Physical loading creating high peak strains on the skeleton at high strain rates is suggested to be the most effective type of activity in terms of bone mineral acquisition. This study assessed the effects of sudden impact loading on mineral and mechanical bone properties in 13-week-old Sprague-Dawley rats. The rats were randomly assigned as sedentary controls (SED, n ؍ 10), control animals receiving low-intensity exercise (EX, n ؍ 15), and experimental animals receiving low-intensity exercise combined with sudden impact-loading (EX ؉ IMP, n ؍ 15). In the EX group, the rats walked in a walking mill at a speed of 10 cm/s for 20 minutes/day, 5 days/week for 9 weeks. In the EX ؉ IMP group, the program was identical to the EX group except for the additional sudden impacts administered to their skeleton during the walking exercise. At the start, there were 50 impacts per session, after which their number was gradually increased to 200 impacts per session by week 6 and then kept constant until the end of the experiment, week 9. These horizontally and vertically directed body impacts were produced by a custom-made walking mill equipped with computer-controlled high-pressure air cylinders. After sacrifice, both femora of each rat were removed and their dimensions, bone mineral content (BMC) by dual-energy X-ray absorptiometry, and mechanical properties by femoral shaft three-point bending and femoral neck compression were determined. The cortical wall thickness increased significantly in the EX and EX ؉ IMP groups as compared with SEDs (؉7.6%, p ؍ 0.049 and ؉10%, p ؍ 0.020, respectively). The EX ؉ IMP group showed ؉9.0% ( p ؍ 0.046) higher cross-sectional moment of inertia values than the EX group. No significant intergroup differences were seen in the BMC values, while the breaking load of the femoral shaft (EX ؉ IMP vs. SED ؉8.8%, p ؍ 0.047) and femoral neck (EX ؉ IMP vs. SED ؉14.1%, p ؍ 0.013) was significantly enhanced by the impact loading. In conclusion, this study indicates that mechanical loading can substantially improve the mechanical characteristics of a rat femur without simultaneous gain in its mineral mass. If this is true in humans too, our finding gives an interesting perspective to the numerous longitudinal exercise studies (of women) in which the exercise-induced gains in bone mass and density have remained mild to moderate
High calcium diet down-regulated kidney ACE, reduced albuminuria and blood pressure, and favorably influenced kidney morphology in experimental renal failure. These findings suggest a link between calcium metabolism and kidney ACE expression, which may play a role in the progression of renal damage.
Abstract-It is not known whether angiotensin II type 1 receptor antagonists can influence the function and morphology of small arteries in renal failure. We investigated the effect of 8-week losartan therapy (20 mg/kg per day) on isolated mesenteric resistance arteries by wire and pressure myographs in 5/6 nephrectomized rats. Plasma urea nitrogen was elevated 1.6-fold after nephrectomy, and ventricular synthesis of atrial and B-type natriuretic peptides was increased 2.2-fold and 1.7-fold, respectively, whereas blood pressure was not affected. Losartan did not influence these variables. The endothelium-mediated relaxation to acetylcholine was impaired in nephrectomized rats in the absence and presence of nitric oxide synthase and cyclooxygenase inhibition. Blockade of calcium-activated potassium channels by charybdotoxin and apamin reduced the remaining acetylcholine response, and this effect was less marked in nephrectomized than in sham-operated rats. Relaxation to levcromakalim, a vasodilator acting through adenosine triphosphate-sensitive potassium channels, was also impaired after nephrectomy. The arteries of nephrectomized rats showed eutrophic inward remodeling: Wall-to-lumen ratio was increased without change in wall cross-sectional area. All changes in arterial relaxation and morphology were normalized by losartan therapy. Aortic ACE content, measured by autoradiography, directly correlated to the plasma level of urea nitrogen, suggesting that renal failure has an enhancing influence on the vascular renin-angiotensin system. Losartan normalized relaxation and morphology of resistance arteries in experimental renal failure, independent of its influence on blood pressure, impaired kidney function, or volume overload. The mechanism of improved vasodilation by losartan may include enhanced relaxation through potassium channels. Key Words: arteries Ⅲ receptors, angiotensin II Ⅲ endothelium-derived factors Ⅲ angiotensin II Ⅲ potassium channels Ⅲ kidney failure C hronic renal failure is associated with a high prevalence of cardiovascular disease. 1 Large arteries in renal failure are characterized by reduced compliance, 2 the possible explanations of which are increased extracellular matrix content, hyperplasia of smooth muscle, and calcification in media. 3,4 However, increased vascular stiffness has also been observed in the absence of vascular hypertrophy, 5 and decreased endothelial vasodilator function may contribute to vascular pathophysiology in renal failure. 6 Indeed, endothelium-dependent vasodilation is impaired in the forearm circulation of hemodialysis patients. 7 We found that in experimental renal failure, endotheliumdependent vasorelaxation is impaired by a mechanism involving K ϩ channels in arterial smooth muscle. 8 In hypertension, the impaired endothelium-mediated relaxation is ameliorated by treatment with angiotensin II type 1 (AT 1 ) receptor blockers. 9,10 Angiotensin II receptor antagonists have the potential to modulate K ϩ channel-mediated vasorelaxation, since stimulation of AT 1 r...
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