scholarly journals Renal autoregulation dynamics monitored across the renal surface

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Christopher Scully ◽  
Nicholas Mitrou ◽  
Branko Braam ◽  
William Cupples ◽  
Ki Chon
Keyword(s):  
Renal Autoregulation

A nonlinear property of the renal autoregulation

1972 ◽  
Vol 28 (5) ◽  
pp. 527-528 ◽  
Author(s):  
Th. Kenner ◽  
K. Ono ◽  
J. Rubenstein
Keyword(s):  
Nonlinear Property ◽  
Renal Autoregulation

KV7.1 channel blockade inhibits neonatal renal autoregulation triggered by a step decrease in arterial pressure

2022 ◽  
Author(s):  
Dieniffer Peixoto-Neves ◽  
Praghalathan Kanthakumar ◽  
Jeremiah M Afolabi ◽  
Hitesh Soni ◽  
Randal K Buddington ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Functional Expression ◽  
Renal Autoregulation ◽  
Neonatal Pigs ◽  
Vascular Smcs ◽  
Neonatal Pig ◽  
Kidney Maturation ◽  
Renal Vascular ◽  
Renal Vascular Tone ◽  
Fetal Pig

KV7, the voltage-gated potassium channels encoded by KCNQ genes, mediate heterogeneous vascular responses in adult rodents. Postnatal changes in the functional expression of KV7 channels have been reported in rodent saphenous arteries, but their physiological function in the neonatal renal vascular bed is unclear. Here, we report that, unlike adult pigs, only KCNQ1 (KV7.1) out of the five members of KCNQ genes was detected in neonatal pig renal microvessels. KCNQ1 is present in fetal pig kidneys as early as day 50 of gestation, and the level of expression remains the same up to postnatal day 21. Activation of the renal vascular smooth muscle cell (SMC) KV7.1 stimulated whole-cell currents, inhibited by HMR1556 (HMR), a selective KV7.1 blocker. HMR did not change the steady-state diameter of isolated renal microvessels. Similarly, intrarenal artery infusion of HMR did not alter the mean arterial pressure (MAP), renal blood flow (RBF), and renal vascular resistance (RVR) in the pigs. An approximately 20 mmHg reduction in the MAP evoked effective autoregulation of the RBF, which HMR inhibited. We conclude that 1) The expression of KCNQ isoforms in porcine renal microvessels is dependent on kidney maturation, 2) KV7.1 is functionally expressed in neonatal pig renal vascular SMCs, 3) a decrease in arterial pressure up to 20 mmHg induces renal autoregulation in neonatal pigs, and 4) SMC KV7.1 does not control basal renal vascular tone but contributes to neonatal renal autoregulation triggered by a step decrease in arterial pressure.

Parametric and Nonparametric Nonlinear Modeling of Renal Autoregulation Dynamics

1994 ◽  
pp. 195-210 ◽  
Author(s):  
Ki H. Chon ◽  
Niels H. Holstein-Rathlou ◽  
Donald J. Marsh ◽  
Vasilis Z. Marmarelis
Keyword(s):  
Nonlinear Modeling ◽  
Renal Autoregulation

Direct measurement of renal medullary blood flow in the dog

1994 ◽  
Vol 267 (1) ◽  
pp. R253-R259 ◽  
Author(s):  
D. M. Strick ◽  
M. J. Fiksen-Olsen ◽  
J. C. Lockhart ◽  
R. J. Roman ◽  
J. C. Romero
Keyword(s):  
Blood Flow ◽  
Pressure Range ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Flow Probe ◽  
Renal Autoregulation ◽  
Renal Perfusion Pressure ◽  
Medullary Blood Flow ◽  
Renal Medullary Blood Flow ◽  
Doppler Flowmeter

We studied the responses of total renal blood flow (RBF) and renal medullary blood flow (RMBF) to changes in renal perfusion pressure (RPP) within and below the range of renal autoregulation in the anesthetized dog (n = 7). To measure RMBF, we developed a technique in which the medulla is exposed by excising a section of infarcted cortex and a multiple optical fiber flow probe, connected to a laser-Doppler flowmeter, is placed on the medulla. At the baseline RPP of 120 +/- 1 mmHg, RBF was 2.58 +/- 0.33 ml.min-1.g perfused kidney wt-1, and RMBF was 222 +/- 45 perfusion units. RPP was then decreased in consecutive 20-mmHg steps to 39 +/- 1 mmHg. At 80 +/- 1 mmHg, RBF remained at 89 +/- 4% of the baseline value; however, RMBF had decreased significantly (P < 0.05) to 73 +/- 4% of its baseline value. The efficiency of autoregulation of RBF and of RMBF within the RPP range of 120 to 80 mmHg was determined by calculating an autoregulatory index (AI) for each parameter using the formula AI = (%delta blood flow)/(%delta RPP). An AI of 0 indicates perfect autoregulation, and an index of 1 indicates a system with a fixed resistance. The AI for RBF averaged 0.33 +/- 0.12 over this pressure range and showed a significantly greater (P < 0.05) autoregulatory ability than did the RMBF (0.82 +/- 0.13). Decreasing perfusion pressure < 80 mmHg produced significant decreases in both RBF and RMBF.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Anti‐inflammatory treatment improves renal autoregulation in DOCA‐salt hypertensive rats

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Zhengrong Guan ◽  
Anthony K Cook ◽  
Edward W Inscho
Keyword(s):  
Hypertensive Rats ◽  
Renal Autoregulation ◽  
Anti Inflammatory

scholarly journals Consequences of the laser speckle imaging computation method on analysis of renal autoregulation dynamics

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Christopher Scully ◽  
Nicholas Mitrou ◽  
Jennifer Waring ◽  
Branko Braam ◽  
William A. Cupples ◽  
...  
Keyword(s):  
Laser Speckle ◽  
Computation Method ◽  
Laser Speckle Imaging ◽  
Speckle Imaging ◽  
Renal Autoregulation

scholarly journals Renal Autoregulation in Health and Disease

2015 ◽  
Vol 95 (2) ◽  
pp. 405-511 ◽  
Author(s):  
Mattias Carlström ◽  
Christopher S. Wilcox ◽  
William J. Arendshorst
Keyword(s):  
Intracellular Signaling ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Tubuloglomerular Feedback ◽  
Free Calcium ◽  
Myogenic Response ◽  
Renal Vasculature ◽  
Renal Autoregulation ◽  
Positive Balance ◽  
Health And Disease

Intrarenal autoregulatory mechanisms maintain renal blood flow (RBF) and glomerular filtration rate (GFR) independent of renal perfusion pressure (RPP) over a defined range (80–180 mmHg). Such autoregulation is mediated largely by the myogenic and the macula densa-tubuloglomerular feedback (MD-TGF) responses that regulate preglomerular vasomotor tone primarily of the afferent arteriole. Differences in response times allow separation of these mechanisms in the time and frequency domains. Mechanotransduction initiating the myogenic response requires a sensing mechanism activated by stretch of vascular smooth muscle cells (VSMCs) and coupled to intracellular signaling pathways eliciting plasma membrane depolarization and a rise in cytosolic free calcium concentration ([Ca2+]i). Proposed mechanosensors include epithelial sodium channels (ENaC), integrins, and/or transient receptor potential (TRP) channels. Increased [Ca2+]ioccurs predominantly by Ca2+influx through L-type voltage-operated Ca2+channels (VOCC). Increased [Ca2+]iactivates inositol trisphosphate receptors (IP3R) and ryanodine receptors (RyR) to mobilize Ca2+from sarcoplasmic reticular stores. Myogenic vasoconstriction is sustained by increased Ca2+sensitivity, mediated by protein kinase C and Rho/Rho-kinase that favors a positive balance between myosin light-chain kinase and phosphatase. Increased RPP activates MD-TGF by transducing a signal of epithelial MD salt reabsorption to adjust afferent arteriolar vasoconstriction. A combination of vascular and tubular mechanisms, novel to the kidney, provides for high autoregulatory efficiency that maintains RBF and GFR, stabilizes sodium excretion, and buffers transmission of RPP to sensitive glomerular capillaries, thereby protecting against hypertensive barotrauma. A unique aspect of the myogenic response in the renal vasculature is modulation of its strength and speed by the MD-TGF and by a connecting tubule glomerular feedback (CT-GF) mechanism. Reactive oxygen species and nitric oxide are modulators of myogenic and MD-TGF mechanisms. Attenuated renal autoregulation contributes to renal damage in many, but not all, models of renal, diabetic, and hypertensive diseases. This review provides a summary of our current knowledge regarding underlying mechanisms enabling renal autoregulation in health and disease and methods used for its study.

scholarly journals 20-HETE and the kidney: resolution of old problems and new beginnings

1999 ◽  
Vol 277 (3) ◽  
pp. R607-R623 ◽  
Author(s):  
John C. McGiff ◽  
John Quilley
Keyword(s):  
Thick Ascending Limb ◽  
Renal Circulation ◽  
Large Measure ◽  
Water Excretion ◽  
Renal Autoregulation ◽  
Blood Pressure Homeostasis ◽  
Calcium Activated Potassium Channels ◽  
New Beginnings ◽  
Cytochrome P 450 ◽  
Preglomerular Arterioles

The protean properties of 20-hydroxyeicosatetraenoic acid (HETE), vasoactivity, mitogenicity, and modulation of transport in key nephron segments, serve as the basis for the essential roles of 20-HETE in the regulation of the renal circulation and electrolyte excretion and as a second messenger for endothelin-1 and mediator of selective renal effects of ANG II. Renal autoregulation and tubular glomerular feedback are mediated by 20-HETE through constriction of preglomerular arterioles, responses that are maintained by 20-HETE inhibition of calcium-activated potassium channels. 20-HETE modulates ion transport in the proximal tubules and the thick ascending limb by affecting the activities of Na+-K+-ATPase and the Na+-K+-2Cl−cotransporter, respectively. The range and diversity of activity of 20-HETE derives in large measure from COX-dependent transformation of 20-HETE to products affecting vasomotion and salt and water excretion. Nitric oxide (NO) exerts a negative modulatory effect on 20-HETE formation; inhibition of NO synthesis produces marked perturbation of renal function resulting from increased 20-HETE production. 20-HETE is an essential component of interactions involving several hormonal systems that have central roles in blood pressure homeostasis, including angiotensins, endothelins, NO, and cytokines. 20-HETE is the preeminent renal eicosanoid, overshadowing PGE2 and PGI2. This review is intended to provide evidence for the physiological roles for cytochrome P-450-derived eicosanoids, particularly 20-HETE, and seeks to extend this knowledge to a conceptual framework for overall cardiovascular function.

scholarly journals Renal autoregulation in medical therapy of renovascular hypertension

2010 ◽  
Vol 6 ◽  
pp. 912-918 ◽  
Author(s):  
Arkadiusz Lubas ◽  
Grzegorz Żelichowski ◽  
Agnieszka Próchnicka ◽  
Magdalena Wiśniewska ◽  
Zofia Wańkowicz
Keyword(s):  
Renovascular Hypertension ◽  
Medical Therapy ◽  
Renal Autoregulation

Juxtaglomerular interstitial hypertonicity in Amphiuma: tubular origin-TGF signal

1988 ◽  
Vol 254 (3) ◽  
pp. F445-F449 ◽  
Author(s):  
B. E. Persson ◽  
T. Sakai ◽  
D. J. Marsh
Keyword(s):  
Feedback Inhibition ◽  
Distal Tubule ◽  
Juxtaglomerular Apparatus ◽  
Nacl Transport ◽  
Renal Autoregulation ◽  
Rate Dependent ◽  
Single Nephron ◽  
Tubular Flow ◽  
Renal Vascular ◽  
Vascular Autoregulation

One of the mechanisms mediating renal vascular autoregulation in mammals senses tubular flow rate-dependent changes in luminal NaCl concentrations and signals renal arterioles to change diameter. A similar mechanism operates in the salamander, Amphiuma means. To trace the signal, we measured chloride activity in juxtaglomerular interstitial spaces in Amphiuma during perfusion of the early distal tubule belonging to the same nephron. Interstitial Cl- activity exceeded systemic levels and increased when perfusion rate in the adjacent early distal tubule was increased, reaching values more than five times isotonic. Bumetanide, which inhibits NaCl transport by the early distal tubule, eliminated the hypertonicity. Regions of the interstitial space not a part of the juxtaglomerular apparatus (JGA) were not hypertonic. The Cl- concentration was 80% greater than isotonic in the JGA of nephrons studied under free-flow conditions. Single-nephron blood flow, measured by counting the flux of erythrocytes labeled with a fluorescent molecule, showed typical feedback inhibition with maximum sensitivity to the same rates of tubular perfusion that caused the maximum change in JGA interstitial hypertonicity. Juxtaglomerular interstitial hypertonicity could be an important part of the signal for renal autoregulation.

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