scholarly journals Diffusive shunting of gases and other molecules in the renal vasculature: physiological and evolutionary significance

2016 ◽  
Vol 311 (5) ◽  
pp. R797-R810 ◽  
Author(s):  
Jennifer P. Ngo ◽  
Connie P.C. Ow ◽  
Bruce S. Gardiner ◽  
Saptarshi Kar ◽  
James T. Pearson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Carbon Dioxide ◽  
Hydrogen Sulfide ◽  
Mathematical Models ◽  
Renal Cortex ◽  
Renal Medulla ◽  
Evolutionary Significance ◽  
Renal Vasculature ◽  
Vasa Recta ◽  
Arteries And Veins

Countercurrent systems have evolved in a variety of biological systems that allow transfer of heat, gases, and solutes. For example, in the renal medulla, the countercurrent arrangement of vascular and tubular elements facilitates the trapping of urea and other solutes in the inner medulla, which in turn enables the formation of concentrated urine. Arteries and veins in the cortex are also arranged in a countercurrent fashion, as are descending and ascending vasa recta in the medulla. For countercurrent diffusion to occur, barriers to diffusion must be small. This appears to be characteristic of larger vessels in the renal cortex. There must also be gradients in the concentration of molecules between afferent and efferent vessels, with the transport of molecules possible in either direction. Such gradients exist for oxygen in both the cortex and medulla, but there is little evidence that large gradients exist for other molecules such as carbon dioxide, nitric oxide, superoxide, hydrogen sulfide, and ammonia. There is some experimental evidence for arterial-to-venous (AV) oxygen shunting. Mathematical models also provide evidence for oxygen shunting in both the cortex and medulla. However, the quantitative significance of AV oxygen shunting remains a matter of controversy. Thus, whereas the countercurrent arrangement of vasa recta in the medulla appears to have evolved as a consequence of the evolution of Henle’s loop, the evolutionary significance of the intimate countercurrent arrangement of blood vessels in the renal cortex remains an enigma.

scholarly journals Chronic ouabain treatment induces vasa recta endothelial dysfunction in the rat

2009 ◽  
Vol 296 (1) ◽  
pp. F98-F106 ◽  
Author(s):  
Chunhua Cao ◽  
Kristie Payne ◽  
Whaseon Lee-Kwon ◽  
Zhong Zhang ◽  
Sun Woo Lim ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Methyl Ester ◽  
Endothelial Dysfunction ◽  
Chronic Exposure ◽  
Renal Medulla ◽  
Renal Vasculature ◽  
Vasa Recta

Descending vasa recta (DVR) are 15-μm vessels that perfuse the renal medulla. Ouabain has been shown to augment DVR endothelial cytoplasmic Ca2+ ([Ca2+]CYT) signaling. In this study, we examined the expression of the ouabain-sensitive Na-K-ATPase α2 subunit in the rat renal vasculature and tested effects of acute ouabain exposure and chronic ouabain treatment on DVR. Immunostaining with antibodies directed against the α2 subunit verified its expression in both DVR pericytes and endothelium. Acute application of ouabain (100 or 500 nM) augmented the DVR nitric oxide generation stimulated by acetylcholine (ACh; 10 μM). At a concentration of 1 mM, ouabain constricted microperfused DVR, whereas at 100 nM, it was without effect. Acute ouabain (100 nM) did not augment constriction by angiotensin II (0.5 or 10 nM), whereas l-nitroarginine methyl ester-induced contraction of DVR was slightly enhanced. Ouabain-hypertensive (OH) rats were generated by chronic ouabain treatment (30 μg·kg−1·day−1, 5 wk). The acute endothelial [Ca2+]CYT elevation by ouabain (100 nM) was absent in DVR endothelia of OH rats. The [Ca2+]CYT response to 10 nM ACh was also eliminated, whereas the response to 10 μM ACh was not. The endothelial [Ca2+]CYT response to bradykinin (100 nM) was significantly attenuated. We conclude that endothelial responses may offset the ability of acute ouabain exposure to enhance DVR vasoconstriction. Chronic exposure to ouabain, in vivo, leads to hypertension and DVR endothelial dysfunction, manifested as reduced [Ca2+]CYT responses to both ouabain- and endothelium-dependent vasodilators.

scholarly journals Increased activity and expression of Ca2+-dependent NOS in renal cortex of ANG II-infused hypertensive rats

1999 ◽  
Vol 277 (5) ◽  
pp. F797-F804 ◽  
Author(s):  
So Yeon Chin ◽  
Kailash N. Pandey ◽  
Shang-Jin Shi ◽  
Hiroyuki Kobori ◽  
Carol Moreno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Renal Cortex ◽  
Renal Medulla ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Differential Distribution ◽  
Cortical Blood Flow ◽  
Renal Cortical Blood Flow

We have previously demonstrated that nitric oxide (NO) exerts a greater modulatory influence on renal cortical blood flow in ANG II-infused hypertensive rats compared with normotensive rats. In the present study, we determined nitric oxide synthase (NOS) activities and protein levels in the renal cortex and medulla of normotensive and ANG II-infused hypertensive rats. Enzyme activity was determined by measuring the rate of formation ofl-[14C]citrulline froml-[14C]arginine. Western blot analysis was performed to determine the regional expression of endothelial (eNOS), neuronal (nNOS), and inducible (iNOS) isoforms in the renal cortex and medulla of control and ANG II-infused rats. Male Sprague-Dawley rats were prepared by the infusion of ANG II at a rate of 65 ng/min via osmotic minipumps implanted subcutaneously for 13 days and compared with sham-operated rats. Systolic arterial pressures were 127 ± 2 and 182 ± 3 mmHg in control ( n = 13) and ANG II-infused rats ( n = 13), respectively. The Ca2+-dependent NOS activity, expressed as picomoles of citrulline formed per minute per gram wet weight, was higher in the renal cortex of ANG II-infused rats (91 ± 11) than in control rats (42 ± 12). Likewise, both eNOS and nNOS were markedly elevated in the renal cortex of the ANG II-treated rats. In both groups of rats, Ca2+-dependent NOS activity was higher in the renal medulla than in the cortex; however, no differences in medullary NOS activity were observed between the groups. Also, no differences in medullary eNOS levels were observed between the groups; however, medullary nNOS was decreased by 45% in the ANG II-infused rats. For the Ca2+-independent NOS activities, the renal cortex exhibited a greater activity in the control rats (174 ± 23) than in ANG II-infused rats (101 ± 10). Similarly, cortical iNOS was greater by 47% in the control rats than in ANG II-treated rats. No differences in the activity were found for the renal medulla between the groups. There was no detectable signal for iNOS in the renal medulla for both groups. These data indicate that there is a differential distribution of NOS activity, with the Ca2+-dependent activity and protein expression higher in the renal cortex of ANG II-infused rats compared with control rats, and support the hypothesis that increased constitutive NOS activity exerts a protective effect in ANG II-induced hypertension to maintain adequate renal cortical blood flow.

Effect of norepinephrine and acetylcholine on outer medullary descending vasa recta

1995 ◽  
Vol 269 (2) ◽  
pp. H710-H716 ◽  
Author(s):  
S. Yang ◽  
E. P. Silldorff ◽  
T. L. Pallone
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Regional Blood Flow ◽  
Renal Medulla ◽  
Cholinergic Innervation ◽  
Vascular Bundles ◽  
Nitric Oxide Synthase Inhibitor ◽  
Vasa Recta ◽  
Oxide Synthase

To examine their responsiveness to norepinephrine (NE) and acetylcholine (ACh), outer medullary descending vasa recta (OMDVR) have been dissected from vascular bundles of the rat and perfused in vitro. Abluminal application of NE produced graded vasoconstriction in a concentration range of 10(-9)-10(-6) M. When applied with NE, ACh at concentrations of 10(-8)-10(-5) M dilated NE-preconstricted OMDVR. In contrast, ACh applied in the absence of NE caused vasoconstriction. ACh-induced vasodilation was blocked by addition of the nitric oxide synthase inhibitor N omega-nitro-L-arginine (L-NNA, 2 x 10(-4) M). L-NNA in the absence of ACh enhanced NE-induced vasoconstriction. Supraphysiological (10(-3) M) L-arginine (L-Arg) reversed the effects of L-NNA, and abluminal application of L-NNA alone resulted in OMDVR vasoconstriction. At concentrations of 10(-6)-10(-3) M, abluminal application of L-Arg produced graded vasodilation of NE-constricted OMDVR. These results suggest that adrenergic and cholinergic innervation could influence OMDVR vasomotor tone to modulate total and regional blood flow to the renal medulla. The data also favor a role for the activity of constitutively expressed nitric oxide synthase to modulate OMDVR vasoactivity.

scholarly journals Impact of nitric-oxide-mediated vasodilation and oxidative stress on renal medullary oxygenation: a modeling study

2016 ◽  
Vol 310 (3) ◽  
pp. F237-F247 ◽  
Author(s):  
Brendan C. Fry ◽  
Aurélie Edwards ◽  
Anita T. Layton
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Sodium Transport ◽  
Renal Medulla ◽  
Vascular Bundles ◽  
Active Sodium ◽  
Transport Efficiency ◽  
Active Sodium Transport ◽  
Vasa Recta ◽  
Radial Organization

The goal of this study was to investigate the effects of nitric oxide (NO)-mediated vasodilation in preventing medullary hypoxia, as well as the likely pathways by which superoxide (O2−) conversely enhances medullary hypoxia. To do so, we expanded a previously developed mathematical model of solute transport in the renal medulla that accounts for the reciprocal interactions among oxygen (O2), NO, and O2− to include the vasoactive effects of NO on medullary descending vasa recta. The model represents the radial organization of the vessels and tubules, centered around vascular bundles in the outer medulla and collecting ducts in the inner medulla. Model simulations suggest that NO helps to prevent medullary hypoxia both by inducing vasodilation of the descending vasa recta (thus increasing O2 supply) and by reducing the active sodium transport rate (thus reducing O2 consumption). That is, the vasodilative properties of NO significantly contribute to maintaining sufficient medullary oxygenation. The model further predicts that a reduction in tubular transport efficiency (i.e., the ratio of active sodium transport per O2 consumption) is the main factor by which increased O2− levels lead to hypoxia, whereas hyperfiltration is not a likely pathway to medullary hypoxia due to oxidative stress. Finally, our results suggest that further increasing the radial separation between vessels and tubules would reduce the diffusion of NO towards descending vasa recta in the inner medulla, thereby diminishing its vasoactive effects therein and reducing O2 delivery to the papillary tip.

scholarly journals Intrinsic nitric oxide and superoxide production regulates descending vasa recta contraction

2010 ◽  
Vol 299 (5) ◽  
pp. F1056-F1064 ◽  
Author(s):  
Chunhua Cao ◽  
Aurélie Edwards ◽  
Mauricio Sendeski ◽  
Whaseon Lee-kwon ◽  
Lan Cui ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Medulla ◽  
Ros Generation ◽  
No Production ◽  
Oxygen Species ◽  
Direct Effects ◽  
Vasa Recta ◽  
Luminal Perfusion ◽  
Oxide Synthase ◽  
Hydrophilic Solutes

Descending vasa recta (DVR) are 12- to 15-μm microvessels that supply the renal medulla with blood flow. We examined the ability of intrinsic nitric oxide (NO) and reactive oxygen species (ROS) generation to regulate their vasoactivity. Nitric oxide synthase (NOS) inhibition with Nω-nitro-l-arginine methyl ester (l-NAME; 100 μmol/l), or asymmetric NG, NG-dimethyl-l-arginine (ADMA; 100 μmol/l), constricted isolated microperfused DVR by 48.82 ± 4.34 and 27.91 ± 2.91%, respectively. Restoring NO with sodium nitroprusside (SNP; 1 mmol/l) or application of 8-Br-cGMP (100 μmol/l) reversed DVR vasoconstriction by l-NAME. The superoxide dismutase mimetic Tempol (1 mmol/l) and the NAD(P)H inhibitor apocynin (100, 1,000 μmol/l) also blunted ADMA- or l-NAME-induced vasoconstriction, implicating a role for concomitant generation of ROS. A role for ROS generation was also supported by an l-NAME-associated rise in oxidation of dihydroethidium that was prevented by Tempol or apocynin. To test whether H2O2 might play a role, we examined its direct effects. From 1 to 100 μmol/l, H2O2 contracted DVR whereas at 1 mmol/l it was vasodilatory. The H2O2 scavenger polyethylene glycol-catalase reversed H2O2 (10 μmol/l)-induced vasoconstriction; however, it did not affect l-NAME-induced contraction. Finally, the previously known rise in DVR permeability to 22Na and [3H]raffinose that occurs with luminal perfusion was not prevented by NOS blockade. We conclude that intrinsic production of NO and ROS can modulate DVR vasoactivity and that l-NAME-induced vasoconstriction occurs, in part, by modulating superoxide concentration and not through H2O2 generation. Intrinsic NO production does not affect DVR permeability to hydrophilic solutes.

The influence of nitric oxide synthase 1 on blood flow and interstitial nitric oxide in the kidney

2001 ◽  
Vol 281 (1) ◽  
pp. R91-R97 ◽  
Author(s):  
Masao Kakoki ◽  
Ai-Ping Zou ◽  
David L. Mattson
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Renal Cortex ◽  
In Vivo Microdialysis ◽  
Sprague Dawley ◽  
Selective Inhibitors ◽  
Renal Vasculature ◽  
Doppler Flowmetry ◽  
Arterial Blood

The role of nitric oxide (NO) produced by NO synthase 1 (NOS1) in the renal vasculature remains undetermined. In the present study, we investigated the influence of systemic inhibition of NOS1 by intravenous administration of N ω-propyl-l-arginine (l-NPA; 1 mg · kg−1 · h−1) and N 5-(1-imino-3-butenyl)-l-ornithine (v-NIO; 1 mg · kg−1 · h−1), highly selective NOS1 inhibitors, on renal cortical and medullary blood flow and interstitial NO concentration in Sprague-Dawley rats. Arterial blood pressure was significantly decreased by administration of both NOS1-selective inhibitors (−11 ± 1 mmHg with l-NPA and −7 ± 1 mmHg with v-NIO; n = 9/group). Laser-Doppler flowmetry experiments demonstrated that blood flow in the renal cortex and medulla was not significantly altered following administration of either NOS1-selective inhibitor. In contrast, the renal interstitial level of NO assessed by an in vivo microdialysis oxyhemoglobin-trapping technique was significantly decreased in both the renal cortex (by 36–42%) and medulla (by 32–40%) following administration of l-NPA ( n = 8) or v-NIO ( n = 8). Subsequent infusion of the nonspecific NOS inhibitor N ω-nitro-l-arginine methyl ester (l-NAME; 50 mg · kg−1 · h−1) to rats pretreated with either of the NOS1-selective inhibitors significantly increased mean arterial pressure by 38–45 mmHg and significantly decreased cortical (25–29%) and medullary (37–43%) blood flow. In addition, l-NAME further decreased NO in the renal cortex (73–77%) and medulla (62–71%). To determine if a 40% decrease in NO could alter renal blood flow, a lower dose ofl-NAME (5 mg · kg−1 · h−1; n = 8) was administered to a separate group of rats. The low dose of l-NAME reduced interstitial NO (cortex 39%, medulla 38%) and significantly decreased blood flow (cortex 23–24%, medulla 31–33%). These results suggest that NOS1 does not regulate basal blood flow in the renal cortex or medulla, despite the observation that a considerable portion of NO in the renal interstitial space appears to be produced by NOS1.

Renal Vasculature of 2 Dasyurid Marsupials, Sminthopsis-Dolichura and S-Crassicaudata

1995 ◽  
Vol 43 (3) ◽  
pp. 259 ◽  
Author(s):  
BM Brooker ◽  
JE Oshea ◽  
T Stewart
Keyword(s):  
Renal Medulla ◽  
Urine Concentration ◽  
Corrosion Casts ◽  
Water Reabsorption ◽  
Renal Vasculature ◽  
Vasa Recta ◽  
Current Water ◽  
Afferent Arterioles ◽  
Counter Current ◽  
Vascular Corrosion Casts

The renal vasculature of two dasyurid marsupials, Sminthopsis dolichura and S. crassicaudata, was examined using scanning electron microscopy of vascular corrosion casts of the kidney. Each species had a pair of unipapillary kidneys and the structural organisation of the major renal arterial vessels was similar to that of other placental mammals. The glomerulus of both species consisted of a network of dividing and anastomosing capillary loops. The glomeruli varied markedly in size, shape and complexity. Some afferent arterioles extended back towards the renal medulla, positioning the glomeruli closer to the cortico-medullary border. This placement of glomeruli may extend the loop of the nephron further into the medulla and thereby enhance counter-current water reabsorption and the final urine concentration. In both S. crassicaudata and S. dolichura, a dense mesh of numerous fine capillaries lined the wall of the renal pelvis adjacent to the inner medulla, with a unique configuration in that they were aligned perpendicular to the vasa recta. The function of these fine capillaries is unknown.

Infrared Spectrophotometric Analysis of Medicinal Gases for Trace Impurities

1976 ◽  
Vol 59 (6) ◽  
pp. 1404-1408
Author(s):  
Wilson L Brannon ◽  
Walter R Benson ◽  
George Schwartzman
Keyword(s):  
Nitric Oxide ◽  
Carbon Dioxide ◽  
Carbon Monoxide ◽  
Hydrogen Sulfide ◽  
Sulfur Dioxide ◽  
Spectrophotometric Analysis ◽  
Gas Cell ◽  
Trace Impurities ◽  
Infrared Spectrophotometer ◽  
Low Levels

Abstract The feasibility of examining medicinal gases for trace impurities, using an infrared spectrophotometer in conjunction with a 10 m gas cell, was investigated. Many of the impurities for which the USP includes limits were detected and measured at concentrations at or below those permitted by the USP; these include sulfur dioxide, carbon dioxide, carbon monoxide, and water. However, others (hydrogen sulfide, nitric oxide, and nitrogen dioxide) were not detected at these levels by this technique. Methane was found at low levels in some samples.

Sodium Status Affects Gc-B Natriuretic Peptide Receptor mRNA Levels, but Not Gc-A Or C Receptor Mrna Levels, in the Sheep Kidney

1994 ◽  
Vol 86 (5) ◽  
pp. 517-522 ◽  
Author(s):  
Margaret B. Fraenkel ◽  
G. Peter Aldred ◽  
John G. McDougall
Keyword(s):  
Natriuretic Peptide ◽  
Transcriptional Control ◽  
Renal Cortex ◽  
Renal Medulla ◽  
Mrna Levels ◽  
Binding Studies ◽  
Renal Vasculature ◽  
Receptor Mrna ◽  
Natural Ligand ◽  
Significant Difference

1. In humans and experimental animals the natriuresis and diuresis resulting from infusion of atrial natriuretic peptide varies with the sodium status of the subject. Tissue binding studies have suggested that this may be related to changes in the renal receptors for the hormone. 2. In order to establish whether these changes are under transcriptional control, we examined the levels of mRNA for the three natriuretic peptide receptors [GC-A, GC-B and clearance (C) receptors] in renal cortex and medulla from six sodium-loaded, six sodium-depleted and four control sheep. cDNA probes specific to each receptor were generated using the polymerase chain reaction. 3. GC-B receptor mRNA levels were increased approximately two-fold in the renal cortex of sodium-depleted animals, whereas there was no influence on GC-B receptor mRNA levels in the renal medulla. There was no significant difference in mRNA levels for the GC-A and C receptors. 4. At present the role of the GC-B receptor and its natural ligand C-type natriuretic peptide in the control of renal function is unknown. The present experiments imply some intrarenal function for the GC-B receptor and its natural ligand, although the site of any such function, e.g. renal vasculature or tubules, remains unclear. In addition, we have shown that if GC-A and C receptor levels in the sheep are modulated by sodium, the regulation occurs beyond the level of gene transcription.

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