Renin measurement in blood collected from the efferent arteriole of the kidney of the rat

1975 ◽  
Vol 356 (3) ◽  
pp. 277-286 ◽  
Author(s):  
C. I. Johnston ◽  
P. G. Matthews ◽  
J. M. Davis ◽  
T. Morgan
Keyword(s):  
Efferent Arteriole

Morphometric analysis of the actions of angiotensin II on renal arterioles and glomeruli

1992 ◽  
Vol 262 (3) ◽  
pp. F367-F372 ◽  
Author(s):  
K. M. Denton ◽  
P. A. Fennessy ◽  
D. Alcorn ◽  
W. P. Anderson
Keyword(s):  
Electron Microscopy ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Morphometric Analysis ◽  
Unit Length ◽  
Average Difference ◽  
Outer Cortex ◽  
Efferent Arteriole ◽  
Transmission Electron ◽  
The Right

To study the effects of angiotensin II on afferent and efferent arteriole diameters and on intraglomerular dimensions, angiotensin II (20 ng.kg-1.min-1) or saline vehicle was infused intravenously for 20 min into anesthetized rabbits pretreated with enalapril. Both kidneys were perfusion fixed (glutaraldehyde), and vascular casts were made of the right kidneys using methacrylate. Morphometric analysis of the left kidneys using transmission electron microscopy revealed no significant effects of angiotensin II within the glomerulus, including the degree of mesangial contraction. The diameters of the afferent and efferent arteriole casts from the right kidneys were measured at 20, 50, and 75 microns from the glomerulus by scanning electron microscopy. In the outer cortex the mean diameters of the afferent and efferent arterioles were 14.1 +/- 0.8 and 9.7 +/- 0.5 microns, respectively, in the angiotensin II-infused rabbits, significantly less than in the control (vehicle) rabbits, 17.0 +/- 0.7 microns (P less than 0.001) and 10.7 +/- 0.4 microns (P less than 0.005), respectively. Calculation of the relative changes in vascular resistance, however, indicated that the effects of angiotensin II on efferent arteriole resistance (average difference 2.4 +/- 1.2 units/microns) were significantly greater per unit length than the effects on afferent arteriole resistance (average difference 0.9 +/- 0.3 units/microns). Thus infused angiotensin II caused greater reduction in afferent arteriolar diameter than in efferent, but the calculated increase in vascular resistance per micron was greater in efferent vessels due to their smaller resting diameter.

Renal microvascular effects of endothelin

1990 ◽  
Vol 259 (2) ◽  
pp. F217-F221 ◽  
Author(s):  
R. M. Edwards ◽  
W. Trizna ◽  
E. H. Ohlstein
Keyword(s):  
Response Curve ◽  
Contractile Response ◽  
Maximum Response ◽  
Lumen Diameter ◽  
Rabbit Kidney ◽  
Significant Shift ◽  
Efferent Arteriole ◽  
Endothelin 1 ◽  
Afferent Arterioles ◽  
Concentration Response Curve

The effects of endothelin 1, 2, and 3 (ET-1, -2, -3) on lumen diameter of individual afferent and efferent arterioles dissected from rabbit kidney were examined. ET-1 produced concentration-dependent and long-lasting decreases in lumen diameter in both arterioles. The 50% maximum response (EC50) values were 1.4 +/- 0.41 and 0.9 +/- 0.65 nM for afferent and efferent arterioles, respectively. In afferent arterioles, ET-2 produced decreases in lumen diameter (EC50 = 3.3 +/- 1.75 nM) that were indistinguishable from ET-1. However, ET-3 was considerably less potent (EC50 = 21.9 +/- 6.0 nM, P less than 0.05) than ET-1 or ET-2. Similar results were obtained in the efferent arteriole in which the EC50 for ET-2 (0.25 +/- 0.1 nM) was similar to ET-1, but ET-3 was significantly less potent (EC50 = 2.6 +/- 0.4 nM, P less than 0.05). Nicardipine (0.01-1 microM) produced concentration-dependent shifts in the ET-1 concentration-response curve in afferent arterioles. Verapamil (1 microM) also caused a significant shift in the ET-1 response curve. The contractile response to ET-1 was significantly more sensitive to nicardipine than was the response to norepinephrine. In contrast, the response of efferent arterioles to ET-1 and norepinephrine was unaffected by nicardipine or verapamil. The results demonstrate that ETs are potent vasoconstrictors of both the pre- and postglomerular microvasculature and may play a role in the regulation of renal hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of angiotensin II on regional afferent and efferent arteriole dimensions and the glomerular pole

2000 ◽  
Vol 279 (2) ◽  
pp. R629-R638 ◽  
Author(s):  
Kate M. Denton ◽  
Warwick P. Anderson ◽  
Raja Sinniah
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Capillary Pressure ◽  
Ang Ii ◽  
Similar Extent ◽  
Outer Cortex ◽  
Efferent Arteriole ◽  
Vascular Casting ◽  
Cortical Regions ◽  
Inner Cortex

The diversity of renal arteriole diameters in different cortical regions has important consequences for control of glomerular capillary pressure. We examined whether intrarenal angiotensin II (ANG II; 0.1, 1, or 5 ng · kg−1 · min−1) in anesthetized rabbits acts preferentially on pre- or postglomerular vessels using vascular casting. ANG II produced dose-related reductions in afferent and efferent diameters in the outer, mid, and inner cortex, without effecting arterial pressure. Afferent diameter decreased more than efferent in the outer and mid cortex ( P < 0.05) but by a similar extent in juxtamedullary nephrons ( P = 0.58). Calculated efferent resistance increased more than afferent, especially in the outer cortex (127 vs. 24 units; 5 ng · kg−1 · min−1 ANG II). ANG II produced significant dose-related increases in the distance between the arterioles at the entrance to the glomerular pole in all regions. Thus afferent diameter decreased more in response to ANG II, but efferent resistance rose more due to smaller resting luminal dimensions. The results also indicate that glomerular pole dimensions change in response to ANG II.

scholarly journals P0089KEAP1/NRF2 PATHWAY REGULATES GFR BY INCREASING THE GLOMERULAR EFFECTIVE AREA WITHOUT AFFECTING THE AFFERENT/EFFERENT ARTERIOLE RATIO

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
KENGO KIDOKORO ◽  
Yoshihisa Wada ◽  
Megumi Kondo ◽  
Atsuyuki Tokuyama ◽  
Seiji Itano ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Kidney Disease ◽  
Mesangial Cells ◽  
Calcium Influx ◽  
Imaging Techniques ◽  
Glomerular Permeability ◽  
Antioxidant Genes ◽  
Efferent Arteriole ◽  
Nrf2 Pathway ◽  
Nrf2 Activator

Abstract Background and Aims The Keap1/Nrf2 pathway regulates the expression of a series of cytoprotective, anti-inflammatory and antioxidant genes. The Nrf2 activator, bardoxolone methyl (BARD), has consistently increased estimated GFR (eGFR) in clinical studies in patients with chronic kidney disease. BARD demonstrated improvement of renal function assessed by inulin clearance, the clinical gold standard for measuring GFR, in diabetic kidney disease patients. These findings suggest the Keap1/Nrf2 system is deeply involved in the regulatory mechanisms of GFR. However, the precise mechanisms are not fully elucidated. We pharmacologically and genetically investigated the mechanisms of GFR regulation by Keap1/Nrf2 system using in vivo multiphoton microscope (MPM) imaging techniques. Method C57BL/6 (Cont), Nrf2 knockout (Nrf2-KO), and Nrf2-activated Keap1-knockdown mice (Keap1-KD) were used. The mice were treated the synthetic triterpenoid RTA dh404 (10 mg/kg/day by gavage) which is a Nrf2 activator for rodents, for a week. We successfully developed the technique to evaluate single-nephron GFR (SNGFR) using MPM (Circulation 2019). The glomerular hemodynamics, diameter of the afferent/efferent arterioles and glomerular permeability were also evaluated. The calcium influx into cells in response to ATP and angiotensin II stimulation and the effect on [Ca2+]i by RTAdh404 were evaluated using Fluo 4 and Fura red in cultured mesangial cells and podocytes. Production of reactive oxygen species and nitric oxide (NO) availability were assessed by fluorescent method using CellROX® Deep Red and diaminofluorescein-FM diacetate (DAF-FM DA) upon the exposure to these stimuli. Results SNGFR in Keap1-KD mice was significantly higher than in the control (9.13±0.55 vs 4.40±0.39 nl/min, Figure 1). RTA dh404 increased SNGFR in the control but not in the Nrf2-KO mice (6.00±0.40 vs 4.66±0.35 nl/min, Figure 1). There was no significant change in the ratio of the glomerular afferent/efferent arteriole diameter in all groups. RTA dh404 treatment increased glomerular volume but did not affect the glomerular permeability of albumin and 40kd-dextran. RTA dh404-treatment inhibited calcium influx into cultured podocytes and mesangial cells induced by angiotensin II or ATP, thereby affecting contractile responses. Oxidative stress and NO-bioavailablity were also ameliorated with RTA dh404. Conclusion The Keap1/Nrf2 pathway plays a pivotal role in controlling GFR and presumably underlies the effect of BARD on GFR in patients.

scholarly journals Influence of Ca2+-activated K+ channels on rat renal arteriolar responses to depolarizing agonists

2001 ◽  
Vol 280 (4) ◽  
pp. F583-F591 ◽  
Author(s):  
Rachel W. Fallet ◽  
Joseph P. Bast ◽  
Keiji Fujiwara ◽  
Naohito Ishii ◽  
Steven C. Sansom ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Arginine Vasopressin ◽  
Ang Ii ◽  
Channel Blockade ◽  
Experimental Conditions ◽  
Efferent Arteriole ◽  
K Channels ◽  
Channel Opener ◽  
Arteriolar Diameter ◽  
Channel Agonist

Experiments were performed to evaluate the hypothesis that opening of Ca2+-activated K+ channels (BKCachannels) promotes juxtamedullary arteriolar dilation and curtails constrictor responses to depolarizing agonists. Under baseline conditions, afferent and efferent arteriolar lumen diameters averaged 23.4 ± 0.9 ( n = 36) and 22.8 ± 1.1 ( n= 13) μm, respectively. The synthetic BKCa channel opener NS-1619 evoked concentration-dependent afferent arteriolar dilation. BKCa channel blockade (1 mM tetraethylammonium; TEA) decreased afferent diameter by 15 ± 3% and prevented the dilator response to 30 μM NS-1619. ANG II (10 nM) decreased afferent arteriolar diameter by 44 ± 4%, a response that was reduced by 30% during NS-1619 treatment; however, TEA failed to alter afferent constrictor responses to either ANG II or arginine vasopressin. Neither NS-1619 nor TEA altered agonist-induced constriction of the efferent arteriole. Thus, although the BKCa channel agonist was able to curtail afferent (but not efferent) arteriolar constrictor responses to ANG II, BKCa channel blockade did not allow exaggerated agonist-induced arteriolar constriction. These observations suggest that the BKCa channels evident in afferent arteriolar smooth muscle do not provide a prominent physiological brake on agonist-induced constriction under our experimental conditions.

The Intrarenal Release of Renin in the Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 81s-83s
Author(s):  
T. O. Morgan ◽  
J. Davis ◽  
A. Gillies
Keyword(s):  
Renal Artery ◽  
Renal Vein ◽  
Control Mechanism ◽  
Venous Blood ◽  
Local Formation ◽  
Efferent Arteriole ◽  
Arterial Blood

1. A technique was developed to measure renin concentration in nanolitre volumes of blood. 2. The renin concentration in renal venous blood was higher than in renal arterial blood. 3. The renin concentration in blood from the efferent arteriole was less than in blood from the renal artery and renal vein. 4. Renin enters the circulation distal to the efferent arteriole. 5. The release of renin into the interstitium would allow local formation of angiotensin and the system could act as an intrarenal control mechanism.

scholarly journals Proinsulin C-peptide reduces diabetes-induced glomerular hyperfiltration via efferent arteriole dilation and inhibition of tubular sodium reabsorption

2009 ◽  
Vol 297 (5) ◽  
pp. F1265-F1272 ◽  
Author(s):  
Lina Nordquist ◽  
Russell Brown ◽  
Angelica Fasching ◽  
Patrik Persson ◽  
Fredrik Palm
Keyword(s):  
Filtration Rate ◽  
Diabetic Rats ◽  
Glomerular Hyperfiltration ◽  
Proximal Tubular Cells ◽  
Filtration Fraction ◽  
C Peptide ◽  
Efferent Arteriole ◽  
Tubular Cells ◽  
Proximal Tubular ◽  
Stop Flow

C-peptide reduces diabetes-induced glomerular hyperfiltration in diabetic patients and experimental animal models. However, the mechanisms mediating the beneficial effect of C-peptide remain unclear. We investigated whether altered renal afferent-efferent arteriole tonus or alterations in tubular Na+ transport (TNa) in response to C-peptide administration mediate the reduction of diabetes-induced glomerular hyperfiltration. Glomerular filtration rate, filtration fraction, total and cortical renal blood flow, total kidney O2 consumption (Qo2), TNa, fractional Na+ and Li+ excretions, and tubular free-flow and stop-flow pressures were measured in anesthetized adult male normoglycemic and streptozotocin-diabetic Sprague-Dawley rats. The specific effect of C-peptide on transport-dependent Qo2 was investigated in vitro in freshly isolated proximal tubular cells. C-peptide reduced glomerular filtration rate (−24%), stop-flow pressure (−8%), and filtration fraction (−17%) exclusively in diabetic rats without altering renal blood flow. Diabetic rats had higher baseline TNa (+40%), which was reduced by C-peptide. Similarly, C-peptide increased fractional Na+ (+80%) and Li+ (+47%) excretions only in the diabetic rats. None of these parameters was affected by vehicle treatments in either group. Baseline Qo2 was 37% higher in proximal tubular cells from diabetic rats than controls and was normalized by C-peptide. C-peptide had no effect on ouabain-pretreated diabetic cells from diabetic rats. C-peptide reduced diabetes-induced hyperfiltration via a net dilation of the efferent arteriole and inhibition of tubular Na+ reabsorption, both potent regulators of the glomerular net filtration pressure. These findings provide new mechanistic insight into the beneficial effects of C-peptide on diabetic kidney function.

Determinants of renal microvascular response to ACh: afferent and efferent arteriolar actions of EDHF

2002 ◽  
Vol 282 (1) ◽  
pp. F124-F132 ◽  
Author(s):  
Xuemei Wang ◽  
Rodger Loutzenhiser
Keyword(s):  
Rat Kidney ◽  
K Channel ◽  
Channel Blockers ◽  
Efferent Arteriole ◽  
Microvascular Response ◽  
Vascular Beds ◽  
Underlying Mechanisms ◽  
Oxide Synthase

The renal microvascular actions of ACh were investigated using the in vitro perfused hydronephrotic rat kidney. ACh reversed ANG II-induced vasoconstriction in the afferent and efferent arteriole by 106 ± 2 and 75 ± 5%, respectively. Inhibition of nitric oxide synthase [NOS; 100 μmol/l N G-nitro-l-arginine methyl ester (l-NAME)] and cyclooxygenase (COX; 10 μmol/l ibuprofen) prevented the sustained response of the afferent arteriole but did not reduce the magnitude of the initial dilation (97 ± 7%). However, NOS/COX inhibition abolished the response of the efferent arteriole. The underlying mechanisms mediating this endothelium-derived hyperpolarizing factor (EDHF)-like response were characterized using K channel blockers. Ba (100 μmol/l), tetraethylammonium (1 mmol/l), and ouabain (3 mmol/l) had no effect, arguing against a role of an inward rectifier K channel, large-conductance Ca-activated K channel, or Na,K-ATPase. Charybdotoxin (10 nmol/l) and apamin (1.0 μmol/l) attenuated the response when administered alone (63 ± 7% and 37 ± 5%, respectively) and abolished the response when coadministered (0.1 ± 1.0%). These findings indicate that, as in other vascular beds, the renal EDHF-like response to ACh involves K channels that are sensitive to a combination of apamin and charybdotoxin. Our finding that EDHF modulates preglomerular, but not postglomerular, tone is consistent with the evolving concept that vasomotor mechanisms in cortical efferent arterioles do not involve voltage-gated Ca entry.

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