Renal blood flow > Background Section
Regional renal blood flow can be determined in renal cortical and medullary blood flow with a Transonic systems Laser Doppler flow meter (BLF21D) and probe which we have provided important information regarding the effects of. COX1 and COX2 inhibition on renal blood flow (22). These studies show that renal medullary blood flow is preserved during AngII infusion while renal cortical blood flow falls. The studies also show renal medullary blood flow but not cortical blood flow is sensitive to COX2 inhibition. The findings support the utility of this technique in provide important information for studies of drug/diabetes/renal interactions. Detailed methodolgy is provided on the protocol page for this segment.
To measure regional renal blood flow, the left kidney can be exposed by midline laparotomy. A laser-Doppler flowmeter (model BLF 21D, Transonic System Inc., Ithaca, New York) equipped with two flow probes will be used to measure renal cortical blood flow (CBF), and medullary blood flow (MBF). One flow probe (type N probe with a 3 mm diameter) is placed on the surface of the kidney to measure CBF. MBF is measured by a monofilament fiber optic flow-probe (diameter: 0.5 mm) implanted into renal medulla. The location of the implanted fiber probe will be confirmed at the end of each experiment by dissecting the kidney and examining the region surrounding the fiber tip.
Data from incorrectly positioned fibers are discarded. After anesthesia, the mice receive continuous infusion of 0.9% sodium chloride containing 1% of bovine serum albumin at a rate of 0.5 ml/hour and allowed to equilibrate for around 120 minutes. MAP is analyzed using a Blood Pressure Analyzer (BPA Model 300, Micro-Med. Inc., Louisville, Kentucky).
Publications for Renal blood flow (1)
Qi Z, Hao CM, Langenbach RI, Breyer RM, Redha R, Morrow JD, Breyer MD. Opposite effects of cyclooxygenase-1 and -2 activity on the pressor response to
angiotensin II. J Clin Invest (2002) 110:61-9
View abstract View in PubMed
Therapeutic use of cyclooxygenase-inhibiting (COX-inhibiting) nonsteroidal antiinflammatory drugs (NSAIDs) is often complicated by renal side effects including hypertension and edema. The present studies were undertaken to elucidate the roles of COX1 and COX2 in regulating blood pressure and renal function. COX2 inhibitors or gene knockout dramatically augment the pressor effect of angiotensin II (Ang II). Unexpectedly, after a brief increase, the pressor effect of Ang II was abolished by COX1 deficiency (either inhibitor or knockout). Ang II infusion also reduced medullary blood flow in COX2-deficient but not in control or COX1-deficient animals, suggesting synthesis of COX2-dependent vasodilators in the renal medulla. Consistent with this, Ang II failed to stimulate renal medullary prostaglandin E(2) and prostaglandin I(2) production in COX2-deficient animals. Ang II infusion normally promotes natriuresis and diuresis, but COX2 deficiency blocked this effect. Thus, COX1 and COX2 exert opposite effects on systemic blood pressure and renal function. COX2 inhibitors reduce renal medullary blood flow, decrease urine flow, and enhance the pressor effect of Ang II. In contrast, the pressor effect of Ang II is blunted by COX1 inhibition. These results suggest that, rather than having similar cardiovascular effects, the activities of COX1 and COX2 are functionally antagonistic.
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Last updated on 2013-11-06 Moderated by Jimmy Hao