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Ho-Shiang Huang

Publications and source records attributed to Ho-Shiang Huang.

6 recordsLinked to original sources

Changes in renal hemodynamics and urodynamics in rats with chronic hyperoxaluria and after acute oxalate infusion: role of free radicals.

AIMS: The aim of this study was to evaluate possible changes in renal hemodynamic and urodynamic parameters in rats with chronic hyperoxaluria and after acute oxalate challenge. We also evaluated the possible association between free radical (FR) production, hyperoxaluria, and calcium oxalate (CaOx) calculi formation. METHODS: Chronic hyperoxaluria was induced by adding 0.75% ethylene glycol (EG) to the drinking water of male Wistar rats. After 7, 21, and 42 days of treatment, urinary biochemistry, oxalate levels, and lipid peroxides were measured. Kidney calculi were examined by polarizing microscopy. In the second part of the experiments, 1, 10, 20, and 30 mg kg(-1) hr(-1) oxalate was infused, by means of an intrarenal arterial catheter (IRA), into normal rats sequentially. Superoxide dismutase (SOD) infusion by means of IRA, in addition to oxalate, was also performed to check its influence on the altered renal function after oxalate infusion. In both the acute and chronic groups, renal blood flow (RBF), cortical microvascular blood flow (CMVBF), glomerular filtration rate (GFR), urine flow (UV), and urinary sodium excretion (U(Na)V) were measured, and chemiluminescence (CL) was examined in the renal venous blood. RESULTS: Levels of urinary lipid peroxides and enzymuria had increased since day 7, and increased the size of numbers of CaOx crystals in the kidney were noted beginning on day 21, but elevated CL was detectable only on day 7 after 0.75% EG treatment. Decreased UV and U(Na)V were noted in the 42-day EG group, although the 24-hr creatinine clearance values were normal in all experimental groups. On the other hand, RBF, GFR, and CMVBF were attenuated with elevated FR when the oxalate concentration was higher than 10 mg kg(-1) hr(-1) in the acute oxalate infusion group. With SOD pretreatment, the decreased RBF, GFR, and CMVBF could be reversed at 10 mg kg(-1) hr(-1) of oxalate, and be partially reversed at 20. FR also could be reduced significantly at 10 and 20 mg kg(-1) hr(-1) of oxalate. CONCLUSIONS: Decreased urine flow and sodium excretion were the main renal functions affected by chronic hyperoxaluria. However, that only the 42-day EG group had a decreased tubular function cannot be fully explained by the persistent tubular enzymuria and increased lipid peroxides that began on day 7 after EG treatment. With acute oxalate infusion, the major insult to renal function was renal hemodynamics. Pretreated SOD could reverse the attenuated hemodynamics and reduce the elevated FR partly, which suggested that FR is responsible for oxalate toxicity.

Acute Disease↗

Impaired renal sensory responses after renal ischemia in the rat.

Renal sensory responses and reflex function were examined in rats 24 h after 45 min of ischemic injury caused by unilateral renal arterial occlusion (RAO). The integrity of renal pelvic mechanoreceptor (MRu)-mediated renorenal reflex was examined. An increase in ipsilateral afferent renal nerve activity (ARNA) and a reflex decrease in efferent renal nerve activity (ERNA) and contralateral diuresis and natriuresis produced by increasing the intrapelvic pressure were seen in sham-operated (Sham) rats, but it was largely attenuated in RAO rats. Using single-fiber recordings of the renal MRu discharge, graded increases in intrapelvic pressure or renal pelvic administration of substance P (SP) resulted in pressure- or concentration-dependent increases in ARNA in the control kidney of Sham rats, whereas attenuated responses were seen in the postischemic kidney of RAO rats. The unresponsiveness of renal MRus in RAO rats was accompanied by an insufficient release of SP. However, the baseline SP release is higher in RAO kidneys due to a reduced neutral endopeptidase (NEP) activity in the renal pelvis of the postischemic kidney. No changes in NK-1 receptor mRNA levels were demonstrated; however, the expression of NK-1 receptors in the plasma membrane of RAO pelvis were decreased, possibly resulting from the internalization of the receptors associated with beta-arrestin trafficking. Renal excretory responses after saline loading were significantly lower in the postischemic kidney of RAO rats than in Sham rats. Responses of ARNA and ERNA were also lower. It is concluded that the defective activation of renal sensory mechanoreceptors in the postischemic kidney results from an inadequate release of SP after mechanostimulation and the reduced functional NK-1 receptors.

Animals↗

Temporal decrease in renal sensory responses in rats after chronic ligation of the bile duct.

Renal responses to renal sensory receptor activation were examined in rats after 1 and 4 wk of common bile duct ligation (CBDL). Compared with sham-operated rats (Sham), urine and sodium excretion after acute saline loading was significantly reduced at both times after CBDL. The blunted excretory responses in CBDL rats, accompanied by less activation of afferent renal nerve activity (ARNA), were already apparent at 1 wk and became severe at 4 wk. The defect in ARNA activation in CBDL rats was further studied using specific stimuli to activate renal sensory receptors. Graded increases in intrapelvic pressure or renal pelvic perfusion of substance P (SP) elicited an increase in ARNA in Sham rats, these responses being temporally attenuated in CBDL rats. Despite no significant change in renal pelvic SP release, no renorenal reflex was demonstrable in 4-wk CBDL rats. Immunoblotting showed that expression of renal pelvic neurokinin 1 (NK-1) receptors was 32 and 47% lower in 1- and 4-wk CBDL rats, respectively, than in Sham rats, this decrease correlating well with plasma SP levels. The quantitative real-time RT-PCR showed similar levels of NK-1 receptor mRNA in the renal pelvis in the Sham and 4-wk CBDL groups. We conclude that impairment of renal excretory and sensory responses increases with the duration of cirrhosis. An impaired renorenal reflex in cirrhotic rats is involved in the defective activation of the renal sensory receptors could be due, in part, to the low expression of NK-1 receptors, which is dependent on the duration of CBDL. The decrease in NK-1 receptor protein levels is not due to a decrease in mRNA levels.

Animals↗

Impaired renal sensory responses after unilateral ureteral obstruction in the rat.

Renal responses to the activation of renal sensory receptors were examined in rats after release of 24-h unilateral ureteral obstruction of the left kidney. The integrity of the renorenal reflex was examined in both 24-h unilateral ureteral obstruction-treated (UUO) and sham-operated (Sham) rats. Increased ipsilateral afferent renal nerve activity (ARNA) and reflexly decreased efferent renal nerve activity (ERNA) and increased contralateral diuresis and natriuresis produced by increasing the left intrapelvic pressure were observed in Sham rats but not in UUO rats. The lack of responsiveness of the renorenal reflex in UUO rats was associated with lower release of substance P (SP) and increased neutral endopeptidase (NEP) activity in the renal pelvis in the postobstructive kidney. Compared with Sham rats, urine and sodium excretion after acute saline loading was significantly reduced in the postobstructive kidney. The blunted excretory responses were accompanied by lower activation of ARNA and less reflex inhibition of ERNA. Renal sensory dysfunction in the postobstructive kidney was further examined by stimulation of renal mechanoreceptors and chemoreceptors. Graded increases in intrapelvic pressure or renal pelvic perfusion with hypertonic saline solution elicited, respectively, a pressure- or concentration-dependent increase in ARNA in the control kidney of Sham rats, this response being greatly attenuated in the postobstructive kidney. Western blots showed no quantitative difference in the expression of renal pelvic neurokinin 1 (NK-1) receptors between the two groups. It was concluded that renal sensory function is impaired in the postobstructive kidney of UUO rats and that this defective activation of renal sensory receptors results in an impaired renorenal reflex, which is associated with enhanced NEP activity and catabolism of SP released in the renal pelvis and is not related to the expression of NK-1 receptor protein.

Afferent Pathways↗

Association of changes in the pattern of urinary calculi in Taiwanese with diet habit change between 1956 and 1999.

OBJECTIVE: Due to rapid economic development over the past four decades, urinary stone components may have changed in Taiwan. We studied the changes in urinary stone components over time and the possible association with dietary changes during the same period. MATERIALS AND METHODS: From 1956 to 1999, 9,715 urinary calculi were collected at a single institution and analyzed using polarizing microscopy. Dietary information was obtained from an official national report. Linear regression was used to analyze the possible correlation between the change in stone components with daily consumption of animal protein, vegetable protein, and lipid. RESULTS: Eleven distinct components were identified. Calcium oxalate (Jensen type I stone; found in sterile, acidic urine) was found most frequently (87.3%), and its incidence increased gradually with time. However, the incidence of Jensen type III stone (caused by metabolic abnormality) gradually decreased from 1956 to 1999. The male to female ratio among subjects was 2.3:1, and the modal age was in the forties. Female patients were more likely to suffer from type II stones (found in infected, alkaline urine), whereas type I and III stones were more prevalent in males. Among the dietary components, consumption of animal and vegetable proteins and lipid increased significantly during the same period, and appeared to be coincident with the increased incidence of type I stones during the study period. CONCLUSIONS: Patterns of urinary tract stones in Taiwan have progressively changed in the past four decades and are now similar to those in western populations. The incidence of type I stones has increased during the past four decades, which may reflect the Westernization of dietary habits in Taiwanese during the same period.

Adult↗

Changes in the oxidant-antioxidant balance in the kidney of rats with nephrolithiasis induced by ethylene glycol.

PURPOSE: We investigated the possible mechanism of increased free radicals, the role of antioxidant enzymes and their correlation with renal tubular damage in the kidney after feeding 0.75% ethylene glycol to male Wistar rats. MATERIALS AND METHODS: Rats were divided into 7 experimental groups according to the duration of ethylene glycol feeding (1, 3, 5, 7, 9, 21 or 42 days) and into age matched control groups. Chemiluminescence levels were examined in blood samples (renal artery and vein) and in the kidney. The activities of oxidase and antioxidant enzymes were measured in kidney homogenates. The nitroblue tetrazolium perfusion method and immunohistochemical stains with ED1 and CD45 were performed. Urinary levels of alpha and mu-glutathione S-transferase (GST) were also measured and expressed in gm. urinary creatinine. RESULTS: Chemiluminescence levels of renal venous blood samples were elevated on days 1, 3 and 7 (p <0.05), and those of the kidney were elevated only on days 3 and 42 (p <0.05) compared with controls. The infiltration of CD45 positive cells in the kidney increased on day 7 and a further increase in these positive cells was noted on day 21. Fused ED1 positive cells surrounding the calcium oxalate crystals and adjacent to the nitroblue tetrazolium positive area were found on day 42. Xanthine oxidase activity showed no significant change, whereas nicotinamide adenine dinucleotide dependent oxidase activity was higher on day 5 and nicotinamide adenine dinucleotide phosphate dependent activity was elevated in all experimental groups (p <0.05). The activities of catalase and manganese superoxide dismutase were elevated in the early stage. On day 42 almost all antioxidant enzyme activities were attenuated (p <0.05) except that of catalase. The urinary levels of alpha-GST were elevated from day 7 until day 42, whereas levels of mu-GST were elevated from day 3 until day 42 except day 5. CONCLUSIONS: The possible mechanism that causes free radical elevation in the kidney may be different in the course of nephrolithiasis after ethylene glycol treatment. Initially the systemic circulation may bring the toxic substance into the kidney and cause it to produce free radicals. In the late stage gradually infiltrating leukocytes and decreased antioxidant enzyme activities may cause the kidney to remain under excessive oxidative stress.

Animals↗