The effect of losartan and captopril on glomerular basement membrane anionic charge in a diabetic rat model.

OBJECTIVE: Although angiotensin-converting enzyme inhibitors are known to reduce albuminuria by preserving glomerular basement membrane anionic content, the effects of angiotensin II receptor blockage are currently not known. The aim of this study was to evaluate the effects of captopril and losartan on glomerular basement membrane anionic charges in a diabetic rat model. DESIGN: After diabetes induction with streptozotocin, female Wistar rats were divided into three groups: group A, losartan 10 mg/kg by gavage (n = 8); group B, captopril 50 mg/l in drinking water (n = 6); group C, diabetic control rats (n = 8) given only tap water. Group D (eight rats) served as non-diabetic controls. At the end of 8 weeks, erythrocyte membrane charge, serum sialic acid, urinary glycosaminoglycan and albumin were measured and kidney specimens stained with Alcian blue in order to assess basement membrane glycosaminoglycans. RESULTS: Red blood cell anionic charges (ng Alcian blue/ 10(6) red blood cells) were 371.5+/-9.9 for group A, 443.5+/-7.1 for group B, 400.1+/-14.7 for group C, 468.7+/-4 for group D (AD, P<0.01; A>B P<0.01). Albuminuria (microg/day) was 778+/-221 for group A, 719+/-314 for group B, 1724+/-945 for group C, 393+/-263 for group D (A, B

Hyperglycemia-induced attenuation of rectal perception depends upon pattern of rectal balloon inflation.

This study investigated the effects of acute hyperglycemia on conscious rectal perception in response to two different rectal distension paradigms. Eleven healthy males were studied in random order on two separate days during euglycemia and hyperglycemia with blood glucose concentrations clamped to 3.8 +/- 0.6 and 14.8 +/- 0.86 mmol/liter, respectively. In order to evoke sensory responses, rapid phasic and ramplike distensions were applied to an intrarectal balloon. Rectal sensation thresholds for initial sensation, sensation of stool and discomfort, and sensory intensities were recorded. Additionally, anorectal motor responses were investigated during phasic distension. Acute hyperglycemia did not modify rectal sensory pressure thresholds and perception scores in response to phasic distension. Neither did hyperglycemia alter the resting anal sphincter pressure, the pressure threshold for eliciting the rectoanal inhibitory reflex, or the maximal anal squeeze pressure. In contrast, hyperglycemia attenuated rectal perception in response to ramplike distension. The pressure thresholds, 10.0 +/- 1.8 and 17.0 +/- 3.6 mm Hg for initial sensation and discomfort, respectively, during hyperglycemia were significantly higher than the corresponding thresholds of 4.4 +/- 1.4 and 11.4 +/- 1.9 mm Hg observed during euglycemia (P < 0.01). Higher rectal pressures were observed at all intensities of sensation of stool and discomfort during hyperglycemia than those obtained during euglycemia (P < 0.01). Hyperglycemia did not alter the compliance of the rectum. The results of this study demonstrate that acute hyperglycemia attenuates rectal perception, and this attenuation depends upon the type of distension employed. Our findings also demonstrate that anal sphincter motor function is not appreciably modified by hyperglycemia.