• The Korean Journal of Physiology and Pharmacology
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• 제2권1호
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• pp.77-84
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• 1998

Ureteral obstruction causes increase in renal blood flow (RBF) and partial impairment of the autoregulation of RBF. Although increased renal prostaglandin production is responsible for the former, it is not clear whether or not it is also responsible for the latter. Therefore, we investigated the role which prostaglandins play in the autoregulation of RBF during an ureteral pressure elevation (40 $cmH_2O$). Since the major mechanism of RBF autoregulation is the tubuloglomerular feedback, studying the interaction between ureteral pressure and RBF autoregulation may reveal the role of prostaglandin in tubuloglomerular feedback. To pursue the purpose, six anesthetized dogs were prepared for the measurements of RBF, mean sytemic and renal arterial pressure (RAP) and the manipulation of ureteral pressure. The autoregulation curves were determined during both control and elevation of the ureteral pressure, before and after the pretreatment with indomethacin, a cyclooxygenase inhibitor. The desired ureteral pressure was achieved by vertically elevating the water-filled reservoir connected to the ureteral catheter to 40 cm above the kidney level. In response to the elevation of the ureteral pressure, RBF increased from $170{\pm}8 ml{\cdot}min^{-1}\;to\;189{\pm}8$, and the systemic arterial pressure didn't change significantly. During spontaneous urine flow, RBF autoregulation was abolished when RAP was reduced to $59{\pm}3$ mmHg. On the other hand, during the ureteral pressure elevation, the autoregulation curves shifted upward and rightward from control, and the pressure when RBF autoregulation was abolished was $74{\pm}3$ mmHg. The pretreatment of the dogs with indomethacin failed to affect the lower limit of RBF autoregulaion during both control ($63{\pm}5$ mmHg) and the elevated ureteral pressure ($77{\pm}5$ mmHg). Since RBF failed to increase in response to the elevated ureteral pressure, RBF autoregulation curves obtained during the elevated ureteral pressure shifted only rightward from indomethacin control. The results indicate that the increased intrarenal level of prostaglandin or prostaglandin-induced vasodilation does not appear to bear any relation to the reduction in the autoregulatory capacity during partial ureteral obstruction. It seems that the partial impairment of the autoregulation during acute ureteral obstruction is due to the consumption of tubuloglomerular feedback mechanism at spontaneous RAP and that prostaglandin is neither mediator nor effector of tubuloglomerular feedback mechanism.

• 대한한의학회지
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• 제39권2호
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• pp.1-12
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• 2018

Objectives: The objective of this study is to develop a new animal model with Kidney-hypofunction for Sasang Constitutional Medicine, especially for partial Soyangin(one of four constitution which has good digestive function and poor renal function) by Unilateral Ureteral Obstruction, and to estimate the factor related to obesity, dyslipidemia, and metabolic syndrome. Methods: The C57BL/6J mice were divided into 3 groups : normal group, high fat diet(HFD) control group, and HFD group with Unilateral Ureteral Obstruction(UUO). Then, the HFD control group and the experimental group were fed with high fat diet for 6 weeks. Food intake and body weight were measured at regular time by week. After the final experiment, blood was gathered for bloodchemical examination and organs(liver, fatty tissue) were remoed, weighted, and mRNA was analyzed with real-time PCR. Results: The weight growth rate with High fat diet went down by 8.35% in experimental group and had similar FER with the normal group, while HFD control group had higher weight growth rate and FER than any other groups. Also The experimental group had lower triglyceride and LDL cholesterol rate and higher glucose rate in serum. and in mRNA expression, GLUT-9, the protein related to excretion of uric acid and metabolic syndrome, expressed lower rate than that of HFD control group. and IL-6, a kind of cytokine related to obesity and metabolic syndrome, expressed more than HFD control group. Conclusions: It was found that Kidney-hypofunction animal-experimental model is susceptible to metabolic syndrome.