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KMID : 0616620010070010005
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Journal of Soonchunhyang Medical College
2001 Volume.7 No. 1 p.5 ~ p.11
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The Effect of Prostaglandin on Renal Blood Flow at Increased Ureteral Pressure
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Abstract
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Higher ureteral pressure than in normal condition causes increase in renal blood flow (RBF) and partial impairment of the autoregulation of RBF. Higher ureteral pressure increased renal prostaglandin production, it is not clear whether or not it is also responsible for partial impairment of the autoregulation of RBF. Therefore, we investigated the role which prostaglandin play in the autoregulation of RBF, studying the interaction between ureteral pressure and RBF autoregulation may reveal the role of prostaglandin in tubuloglomerular feedback. For the purpose of this experiment, six anesthetized mongrel dogs were prepared for the measurements of RBF, mean systemic and renal arterial pressure (RAP) and the manipulation of ureteral pressure to 0 ㎝H2O, 20 ㎝H2O and 40 ㎝H2O. 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-fidled reservoir connected to the ureteral catheter to 20 ㎝ and 40 ㎝ above the kidney level. In response to the elevation of the ureteral pressure, RBF increased from 167±11 ㎖/min to 185±8 ㎖/min, 204±11 ㎖/min respectively and the renal arterial pressure and the systemic arterial pressure didn´t change significantly. During 0 ㎜Hg of ureteral pressure threshold pressure of RBF autoregulation was 59±3 ㎜Hg. On the other hand, during 20 ㎝H2O, 40 ㎝H2O of ureteral pressure, the autoregulation curves shifted upward and rightward from control, threshold pressure is elevated by 74±3 ㎜Hg. The pretreatment of the dogs with indomethacin failed to affect the lower limit of RBF autoregulation during both control (63±5 ㎜Hg) and the elevated ureteral pressure (77±5 ㎜Hg). 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 by increased ureteral pressure or prostaglandin-induced vasodilation does not appear to bear any relation to the reduction in the autoregulatory capacity during elevated ureteral pressure. It seems that the partial impairment of the autoregulation during acute ureteral obstruction is due to the consumption of tubuloglomerular feedback mechanism at 0 ㎜Hg of ureteral pressure and that prostaglandin is neither mediator nor effector of tubuloglomerular feedback mechanism.
Key Words : renal blood flow, indomethacin, prostaglandin, ureteral pressure
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