Journal articles: 'Renal blood flow'

1

Di Giantomasso, David, Hiroshi Morimatsu, Clive N. May, and Rinaldo Bellomo. "Increasing Renal Blood Flow." Chest 125, no. 6 (June 2004): 2260–67. http://dx.doi.org/10.1378/chest.125.6.2260.

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2

Liang, Fuyou, Tooru Itoga, Ryuhei Yamaguchi, and Hao Liu. "A Numerical Study of Blood Flow in the Human Renal Artery." Proceedings of the Fluids engineering conference 2004 (2004): 280. http://dx.doi.org/10.1299/jsmefed.2004.280.

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3

Kornacka, M. K., E. Burzyńska, and J. Gadzinowski. "Renal Blood Flow in Twins." Acta geneticae medicae et gemellologiae: twin research 47, no. 3-4 (October 1998): 161–69. http://dx.doi.org/10.1017/s0001566000000052.

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AbstractThe aim of this preliminary study was the estimation of renal blood flow in 16 premature newborns from twin pregnancies with mean body weight 1270 g and mean gestational age 29 weeks.In control group we have 16 singleton newborns with mean gestational age 29 weeks and mean birth weight 1240 g. In both intervention and control group we have the similar clinical symptoms. The renal blood flow was carried out in the first day of life with the Acuson 128 XP Colour Doppler using the 6 and 7 MHz linear transducer. The renal blood flow parameters-PI, RI, Vmax, Vmin Vmean were measured in right and left renal arteries in theirs courses from the aorta to the renal hilus, by color sinal. In the investigation group the mean value of RI in right and left renal artery was 0,88. Mean PI in right vessel was 1,67 and in left 1,56. Mean V min in right and in left artery was 0,03 and mean V max in right artery was 0,34 and in left 0,33. Mean value of mean velocity in right vessels was 0,18 and in left 0,19.In control group we observed in right artery mean value of PI 1,74 and in left 1,6. Mean RI was 0,86 and 0,86 in right vessel in left vessel. Mean V min was 0,05 in right and 0,04 in left artery. Mean V max was 0,37 in right and 0,34 in left artery. Mean value of V mean was 0,19 in right artery and 0,18 in left artery.Using the student, Mann-Whitney and Shapiro-Wilk tests we have not observed statistically significant difference of Doppler parameters between control and investigation group and between the left and right artery. Although in newborns with broad PDA we noted significant higher value of RI (0,97, 0,98) than in newborns without PDA (0,78, 0,81).

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4

Mimran, Albert. "Regulation of Renal Blood Flow." Journal of Cardiovascular Pharmacology 10 (1987): S1—S9. http://dx.doi.org/10.1097/00005344-198700105-00002.

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Mimran, Albert. "Regulation of Renal Blood Flow." Journal of Cardiovascular Pharmacology 10 (1987): S1—S9. http://dx.doi.org/10.1097/00005344-198706105-00002.

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6

Kellum, John A. "Endotoxin and Renal Blood Flow." Blood Purification 15, no. 4-6 (1997): 286–91. http://dx.doi.org/10.1159/000170346.

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7

Guglielmi, M., S. Zanotti, M. Zanotti, T. Walker, J. E. Parrillo, and S. M. Hollenberg. "RENAL BLOOD FLOW IN MICE." Shock 25, Supplement 1 (June 2006): 97. http://dx.doi.org/10.1097/00024382-200606001-00292.

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8

Laurent, Stéphane, Pierre Boutouyrie, and Elie Mousseaux. "Aortic Stiffening, Aortic Blood Flow Reversal, and Renal Blood Flow." Hypertension 66, no. 1 (July 2015): 10–12. http://dx.doi.org/10.1161/hypertensionaha.115.05357.

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9

Speiman, F. A., and P. A. Öberg. "Continuous measurement of renal cortical blood flow and renal arterial blood flow during stimulation of the renal nerve." Medical & Biological Engineering & Computing 29, no. 2 (March 1991): 121–28. http://dx.doi.org/10.1007/bf02447096.

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10

Persson, Pontus B. "Renal blood flow autoregulation in blood pressure control." Current Opinion in Nephrology and Hypertension 11, no. 1 (January 2002): 67–72. http://dx.doi.org/10.1097/00041552-200201000-00010.

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11

Pollock, D. M., and R. O. Banks. "Perspectives on Renal Blood Flow Autoregulation." Experimental Biology and Medicine 198, no. 3 (December 1, 1991): 800–805. http://dx.doi.org/10.3181/00379727-198-43321e.

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12

de Leeuw, P. W., and W. H. Birkenhäger. "Renal Blood Flow in Essential Hypertension." Journal of Cardiovascular Pharmacology 10 (1987): S10—S13. http://dx.doi.org/10.1097/00005344-198700105-00003.

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13

de Leeuw, P. W., and W. H. Birkenhäger. "Renal Blood Flow in Essential Hypertension." Journal of Cardiovascular Pharmacology 10 (1987): S10—S13. http://dx.doi.org/10.1097/00005344-198706105-00003.

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14

Jamberg, P.-O., Bettina Marrone, and L. L. Priano. "A572 ENFLURANE PRESERVES RENAL BLOOD FLOW." Anesthesiology 73, no. 3A (September 1, 1990): NA. http://dx.doi.org/10.1097/00000542-199009001-00570.

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15

GOLDMAN, STANFORD M., URSULA A. SCHEFFEL, JOHN HILTON, JOHN P. ENTERLINE, and JAMES H. ANDERSON. "Blood Flow to Experimental Renal Tumors." Investigative Radiology 21, no. 6 (June 1986): 459–64. http://dx.doi.org/10.1097/00004424-198606000-00003.

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16

Schwartz, Arthur E. "Cerebral and Renal Blood Flow Autoregulation." Anesthesiology 120, no. 5 (May 1, 2014): 1281. http://dx.doi.org/10.1097/aln.0000000000000166.

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17

Young, L. S., M. C. Regan, M. K. Barry, J. G. Geraghty, and J. M. Fitzpatrick. "Methods of renal blood flow measurement." Urological Research 24, no. 3 (June 1996): 149–60. http://dx.doi.org/10.1007/bf00304078.

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18

Zou, A. P., J. D. Imig, M. Kaldunski, P. R. Ortiz de Montellano, Z. Sui, and R. J. Roman. "Inhibition of renal vascular 20-HETE production impairs autoregulation of renal blood flow." American Journal of Physiology-Renal Physiology 266, no. 2 (February 1, 1994): F275—F282. http://dx.doi.org/10.1152/ajprenal.1994.266.2.f275.

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The present study evaluated the role of endogenous P-450 metabolites of arachidonic acid (AA) on autoregulation of renal blood flow in rats. Whole kidney and cortical blood flows were well autoregulated when renal perfusion pressure was varied from 150 to 100 mmHg. Infusion of 17-octadecynoic acid (17-ODYA) into the renal artery (33 nmol/min) increased cortical and papillary blood flows by 12.6 +/- 2.5 and 26.5 +/- 4.6%, respectively. After 17-ODYA, autoregulation of whole kidney and cortical blood flows was impaired. Intrarenal infusion of miconazole (8 nmol/min) had no effect on autoregulation of whole kidney, cortical, or papillary blood flows. 17-ODYA (1 microM) inhibited the formation of 20-hydroxyeicosatetraenoic acid (20-HETE) and 11,12- and 14,15-epoxyeicosatrienoic acids (EETs) by renal preglomerular microvessels in vitro by 83.7 +/- 7.4% and 89.0 +/- 4.9%, respectively. Miconazole (1 microM) reduced the formation of EETs by 86.4 +/- 5.7%, but it had no effect on the production of 20-HETE. These results suggest that endogenous P-450 metabolites of AA, particularly 20-HETE, may participate in the autoregulation of renal blood flow.

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19

Langenberg, C., L. Wan, M. Egi, C. N. May, and R. Bellomo. "Renal blood flow in experimental septic acute renal failure." Kidney International 69, no. 11 (June 2006): 1996–2002. http://dx.doi.org/10.1038/sj.ki.5000440.

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20

Tanemoto, Masayuki. "Influence on renal blood flow in renal denervation procedures." Journal of Hypertension 37, no. 2 (February 2019): 453–54. http://dx.doi.org/10.1097/hjh.0000000000001992.

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21

Prowle, John R., Ken Ishikawa, Clive N. May, and Rinaldo Bellomo. "Renal Blood Flow during Acute Renal Failure in Man." Blood Purification 28, no. 3 (2009): 216–25. http://dx.doi.org/10.1159/000230813.

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22

Bergström, G., G. Göthberg, G. Karlström, and J. Rudenstam. "Renal Medullary Blood Flow and Renal Medullary Antihypertensive Mechanisms." Clinical and Experimental Hypertension 20, no. 1 (January 1998): 1–26. http://dx.doi.org/10.3109/10641969809053203.

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23

Ingyinn, Ma, Khodayar Rais-Bahrami, Rebecca Evangelista, Inger Hogan, Oswaldo Rivera, Gerald T. Mikesell, and Billie L. Short. "Comparison of the effect of venovenous versus venoarterial extracorporeal membrane oxygenation on renal blood flow in newborn lambs." Perfusion 19, no. 3 (May 2004): 163–70. http://dx.doi.org/10.1191/0267659104pf736oa.

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Venovenous extracorporeal membrane oxygenation (VV ECMO) using double lumen catheters is an alternative to venoarterial (VA) ECMO and allows for total blood flow using the patient’s cardiac output in comparison to partial blood flow provided during VA ECMO. Objective: To compare the effects of VV versus VA ECMO on renal blood flow. Design: Prospective study. Setting: Research laboratory in a hospital. Subject: Newborn lambs 1-7 days of age (n=15). Interventions: In anesthetized, ventilated lambs, fe-moral artery and vein were cannulated for monitoring and renal venous blood sampling. An ultrasonic flow probe was placed on the left renal artery for continuous renal blood flow measurements. Animals were randomly assigned to control (non-ECMO), VV ECMO and VA ECMO groups. After systemic heparinization, the animals were cannulated and studied at bypass flows of 120 mL-kg/min (partial bypass) for two hours in both ECMO groups and 200 mL/kg/min (full bypass) for an additional 30 min in the VA group. Changes in blood pressure and renal flow on ECMO and during ECMO bridge unclamping were recorded continuously. Plasma renin activity (PRA) levels were sequentially sampled. Results: Systemic blood pressure was not different in VV or VA ECMO at partial bypass flow. However, systemic blood pressure increased significantly at maximal bypass flow in the VA ECMO group. There was no change in renal flow in either VV or VA ECMO groups. PRA levels did not correlate with bypass flow change. During unclamping of the ECMO bridge, blood pressure and renal flow drop significantly in the VA group, but not in the VV group. Conclusion: VV and VA ECMO at partial bypass flows had comparable effect on blood pressure, renal blood flow and PRA level in this short-term study. However, unclamping of the ECMO bridges did differentially affect blood pressure and renal blood flow between VV and VA groups. We speculate that this repeated acute change in long-run VA ECMO support may play a role in the persistent hypertension seen in some patients.

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24

Lu, S., R. J. Roman, D. L. Mattson, and A. W. Cowley. "Renal medullary interstitial infusion of diltiazem alters sodium and water excretion in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 5 (November 1, 1992): R1064—R1070. http://dx.doi.org/10.1152/ajpregu.1992.263.5.r1064.

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The role of renal papillary blood flow in regulation of fluid and electrolyte excretion was examined. The effects of an acute infusion of diltiazem (5 micrograms.kg-1 x min-1) into the renal medullary interstitium on papillary blood flow and sodium and water excretion were studied. Changes of renal blood flow were measured using an electromagnetic flow probe. Cortical and papillary blood flows were measured using laser-Doppler flowmetry. Renal and cortical blood flows were unchanged during medullary interstitial infusion of diltiazem, but papillary blood flow increased 26% (P < 0.05) and remained elevated for 1 h after diltiazem infusion was discontinued. Glomerular filtration rate (GFR) of the infused kidney increased by 21% from a control of 1.0 +/- 0.1 ml.min-1 x g-1 during infusion of diltiazem (P < 0.05), but it returned to control after diltiazem infusion was stopped. Urine flow and sodium excretion increased by 70% (P < 0.05), and fractional sodium excretion rose from 1.5 +/- 0.2 to 2.4 +/- 0.3% of the filtered load during the hour after diltiazem infusion. Renal blood flow, cortical and papillary blood flow, GFR, urine flow, and sodium excretion in the 0.9% sodium chloride vehicle-infused kidney were not significantly altered during the experiment. Intravenous infusion of the same dose of diltiazem (5 micrograms.kg-1 x min-1) increased GFR by 22%, but had no effect on urine flow and sodium excretion. These results indicate that renal medullary interstitial infusion of diltiazem selectively increased renal papillary blood flow, which was associated with an increase of sodium and water excretion.

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25

Cupples, W. A., P. Novak, V. Novak, and F. C. Salevsky. "Spontaneous blood pressure fluctuations and renal blood flow dynamics." American Journal of Physiology-Renal Physiology 270, no. 1 (January 1, 1996): F82—F89. http://dx.doi.org/10.1152/ajprenal.1996.270.1.f82.

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Two mechanisms operating at 0.03-0.05 and 0.1-0.2 Hz are involved in autoregulation of renal blood flow (RBF). To examine the behavior of the faster system, the response of RBF to spontaneous fluctuations of arterial pressure was assessed in Sprague-Dawley rats anesthetized by isoflurane or halothane. During halothane anesthesia, autonomous oscillation of total RBF was observed at 0.10-0.15 Hz, and normalized admittance gain became negative at 0.11 +/- 0.01 Hz. During isoflurane anesthesia, there was autonomous power in blood flow in a broad peak between 0.15 and 0.25 Hz, and gain became negative at 0.15 +/- 0.01 Hz. Increasing inspired isoflurane concentration from 1.4 +/- 0.1% to 2.2 +/- 0.1% reduced pressure by 22 +/- 2 mmHg but did not alter blood flow or the transfer function, indicating that the operating frequency was not changed. In another experiment, changing from isoflurane to halothane increased peak power in the autonomous blood flow oscillation fivefold and reduced its frequency from 0.18 +/- 0.01 to 0.14 +/- 0.01 Hz. Gain became negative at a higher frequency (0.16 +/- 0.01 Hz) during isoflurane than halothane anesthesia (0.12 +/- 0.01 Hz). The results show that the 0.1–0.2 Hz system is reliably detected under unforced conditions and provides modest attenuation of pressure fluctuations at < or = 0.1 Hz. Its operating frequency under isoflurane anesthesia is consistent with previous estimates from barbiturate-anesthetized rats, whereas it operates significantly slower under halothane anesthesia.

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26

Sandgaard, N. C. F., J. L. Andersen, N. H. Holstein-Rathlou, and P. Bie. "Aortic blood flow subtraction: an alternative method for measuring total renal blood flow in conscious dogs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 5 (May 1, 2002): R1528—R1535. http://dx.doi.org/10.1152/ajpregu.00494.2001.

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We have measured total renal blood flow (TRBF) as the difference between signals from ultrasound flow probes implanted around the aorta above and below the renal arteries. The repeatability of the method was investigated by repeated, continuous infusions of angiotensin II and endothelin-1 seven times over 8 wk in the same dog. Angiotensin II decreased TRBF (350 ± 16 to 299 ± 15 ml/min), an effect completely blocked by candesartan (TRBF 377 ± 17 ml/min). Subsequent endothelin-1 infusion reduced TRBF to 268 ± 20 ml/min. Bilateral carotid occlusion (8 sessions in 3 dogs) increased arterial blood pressure by 49% and decreased TRBF by 12%, providing an increase in renal vascular resistance of 69%. Dynamic analysis showed autoregulation of renal blood flow in the frequency range <0.06–0.07 Hz, with a peak in the transfer function at 0.03 Hz. It is concluded that continuous measurement of TRBF by aortic blood flow subtraction is a practical and reliable method that allows direct comparison of excretory function and renal blood flow from two kidneys. The method also allows direct comparison between TRBF and flow in the caudal aorta.

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27

Kishimoto, T., W. Sakamoto, T. Nakatani, T. Ito, K. Iwai, T. Kim, and Y. Abe. "Cardiac Output, Renal Blood Flow and Hepatic Blood Flow in Rats with Glycerol-Induced Acute Renal Failure." Nephron 53, no. 4 (1989): 353–57. http://dx.doi.org/10.1159/000185781.

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28

DiBona, Gerald F., and Linda L. Sawin. "Effect of renal denervation on dynamic autoregulation of renal blood flow." American Journal of Physiology-Renal Physiology 286, no. 6 (June 2004): F1209—F1218. http://dx.doi.org/10.1152/ajprenal.00010.2004.

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Vasoconstrictor intensities of renal sympathetic nerve stimulation elevate the renal arterial pressure threshold for steady-state stepwise autoregulation of renal blood flow. This study examined the tonic effect of basal renal sympathetic nerve activity on dynamic autoregulation of renal blood flow in rats with normal (Sprague-Dawley and Wistar-Kyoto) and increased levels of renal sympathetic nerve activity (congestive heart failure and spontaneously hypertensive rats). Steady-state values of arterial pressure and renal blood flow before and after acute renal denervation were subjected to transfer function analysis. Renal denervation increased basal renal blood flow in congestive heart failure (+35 ± 3%) and spontaneously hypertensive rats (+21 ± 3%) but not in Sprague-Dawley and Wistar-Kyoto rats. Renal denervation significantly decreased transfer function gain (i.e., improved autoregulation of renal blood flow) and increased coherence only in spontaneously hypertensive rats. Thus vasoconstrictor intensities of renal sympathetic nerve activity impaired the dynamic autoregulatory adjustments of the renal vasculature to oscillations in arterial pressure. Renal denervation increased renal blood flow variability in spontaneously hypertensive rats and congestive heart failure rats. The contribution of vasoconstrictor intensities of basal renal sympathetic nerve activity to limiting renal blood flow variability may be important in the stabilization of glomerular filtration rate.

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29

Glahn, R. P., W. G. Bottje, P. Maynard, and R. F. Wideman. "Response of the avian kidney to acute changes in arterial perfusion pressure and portal blood supply." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 2 (February 1, 1993): R428—R434. http://dx.doi.org/10.1152/ajpregu.1993.264.2.r428.

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Domestic fowl kidneys autoregulate total renal blood flow and glomerular filtration rate (GFR) over a wide range of renal arterial perfusion pressure (RAPP). Sustained (approximately 2-4 h) restriction of renal portal blood flow attenuates the autoregulatory responses. The present study was designed to assess the effects of acute (approximately 10 min) alterations of renal portal blood flow on renal function, and to dissociate the renal responses to altered renal portal blood flow from the renal responses to reductions in RAPP. The thermal pulse decay (TPD) technique and p-aminohippuric acid clearance (CPAH) were used to measure blood flow. During acute increases and decreases in renal portal blood flow, regional renal blood flow as measured by the TPD system (RBFTPD) was significantly positively correlated with total kidney blood flow represented by CPAH (RBFPAH). These results indicate that changes in total kidney blood flow induced by alteration of portal perfusion were reflected in the regional measurement of renal blood flow. Changes in renal portal blood flow did not affect the urine flow rate (UFR), GFR, or fractional excretion of sodium (FENa). Reducing RAPP from 120 to 50 mmHg significantly reduced UFR, GFR, and FENa. Overall, these results indicate that large acute changes in renal portal blood flow can significantly alter total renal blood flow without significantly affecting parameters (UFR, GFR, and FENa) primarily influenced by the renal arterial vasculature.

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30

Hintze, T. H., M. G. Currie, and P. Needleman. "Atriopeptins: renal-specific vasodilators in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 4 (April 1, 1985): H587—H591. http://dx.doi.org/10.1152/ajpheart.1985.248.4.h587.

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Conscious dogs were instrumented to study the effects of atriopeptins (I, II, III) on renal, iliac, mesenteric, and coronary blood flow. Intravenous injection of atriopeptins II and III caused a dose-related increase in renal blood flow, whereas atriopeptin I had no effect. Atriopeptins II and III at 5 micrograms/kg increased renal blood flow 27 +/- 5.0% from 252 +/- 29 ml/min and 18 +/- 2.9% from 238 +/- 32 ml/min and reduced renal vascular resistance 24 +/- 3.2% from 0.431 +/- 0.048 mmHg X ml-1 X min and 15.1 +/- 1.2% from 0.443 +/- 0.023 mmHg X ml-1 X min, respectively. Atriopeptin I, II, or III exerted no significant effect on systemic arterial pressure, heart rate, coronary, mesenteric, or iliac blood flows. Doses of nitroglycerin (25 micrograms/kg) that increased renal blood flow (28 +/- 5.0%) to a degree comparable to atriopeptins II and III also caused increases in coronary, iliac, and mesenteric blood flows and produced falls in systemic blood pressure and a reflex tachycardia. Thus in the conscious dog, atriopeptins II and III are potent selective renal vasodilators that do not exhibit systemic hemodynamic effects in contrast to nitroglycerin, a nonselective vasodilator. Cleavage at the carboxy terminal end of these peptides to yield atriopeptin I abolishes the renal vasodilator action entirely.

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31

Burke, Marilyn, Mallikarjuna Pabbidi, Jerry Farley, and Richard Roman. "Molecular Mechanisms of Renal Blood Flow Autoregulation." Current Vascular Pharmacology 12, no. 6 (December 10, 2014): 845–58. http://dx.doi.org/10.2174/15701611113116660149.

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32

Marsh, Donald J., Olga V. Sosnovtseva, Ki H. Chon, and Niels-Henrik Holstein-Rathlou. "Nonlinear interactions in renal blood flow regulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 5 (May 2005): R1143—R1159. http://dx.doi.org/10.1152/ajpregu.00539.2004.

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We have developed a model of tubuloglomerular feedback (TGF) and the myogenic mechanism in afferent arterioles to understand how the two mechanisms are coupled. This paper presents the model. The tubular model predicts pressure, flow, and NaCl concentration as functions of time and tubular length in a compliant tubule that reabsorbs NaCl and water; boundary conditions are glomerular filtration rate (GFR), a nonlinear outflow resistance, and initial NaCl concentration. The glomerular model calculates GFR from a change in protein concentration using estimates of capillary hydrostatic pressure, tubular hydrostatic pressure, and plasma flow rate. The arteriolar model predicts fraction of open K channels, intracellular Ca concentration (Cai), potential difference, rate of actin–myosin cross bridge formation, force of contraction, and length of elastic elements, and was solved for two arteriolar segments, identical except for the strength of TGF input, with a third, fixed resistance segment representing prearteriolar vessels. The two arteriolar segments are electrically coupled. The arteriolar, glomerular, and tubular models are linked; TGF modulates arteriolar circumference, which determines vascular resistance and glomerular capillary pressure. The model couples TGF input to voltage-gated Ca channels. It predicts autoregulation of GFR and renal blood flow, matches experimental measures of tubular pressure and macula densa NaCl concentration, and predicts TGF-induced oscillations and a faster smaller vasomotor oscillation. There are nonlinear interactions between TGF and the myogenic mechanism, which include the modulation of the frequency and amplitude of the myogenic oscillation by TGF. The prediction of modulation is confirmed in a companion study ( 28 ).

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33

Marsh, Donald J., Olga V. Sosnovtseva, Alexey N. Pavlov, Kay-Pong Yip, and Niels-Henrik Holstein-Rathlou. "Frequency encoding in renal blood flow regulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 5 (May 2005): R1160—R1167. http://dx.doi.org/10.1152/ajpregu.00540.2004.

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With a model of renal blood flow regulation, we examined consequences of tubuloglomerular feedback (TGF) coupling to the myogenic mechanism via voltage-gated Ca channels. The model reproduces the characteristic oscillations of the two mechanisms and predicts frequency and amplitude modulation of the myogenic oscillation by TGF. Analysis by wavelet transforms of single-nephron blood flow confirms that both amplitude and frequency of the myogenic oscillation are modulated by TGF. We developed a double-wavelet transform technique to estimate modulation frequency. Median value of the ratio of modulation frequency to TGF frequency in measurements from 10 rats was 0.95 for amplitude modulation and 0.97 for frequency modulation, a result consistent with TGF as the modulating signal. The simulation predicted that the modulation was regular, while the experimental data showed much greater variability from one TGF cycle to the next. We used a blood pressure signal recorded by telemetry from a conscious rat as the input to the model. Blood pressure fluctuations induced variability in the modulation records similar to those found in the nephron blood flow results. Frequency and amplitude modulation can provide robust communication between TGF and the myogenic mechanism.

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34

Pallone, Thomas L., and Erik P. Silldorff. "Pericyte Regulation of Renal Medullary Blood Flow." Nephron Experimental Nephrology 9, no. 3 (April 23, 2001): 165–70. http://dx.doi.org/10.1159/000052608.

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35

Kennedy‐Lydon, T. M., C. Crawford, S. S. P. Wildman, and C. M. Peppiatt‐Wildman. "Renal pericytes: regulators of medullary blood flow." Acta Physiologica 207, no. 2 (November 6, 2012): 212–25. http://dx.doi.org/10.1111/apha.12026.

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36

Castrop, Hayo. "Renal medullary blood flow and essential hypertension." Acta Physiologica 226, no. 3 (May 23, 2019): e13289. http://dx.doi.org/10.1111/apha.13289.

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37

Takahashi, G., and H. Takahashi. "Renal Blood Flow Velocity in Reflux Nephropathy." Aktuelle Urologie 24, S 1 (April 25, 2008): 106–7. http://dx.doi.org/10.1055/s-2008-1058359.

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38

Hashimoto, Junichiro, and Sadayoshi Ito. "Aortic Blood Flow Reversal Determines Renal Function." Hypertension 66, no. 1 (July 2015): 61–67. http://dx.doi.org/10.1161/hypertensionaha.115.05236.

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39

Seikaly, Mouin G., and Billy S. Arant. "Development of Renal Hemodynamics: Glomerular Filtration And Renal Blood Flow." Clinics in Perinatology 19, no. 1 (March 1992): 1–13. http://dx.doi.org/10.1016/s0095-5108(18)30472-x.

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40

McALLISTER, RICHARD M. "Adaptations in control of blood flow with training: splanchnic and renal blood flows." Medicine &amp Science in Sports &amp Exercise 30, no. 3 (March 1998): 375–81. http://dx.doi.org/10.1097/00005768-199803000-00006.

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41

Visscher, C. A., D. De Zeeuw, G. Navis, A. K. Van Zanten, P. E. De Jong, and R. M. Huisman. "Renal 131I-hippurate clearance overestimates true renal blood flow in the instrumented conscious dog." American Journal of Physiology-Renal Physiology 271, no. 2 (August 1, 1996): F269—F274. http://dx.doi.org/10.1152/ajprenal.1996.271.2.f269.

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We evaluated renal 131I-hippurate clearance (ERPFhip) as a measure of renal blood flow (RBF) in chronically instrumented conscious dogs. When adjusted for renal hippurate extraction (Ehip, 0.77 +/- 0.01) and hematocrit (Hct, 39.7 +/- 1%), calculated RBFhip (656 +/- 37 ml/min) markedly exceeded renal blood flow measured with renal artery blood flow probes (RBFprobe, 433 +/- 27 ml/min). The discrepancy could not be explained by flow probe calibration, because in vivo comparison of flow probe values with renal venous outflow showed only a slight underestimation of renal blood flow (slope 0.93, 95% confidence interval 0.89-0.97). Redistribution of hippurate from erythrocytes into renal venous plasma during or shortly after blood sampling led to an underestimation of Ehip by 4 +/- 1% and thus could only explain a small part of the difference. Extrarenal hippurate clearance was excluded, because the amount of 131I-hippurate cleared from plasma equaled that appearing in the urine (303 +/- 17 and 307 +/- 17 ml/min). Applying these corrections, we found that RBFhip still exceeded RBFprobe by 37 +/- 3%. These data indicate that renal blood flow measured by the hippurate clearance technique markedly overestimates true renal blood flow. Because other errors were excluded, a combination of sampling of nonrenal blood and intrarenal hippurate extraction from erythrocytes might play a role.

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Beierwaltes, W. H., D. H. Sigmon, and O. A. Carretero. "Endothelium modulates renal blood flow but not autoregulation." American Journal of Physiology-Renal Physiology 262, no. 6 (June 1, 1992): F943—F949. http://dx.doi.org/10.1152/ajprenal.1992.262.6.f943.

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Inhibition of the production of the endothelium-derived relaxing factor (EDRF) nitric oxide using N omega-nitro-L-arginine methyl ester (L-NAME) increases blood pressure (BP) and decreases renal blood flow (RBF), suggesting that basal EDRF can modulate both systemic resistance and renal perfusion. We tested whether L-NAME inhibition of EDRF could also change the autoregulation of RBF. Blood pressure and RBF were measured in Inactin-anesthetized Sprague-Dawley rats. A bolus of 10 mg/kg body wt of L-NAME produced the maximum pressor response (23 +/- 3 mmHg) and blocked acetylcholine-induced renal vasodilation. In control rats, sequential changes in renal perfusion pressure showed that RBF was well autoregulated down to 95 +/- 2 mmHg. L-NAME increased BP, decreased RBF by 33% (P less than 0.005), and increased renal vascular resistance twofold. Although RBF was decreased, the kidney was still able to autoregulate RBF, although reset around the lower flow. Acute hypertension by carotid occlusion and vagotomy increased BP by 26 +/- 6 mmHg (P less than 0.005) and slightly increased RBF, while autoregulation was maintained. The pressor response to L-NAME was amplified to 38 +/- 6 mmHg (P less than 0.001), but RBF decreased by 35% (P less than 0.01). Autoregulation of RBF was maintained, although reset around the lower flow. We conclude that, although endothelial EDRF production may help maintain RBF, it does not seem to mediate the intrinsic autoregulatory responses of the renal vasculature to altered renal perfusion pressure.

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Zou, Ai-Ping, Kasem Nithipatikom, Pin-Lan Li, and Allen W. Cowley. "Role of renal medullary adenosine in the control of blood flow and sodium excretion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 3 (March 1, 1999): R790—R798. http://dx.doi.org/10.1152/ajpregu.1999.276.3.r790.

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This study determined the levels of adenosine in the renal medullary interstitium using microdialysis and fluorescence HPLC techniques and examined the role of endogenous adenosine in the control of medullary blood flow and sodium excretion by infusing the specific adenosine receptor antagonists or agonists into the renal medulla of anesthetized Sprague-Dawley rats. Renal cortical and medullary blood flows were measured using laser-Doppler flowmetry. Analysis of microdialyzed samples showed that the adenosine concentration in the renal medullary interstitial dialysate averaged 212 ± 5.2 nM, which was significantly higher than 55.6 ± 5.3 nM in the renal cortex ( n = 9). Renal medullary interstitial infusion of a selective A1antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 300 pmol ⋅ kg−1 ⋅ min−1, n = 8), did not alter renal blood flows, but increased urine flow by 37% and sodium excretion by 42%. In contrast, renal medullary infusion of the selective A2 receptor blocker 3,7-dimethyl-1-propargylxanthine (DMPX; 150 pmol ⋅ kg−1 ⋅ min−1, n = 9) decreased outer medullary blood flow (OMBF) by 28%, inner medullary blood flows (IMBF) by 21%, and sodium excretion by 35%. Renal medullary interstitial infusion of adenosine produced a dose-dependent increase in OMBF, IMBF, urine flow, and sodium excretion at doses from 3 to 300 pmol ⋅ kg−1 ⋅ min−1( n = 7). These effects of adenosine were markedly attenuated by the pretreatment of DMPX, but unaltered by DPCPX. Infusion of a selective A3receptor agonist, N 6-benzyl-5′-( N-ethylcarbonxamido)adenosine (300 pmol ⋅ kg−1 ⋅ min−1, n = 6) into the renal medulla had no effect on medullary blood flows or renal function. Glomerular filtration rate and arterial pressure were not changed by medullary infusion of any drugs. Our results indicate that endogenous medullary adenosine at physiological concentrations serves to dilate medullary vessels via A2 receptors, resulting in a natriuretic response that overrides the tubular A1 receptor-mediated antinatriuretic effects.

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Leonard, Bridget L., Roger G. Evans, Michael A. Navakatikyan, and Simon C. Malpas. "Differential neural control of intrarenal blood flow." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 3 (September 1, 2000): R907—R916. http://dx.doi.org/10.1152/ajpregu.2000.279.3.r907.

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To test whether renal sympathetic nerve activity (RSNA) can differentially regulate blood flow in the renal medulla (MBF) and cortex (CBF) of pentobarbital sodium-anesthetized rabbits, we electrically stimulated the renal nerves while recording total renal blood flow (RBF), CBF, and MBF. Three stimulation sequences were applied 1) varying amplitude (0.5–8 V), 2) varying frequency (0.5–8 Hz), and 3) a modulated sinusoidal pattern of varying frequency (0.04–0.72 Hz). Increasing amplitude or frequency of stimulation progressively decreased all flow variables. RBF and CBF responded similarly, but MBF responded less. For example, 0.5-V stimulation decreased CBF by 20 ± 9%, but MBF fell by only 4 ± 6%. The amplitude of oscillations in all flow variables was progressively reduced as the frequency of sinusoidal stimulation was increased. An increased amplitude of oscillation was observed at 0.12 and 0.32 Hz in MBF and to a lesser extent RBF, but not CBF. MBF therefore appears to be less sensitive than CBF to the magnitude of RSNA, but it is more able to respond to these higher frequencies of neural stimulation.

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YOUNGELMAN, DEBBIE F., KIM U. KAHNG, BROOKE D. ROSEN, LISA S. DRESNER, and RICHARD B. WAIT. "EFFECTS OF CHRONIC CYCLOSPORINE ADMINSTRATION ON RENAL BLOOD FLOW AND INTRARENAL BLOOD FLOW DISTRIBUTION." Transplantation 51, no. 2 (February 1991): 503–8. http://dx.doi.org/10.1097/00007890-199102000-00044.

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46

Mattson, D. L., S. Lu, R. J. Roman, and A. W. Cowley. "Relationship between renal perfusion pressure and blood flow in different regions of the kidney." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 3 (March 1, 1993): R578—R583. http://dx.doi.org/10.1152/ajpregu.1993.264.3.r578.

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The present study examined the autoregulation of blood flow in different regions of the renal cortex and medulla in volume-expanded or hydropenic anesthetized rats. Blood flow was measured in the whole kidney by electromagnetic flowmetry, in the superficial cortex with implanted fibers and external probes for laser-Doppler flowmetry, and in the deep cortex and inner and outer medulla with implanted fibers for laser-Doppler flowmetry. At renal perfusion pressure > 100 mmHg, renal blood flow, superficial cortical blood flow, and deep cortical blood flow were all very well autoregulated in both volume-expanded and hydropenic rats. Inner and outer medullary blood flow were also well autoregulated in hydropenia, but blood flow in these regions was very poorly autoregulated in volume-expanded animals. As renal perfusion pressure was decreased below 100 mmHg in volume-expanded and hydropenic animals, renal blood flow, superficial and deep cortical blood flow, and inner and outer medullary blood flow all decreased. The results of these experiments demonstrate that blood flow in both the inner and outer portions of the renal medulla of the kidney is poorly autoregulated in volume-expanded rats but well autoregulated in hydropenic animals. In contrast, blood flow in all regions of the renal cortex is well autoregulated in both volume-expanded and hydropenic animals. These results suggest that changes in resistance in the postglomerular circulation of deep nephrons are responsible for the poor autoregulation of medullary blood flow in volume expansion despite well autoregulated cortical blood flow.

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Meininger, G. A., J. N. Benoit, E. Z. Ostrowska, and S. K. Muckleroy. "Splanchnic circulatory changes during development of renal hypertension." American Journal of Physiology-Gastrointestinal and Liver Physiology 253, no. 2 (August 1, 1987): G146—G154. http://dx.doi.org/10.1152/ajpgi.1987.253.2.g146.

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Total and regional splanchnic blood flows were measured with radiolabeled microspheres (15 micron) in one-kidney, one-clip renal hypertensive rats at 2, 4, and 6 wk after induction of hypertension. Arterial pressures (mean +/- SE, mmHg) for the normotensive rats (N) and age-matched hypertensive rats (H) were 110 +/- 5 and 114 +/- 6 at 2 wk, 104 +/- 4 and 148 +/- 13 at 4 wk, and 117 +/- 6 and 164 +/- 11 at 6 wk, respectively. Total splanchnic blood flow was increased in H compared with N at 4 wk but not at 2 or 6 wk. The blood flow changes among individual splanchnic organs varied in N and H. For example, at 2 and 4 wk, stomach, small intestine, large intestine, pancreas, hepatic artery, and portal venous blood flows in H were unchanged compared with N. At 6 wk, small intestinal and hepatic arterial blood flows were increased in H compared with N, and pancreatic blood flow was decreased. Vascular resistance was not different for any splanchnic organs between N and H at 2 wk, but it was elevated in H for all organs at 4 and 6 wk except for the hepatic artery. In another group of rats, the renal and superior mesenteric arteries (SMA) were instrumented with ultrasonic Doppler flow probes. Acute one-kidney, one-clip hypertension was produced by removing one kidney and mechanically reducing flow to the remaining kidney with a pneumatic occluder. After 2 h of stenosis, mean arterial pressure and SMA flow velocity was decreased by 6%.(ABSTRACT TRUNCATED AT 250 WORDS)

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Buckley, N. M., and I. D. Frasier. "Regional circulatory responses to intestinal work in developing swine." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 4 (April 1, 1990): H1119—H1125. http://dx.doi.org/10.1152/ajpheart.1990.258.4.h1119.

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Circulatory effects of intraduodenal feeding with 2 and 5% glucose were studied in 29 fasted swine (1 day to 1 mo old) anesthetized with pentobarbital. Recordings included aortic and intestinal venous pressures and intestinal, renal, and femoral blood flows. Calculations included vascular resistances, arterial and intestinal venous O2 contents, and intestinal O2 consumption. Observations were made before and at 15 and 30 min after a feeding and at end of experiments. Blood flow autoregulation was evaluated before and after feedings. Glucose induced increases in intestinal O2 consumption and blood flow at all ages, but intestinal blood flow autoregulation was enhanced only in 2 wk olds. Blood flow was redistributed to the working gut from the hindlimb, but not the kidney, at all ages. Renal blood flow autoregulation was sustained in 2-wk-old and 1-mo-old animals and became significant in 1 wk olds during intestinal hyperemia. We concluded that basic mechanisms governing blood flow redistribution from hindlimb to working gut are available at birth in swine and that maintenance of renal blood flow depends only partly on autoregulatory capability.

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49

Gross, V., A. Lippoldt, J. Bohlender, M. Bader, A. Hansson, and F. C. Luft. "Cortical and medullary hemodynamics in deoxycorticosterone acetate-salt hypertensive mice." Journal of the American Society of Nephrology 9, no. 3 (March 1998): 346–54. http://dx.doi.org/10.1681/asn.v93346.

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The effect of acutely increasing renal perfusion pressure or extracellular fluid volume on renal medullary and cortical blood flow was examined in the low-renin deoxycorticosterone acetate (DOCA)-salt hypertension model in mice. A 50-mg DOCA tablet was implanted, and 1% saline was given as drinking water for 3 wk. Medullary and cortical blood flow were determined with laser-Doppler flowmetry, and whole-kidney blood flow was measured with a transit-time ultrasound flowprobe around the renal artery. In control mice, total renal blood flow ranged from 6.3 and 7.6 ml/min per g kidney weight and in DOCA-salt mice from 4.3 and 4.7 ml/min per g kidney weight, respectively, and was minimally affected as renal perfusion pressure was increased. Renal vascular resistance increased correspondingly. During stepwise increases in renal artery pressure from 90 to 140 mmHg, medullary blood flow progressively increased in control mice to 125% of baseline values, whereas cortical blood flow did not change. In DOCA-salt mice, increasing BP from 100 to 154 mmHg had no effect on either cortical or medullary blood flow. Urine flow and sodium excretion were lower in DOCA-salt mice than in controls and increased nearly to the same extent in both groups after volume expansion with isotonic saline. Total renal blood flow increased after saline loading, more in controls than in DOCA-salt mice. Increases in medullary blood flow after saline loading were up to 122% of baseline values in controls and demonstrated a significantly steeper slope than the 110% of baseline increases in DOCA-salt mice. Cortical blood flow, however, was not different between the groups. Thus, medullary blood flow is not as tightly autoregulated as cortical blood flow in normal mice. Natriuresis with acute volume loading is facilitated by increased medullary blood flow. In DOCA-salt mice, the medullary blood flow reaction to renal perfusion pressure increases is abolished, whereas flow increases with extracellular volume expansion are diminished. These results suggest that diminished pressure-natriuresis responses in DOCA-salt mice are related to perturbed medullary blood flow.

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GROSS, VOLKMAR, WOLFGANG SCHNEIDER, WOLF-HAGEN SCHUNCK, EERO MERVAALA, and FRIEDRICH C. LUFT. "Chronic Effects of Lovastatin and Bezafibrate on Cortical and Medullary Hemodynamics in Deoxycorticosterone Acetate-Salt Hypertensive Mice." Journal of the American Society of Nephrology 10, no. 7 (July 1999): 1430–39. http://dx.doi.org/10.1681/asn.v1071430.

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Abstract. Cholesterol synthesis inhibitors and fibrates both exercise effects that could influence BP and renal function in hypertension. To test this issue, transit-time ultrasound flow probes, implanted optical fibers, and laser-Doppler flowmetry were used for measurements of total and regional renal blood flows in lovastatin (40 mg/kg body wt) and bezafibrate (50 mg/kg body wt) chronically treated deoxycorticosterone acetate (DOCA)-salt hypertensive mice. Total renal blood flow was well autoregulated between 70 and 150 mmHg (approximately 3.5 ml/min per g kidney weight in DOCA-salt mice). Both lovastatin and bezafibrate increased renal blood flow to a range between 4.7 and 5.5 ml/min per g kidney weight. In the renal perfusion pressure ranges investigated, renal vascular resistance increased in lovastin- and bezafibrate-treated DOCA-salt mice, but not as steeply as in vehicle-treated DOCA-salt mice. During a stepwise increase in renal perfusion pressure in lovastatin-treated DOCA-salt mice, medullary blood flow increased up to 130% of baseline values, which was not seen in vehicle- or bezafibrate-treated mice. After extra-cellular volume expansion with 1% saline, 1 ml over 1 min, total renal blood flow was also higher in lovastatin- or bezafibrate-treated DOCA-salt mice, whereas medullary blood flow increased more steeply in lovastatin-, compared with bezafibrate- or vehicle-treated mice. Systemic BP was significantly decreased in lovastatin-treated DOCA-salt mice compared with vehicle-treated mice. Lovastatin prevented histologic evidence for hemostasis in the medullary circulation of DOCA-salt mice. The results suggest that both lovastatin and bezafibrate diminished DOCA-salt-induced reductions in total renal blood flow. Lovastatin also abolished the perturbed medullary blood flow reactions to increased perfusion pressure or to volume expansion. Finally, lovastatin decreased systemic BP in DOCA-salt mice. These data suggest that cholesterol synthesis inhibition or fibrate treatment improve disturbed renal function in a mouse model of salt-dependent hypertension.

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Journal articles on the topic 'Renal blood flow'

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