as models for diet-induced hypercholesterolaemia and the hypercholesterolaemia-induced atherosclerosis. Normotensive Wistar-Kyoto rats (WKY) were used as control animals. Twelve-months-old SHR (n=22) and WKY (n=17) male rats, were randomly divided into two groups each and fed one of the following diets for 12 consecutive weeks: the control diet i.e. the basal AIN-93M diet and the hypercholesterolaemic diet (g/100g: cholesterol 1, cholic acid 0.5 and butter 20). The hypercholesterolaemic diet increased highly significantly (P<0.001) serum total cholesterol concentrations in both WKY (control vs high-cholesterol) and SHR (control vs high cholesterol) rats (2.59±0.20 vs 6.54±0.33 and 2.52±0.20 vs 6.64±0.89 mmol/L, respectively). The same was true for LDL-cholesterol (0.75±0.09 vs 4.22±0.26 and 0.84±0.05 vs 4.62±0.69 mmol/L, respectively). HDL-cholesterol concentrations were also moderately increased in cholesterol-fed rats (1.46±0.10 vs 1.95±0.09 and 1.24±0.08 vs 1.53±0.17 mmol/L, respectively) whereas triglicerydes were unaffected. As regards lipid profile, the only effect of animal strain was that noted for SHR rats in which HDL cholesterol concentrations were significantly (P<0.05) lower than in WKY rats (1.39±0.10 vs 1.69 ± 0.09 mmol/L, respectively). Serum concentrations of MCP-1 were elevated in both WKY (control vs high-cholesterol) and SHR rats (control vs high cholesterol, 41.22 ± 7.98 vs 156.10 ± 20.66 and 84.88 ± 49.40 vs 181.65 ± 38.40 pg/mL, respectively) though only in WKY rats this increase reached statistical significance. Either in WKY or SHR rats, the hypercholesterolaemic diet had no significant effect on endothelium-dependent nor endotheliumindependent vasodilation in aorta induced by acetylcholine or SNAP, respectively. Histological examination of proximal aortas from WKY (control vs high-cholesterol) and SHR (control vs highcholesterol) rats did not show any structural changes, indicative of atherosclerotic plaque formation. We conclude that diet induced hypercholesterolaemia does not lead to progression of atherosclerosis in SHR rats. Hence, hypertensive rats, fed hypercholesterolaemic diet, are not appropriate models for human hypercholesterolaemia and atherosclerosis.
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