Renal Micropuncture Techniques

2011 ◽  
Author(s):  
Heino Velazquez ◽  
Fred S. Wright
Keyword(s):  
Renal Micropuncture

Abstract 062: Regulation of Nephron Afferent Arteriole Resistance in Obesity: Role of Connecting Tubule Glomerular Feedback

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Sumit R Monu ◽  
Mani Maheshwari ◽  
Hong Wang ◽  
Ed Peterson ◽  
Oscar Carretero
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Tubuloglomerular Feedback ◽  
Afferent Arteriole ◽  
Connecting Tubule ◽  
Single Nephron ◽  
Renal Micropuncture ◽  
The Difference

In obesity, renal damage is caused by increase in renal blood flow (RBF), glomerular capillary pressure (P GC ), and single nephron glomerular filtration rate but the mechanism behind this alteration in renal hemodynamics is unclear. P GC is controlled mainly by the afferent arteriole (Af-Art) resistance. Af-Art resistance is regulated by mechanism similar to that in other arterioles and in addition, it is regulated by two intrinsic feedback mechanisms: 1) tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to an increase in sodium chloride (NaCl) in the macula densa, via sodium–potassium-2-chloride cotransporter-2 (NKCC2) and 2) connecting tubule glomerular feedback (CTGF) that causes Af-Art dilatation and is mediated by connecting tubule via epithelial sodium channel (ENaC). CTGF is blocked by the ENaC inhibitor benzamil. Attenuation of TGF reduces Af-Art resistance and allows systemic pressure to get transmitted to the glomerulus that causes glomerular barotrauma/damage. In the current study, we tested the hypothesis that TGF is attenuated in obesity and that CTGF contributes to this effect. We used Zucker obese rats (ZOR) while Zucker lean rats (ZLR) served as controls. We performed in-vivo renal micropuncture of individual rat nephrons while measuring stop-flow pressure (P SF ), an index of P GC. TGF response was measured as a decrease in P SF induced by changing the rate of late proximal perfusion from 0 to 40nl/min in stepwise manner.CTGF was calculated as the difference of P SF value between vehicle and benzamil treatment, at each perfusion rate. Maximal TGF response was significantly less in ZOR (6.16 ± 0.52 mmHg) when compared to the ZLR (8.35 ± 1.00mmHg), p<0.05 , indicating TGF resetting in the ZOR. CTGF was significantly higher in ZOR (6.33±1.95 mmHg) when compared to ZLR (1.38±0.89 mmHg), p<0.05 . When CTGF was inhibited with the ENaC blocker Benzamil (1μM), maximum P SF decrease was 12.30±1.72 mmHg in ZOR and 10.60 ± 1.73 mmHg in ZLR, indicating that blockade of CTGF restored TGF response in ZOR. These observations led us to conclude that TGF is reset in ZOR and that enhanced CTGF contributes to this effect. Increase in CTGF may explain higher renal blood flow, increased P GC and higher glomerular damage in obesity.

Glomerular dynamics and salt balance in pregnant rats with renal hypertension

1989 ◽  
Vol 256 (4) ◽  
pp. F728-F734 ◽  
Author(s):  
A. Dal Canton ◽  
M. Altomonte ◽  
G. Conte ◽  
C. Esposito ◽  
G. Fuiano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Hypertension ◽  
Chronic Hypertension ◽  
Marked Rise ◽  
Pregnant Rats ◽  
Hypertension In Pregnancy ◽  
Single Nephron ◽  
Renal Micropuncture ◽  
Glomerular Hemodynamics ◽  
Goldblatt Hypertension

These studies were aimed at investigating whether chronic hypertension in pregnancy causes changes both in salt excretion (NaE) and in glomerular hemodynamics. Metabolic and renal micropuncture studies were performed in pregnant (P) and Virgin (V) Munich-Wistar rats with normal blood pressure (N) and two-kidney Goldblatt hypertension (H). Mean NaE was higher in PN than VN (2.7 vs. 1.7 meq/day, P less than 0.01). Hypertension raised NaE both in P and V rats: in P and V rats with "benign" hypertension (blood pressure less than 180 mmHg) NaE averaged 3.2 and 2.6 meq/day, respectively (P less than 0.05); mean NaE was 5.9 and 3.8 meq/day, respectively (P less than 0.01), in P and V rats with "malignant" hypertension (blood pressure greater than or equal to 180 mmHg). Afferent arteriole resistance (Ra) averaged 1.73 and 3.50 10 dyn.s-1.cm5 in PN and VN, respectively (P less than 0.01). Hypertension raised Ra in V, but not in P rats (4.47 vs. 2.14 10 dyn.s-1.cm5, P less than 0.01). Thus glomerular plasma flow, glomerular capillary hydrostatic pressure, and single-nephron glomerular filtration rate were markedly higher in PH than VH rats: in PH rats single-nephron filtration fraction was significantly lower than in VH. These results show that in PH rats a marked rise in NaE is associated with glomerular vasodilation.

Renal tubular sites of increased phosphate transport and NaPi-2 expression in the juvenile rat

2001 ◽  
Vol 280 (5) ◽  
pp. R1524-R1533 ◽  
Author(s):  
Craig Woda ◽  
Susan E. Mulroney ◽  
Nabil Halaihel ◽  
Lijun Sun ◽  
Paul V. Wilson ◽  
...  
Keyword(s):  
Brush Border Membrane ◽  
Immunofluorescence Microscopy ◽  
Phosphate Transport ◽  
Adult Rats ◽  
Juvenile Rats ◽  
Juvenile Animal ◽  
Male Wistar Rats ◽  
Proximal Tubular ◽  
Renal Micropuncture ◽  
Renal Tubular

To determine the tubular sites and mechanisms involved in enhanced renal phosphate (Pi) reabsorption seen in the juvenile animal, renal micropuncture experiments were performed in acutely thyroparathyroidectomized adult (>14 wk old) and juvenile (4 wk old) male Wistar rats fed either a normal Pi diet (NPD, 0.6% Pi) or low Pi diet (0.07% Pi) for 2 days, in the presence and absence of parathyroid hormone (PTH). Pi reabsorption was greater in proximal convoluted (PCT) and straight tubules (PST) of the juvenile compared with adult rats fed NPD, whether or not PTH was present. These findings were consistent with a greater Piuptake in brush-border membrane (BBM) vesicles from both superficial (SC) and outer juxtamedullary (JMC) cortices of juvenile animals. Western blot analysis revealed a 2- and 1.8-fold higher amount of NaPi-2 protein in the SC and JMC, respectively, in juvenile rats. Immunofluorescence microscopy also indicated that NaPi-2 protein expression was present in the proximal tubule (PT) BBM to a greater extent in juvenile rats. Dietary Pi restriction in juvenile rats resulted in a significant increase in Pi reabsorption in the PCT and PST segments. NaPi-2 expression in the PT BBM was also increased, as was the expression of intracellular NaPi-2 protein. These studies indicate that Pi reabsorption in both the PCT and PST segments of the renal tubule contributes to the attenuated response to PTH in the normal juvenile animal. In addition, dietary Pi restriction in the juvenile rat upregulates BBM NaPi-2 expression, which is associated with a further increase in proximal tubular Pi reabsorption.

Single nephron function during prolactin-induced pseudopregnancy in the rat

1985 ◽  
Vol 107 (1) ◽  
pp. 127-131 ◽  
Author(s):  
J. Walker ◽  
H. O. Garland
Keyword(s):  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Treated Group ◽  
Female Rats ◽  
Fluid Reabsorption ◽  
Single Nephron ◽  
Renal Changes ◽  
Proximal Tubular ◽  
Renal Micropuncture

ABSTRACT Whole kidney and renal micropuncture techniques were used to investigate the effects of chronic prolactin treatment on kidney function in anaesthetized female rats. At the whole kidney level, glomerular filtration rate (GFR) and fluid reabsorption were both significantly (P<0·02) increased in the hormone-treated group. At the single nephron level, GFR and proximal fluid reabsorption were also increased (P<0·05) by prolactin treatment. Fractional reabsorption was also enhanced at the proximal tubular level in hormone-treated animals. Such changes in renal function are similar to those seen in rat pregnancy and cervically stimulated pseudopregnancy. Since circulating prolactin concentrations are increased in both reproductive states, the hormone may play an important role in establishing the characteristic renal changes seen therein. J. Endocr. (1985) 107, 127–131

scholarly journals Genetic heterogeneity and differences in glomerular hemodynamics between inbred colonies of Munich-Wistar rats.

1992 ◽  
Vol 3 (1) ◽  
pp. 66-72
Author(s):  
F J Fenoy ◽  
E St Lezin ◽  
T W Kurtz ◽  
R J Roman
Keyword(s):  
Capillary Pressure ◽  
Genetic Heterogeneity ◽  
Wistar Rats ◽  
Inbred Strains ◽  
The United States ◽  
Dna Fingerprint ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure ◽  
Renal Micropuncture ◽  
Glomerular Hemodynamics

DNA fingerprint analysis and renal micropuncture studies were performed in Munich-Wistar rats purchased from Harlan Industries and Simonsen Laboratories to determine whether these rats are genetically heterogeneous and exhibit differences in glomerular hemodynamics. RBF and GFR were similar in rats from both colonies. Glomerular capillary pressure was lower in rats from the Harlan colony (46 +/- 2 mm Hg) than in those from the Simonsen colony (56 +/- 2 mm Hg). The low glomerular capillary pressure in the Harlan rats was primarily due to a lower postglomerular vascular resistance. The estimated whole-kidney ultrafiltration coefficient (Kf) was significantly greater in the rats obtained from the Harlan colony than in those obtained from the Simonsen colony (0.12 +/- 0.03 versus 0.05 +/- 0.01 mL/min/g kidney wt/mm Hg). The DNA fingerprints of the Simonsen rats were different from those of the Harlan rats. These results provide evidence of physiologic and genetic heterogeneity between commercially available inbred strains of Munich-Wistar rats in the United States and suggest that comparison of results with Munich-Wistar rats from different sources may be more difficult than previously recognized.

Glomerulotubular balance, dietary protein, and the renal response to glycine in diabetic rats

2002 ◽  
Vol 282 (4) ◽  
pp. R1096-R1103 ◽  
Author(s):  
Larry A. Slomowitz ◽  
Aihua Deng ◽  
John S. Hammes ◽  
Francis Gabbai ◽  
Scott C. Thomson
Keyword(s):  
Dietary Protein ◽  
Distal Tubule ◽  
Diabetic Rats ◽  
Tubular Reabsorption ◽  
Protein Restriction ◽  
Tubuloglomerular Feedback ◽  
Vascular Effect ◽  
Dietary Protein Restriction ◽  
Single Nephron ◽  
Renal Micropuncture

The glomerular filtration rate (GFR) normally increases during glycine infusion, which is a test of “renal reserve.” Renal reserve is absent in diabetes mellitus. GFR increases after protein feeding because of increased tubular reabsorption, which reduces the signal for tubuloglomerular feedback (TGF). Dietary protein restriction normalizes some aspects of glomerular function in diabetes. Renal micropuncture was performed in rats 4–5 wk after diabetes was induced by streptozotocin to determine whether renal reserve is lost as a result of altered tubular function and activation of TGF, whether 10 days of dietary protein restriction could restore renal reserve, and whether this results from effects of glycine on the tubule. TGF activation was determined by locating single-nephron GFR (SNGFR) in the early distal tubule along the TGF curve. The TGF signal was determined from the ionic content of the early distal tubule. In nondiabetic rats, SNGFR in the early distal tubule increased during glycine infusion because of primary vasodilation augmented by increased tubular reabsorption, which stabilized the TGF signal. In diabetic rats, glycine reduced reabsorption, thereby activating TGF, which was largely responsible for the lack of renal reserve. In protein-restricted diabetic rats, the tubular response to glycine remained abnormal, but renal reserve was restored by a vascular mechanism. Glycine affects GFR directly and via the tubule. In diabetes, reduced tubular reabsorption dominates. In low-protein diabetes, the vascular effect is enhanced and overrides the effect of reduced tubular reabsorption.

Head-down tilt and restraint on renal function and glomerular dynamics in the rat

1987 ◽  
Vol 63 (2) ◽  
pp. 505-513 ◽  
Author(s):  
B. J. Tucker ◽  
C. A. Mundy ◽  
M. G. Ziegler ◽  
C. Baylis ◽  
R. C. Blantz
Keyword(s):  
Renal Function ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Conscious Rats ◽  
Single Nephron ◽  
Volume Measurements ◽  
Renal Micropuncture ◽  
Glomerular Ultrafiltration

A model utilizing 25 degree head-down tilt (HDT) and incorporated with chronic catheterization and renal micropuncture techniques in rats was employed to study alterations in renal function induced by HDT. Renal function and extracellular volume measurements were performed after 24 h, 4 days, and 7 days of HDT in conscious rats and compared with their own control measurements and to nontilted but similarly restrained rats. After 24 h HDT, glomerular filtration rate (GFR) increased 19 +/- 8% and renal plasma flow (RPF) increased 18 +/- 8% with increases in urine flow rate, Na+, and K+ excretion in conscious rats. These increases after 24 h were associated with an increase in extracellular volume of 16 +/- 3% (P less than 0.01). In the nontilted controls, there was a decrease in extracellular volume after 24 h of suspension. After 7 days of HDT, GFR was decreased by 7 +/- 1% (P less than 0.01), but RPF and extracellular fluid volume were not different from control values. However, RPF and GFR increased in the nontilted rats after 7 days. After 7 days of HDT renal micropuncture studies demonstrated that single-nephron filtration rate was also decreased from 43 +/- 2 to 31 +/- 3 nl/min (P less than 0.05) due solely to reductions in the glomerular ultrafiltration coefficient (0.11 +/- 0.01 to 0.07 +/- 0.01 nl.s-1 X mmHg-1, P less than 0.05). There was a dissociation between GFR and water and Na+ excretion at days 4 and 7 of HDT not observed in the nontilt restraint controls.

scholarly journals Mouse Models and the Urinary Concentrating Mechanism in the New Millennium

2007 ◽  
Vol 87 (4) ◽  
pp. 1083-1112 ◽  
Author(s):  
Robert A. Fenton ◽  
Mark A. Knepper
Keyword(s):  
Water Conservation ◽  
Collecting Duct ◽  
Tubuloglomerular Feedback ◽  
Water Excretion ◽  
Renal Transporters ◽  
Concentrating Mechanism ◽  
New Information ◽  
Renal Micropuncture ◽  
Key Questions

Our understanding of urinary concentrating and diluting mechanisms at the end of the 20th century was based largely on data from renal micropuncture studies, isolated perfused tubule studies, tissue analysis studies and anatomical studies, combined with mathematical modeling. Despite extensive data, several key questions remained to be answered. With the advent of the 21st century, a new approach, transgenic and knockout mouse technology, is providing critical new information about urinary concentrating processes. The central goal of this review is to summarize findings in transgenic and knockout mice pertinent to our understanding of the urinary concentrating mechanism, focusing chiefly on mice in which expression of specific renal transporters or receptors has been deleted. These include the major renal water channels (aquaporins), urea transporters, ion transporters and channels (NHE3, NKCC2, NCC, ENaC, ROMK, ClC-K1), G protein-coupled receptors (type 2 vasopressin receptor, prostaglandin receptors, endothelin receptors, angiotensin II receptors), and signaling molecules. These studies shed new light on several key questions concerning the urinary concentrating mechanism including: 1) elucidation of the role of water absorption from the descending limb of Henle in countercurrent multiplication, 2) an evaluation of the feasibility of the passive model of Kokko-Rector and Stephenson, 3) explication of the role of inner medullary collecting duct urea transport in water conservation, 4) an evaluation of the role of tubuloglomerular feedback in maintenance of appropriate distal delivery rates for effective regulation of urinary water excretion, and 5) elucidation of the importance of water reabsorption in the connecting tubule versus the collecting duct for maintenance of water balance.

scholarly journals Morphologic identification of microperfused-fixed single nephrons during renal micropuncture

1974 ◽  
Vol 5 (4) ◽  
pp. 300-302 ◽  
Author(s):  
Giorgio Olivetti ◽  
Antonio Dal Canton ◽  
Vittorio E. Andreucci
Keyword(s):  
Renal Micropuncture
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