Effects of Carotid Baroreceptor Stimulation and Renal Denervation on the Medullary Concentration Gradient in Rat Kidneys

1975 ◽  
Vol 53 (3) ◽  
pp. 340-344
Author(s):  
R. Keeler
Keyword(s):  
Concentration Gradient ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Tissue Composition ◽  
Solute Content ◽  
Carotid Baroreceptor ◽  
Medullary Tissue ◽  
Unilateral Stimulation ◽  
Humoral Agent ◽  
Desoxycorticosterone Acetate

Unilateral stimulation of carotid baroreceptors in unanesthetized rats treated with desoxycorticosterone acetate caused highly significant decreases in solute content and osmolar concentration in the inner renal medulla. There was also a corresponding decrease in urine osmolality and a large increase in the excretion of sodium. In rats subjected to water diuresis, the changes in medullary tissue composition were similar but sodium excretion was very low, indicating that the natriuretic response was not a result of medullary 'washout' per se.Renal denervation had no significant effect on medullary tissue composition and did not prevent the dissipation of the cortico–medullary concentration gradient following carotid baroreceptor stimulation.It is concluded that the changes in inner medullary composition are mediated by a humoral agent.

Failure of Vasopressin to Prevent the Natriuretic and Diuretic Response to Unilateral Stimulation of Carotid Baroreceptors

1975 ◽  
Vol 53 (6) ◽  
pp. 1193-1197
Author(s):  
R. Keeler
Keyword(s):  
Effective Dose ◽  
Concentration Gradient ◽  
Control Period ◽  
Kidney Tissue ◽  
Urine Osmolality ◽  
Carotid Baroreceptors ◽  
Unilateral Stimulation ◽  
Vasopressin Secretion ◽  
Diuretic Response ◽  
Stimulation Of

Unanesthetized rats treated with deoxycorticosterone acetate were continuously infused with a maximally effective dose of vasopressin (50 μU/min per 100 g). After a control period of 2 h the animals were subjected to a 2 h period of unilateral stimulation of the carotid baroreceptors. There was a large natriuretic response accompanied by diuresis and a fall in urine osmolality. It was concluded that neither the natriuretic nor the diuretic response could be explained by inhibition of vasopressin secretion. Analysis of kidney tissue indicated that the diuresis was associated with partial dissipation of the inner medullary concentration gradient.

scholarly journals Hydration Status Affects Nuclear Distribution of Transcription Factor Tonicity Responsive Enhancer Binding Protein in Rat Kidney

2001 ◽  
Vol 12 (11) ◽  
pp. 2221-2230 ◽  
Author(s):  
JUNG H. CHA ◽  
SEUNG KYOON WOO ◽  
KI H. HAN ◽  
YOUNG H. KIM ◽  
JOSEPH S. HANDLER ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Mrna Expression ◽  
Nuclear Localization ◽  
Binding Protein ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Hydration Status ◽  
Water Loading ◽  
Nuclear Distribution ◽  
Enhancer Binding Protein

Abstract. Tonicity responsive enhancer binding protein (TonEBP) is the transcription factor that regulates tonicity responsive expression of proteins that catalyze cellular accumulation of compatible osmolytes. In cultured MDCK cells, hypertonicity stimulates the activity of TonEBP via a combination of increased protein abundance and increased nuclear localization. For investigating regulation of TonEBP in the kidney, rats were subjected to water loading or dehydration. Water loading lowered urine osmolality and mRNA expression of sodium/myo-inositol cotransporter (SMIT), a target gene of TonEBP, in the renal medulla; dehydration doubled the urine osmolality and increased SMIT mRNA expression. In contrast, overall abundance of TonEBP and its mRNA measured by immunoblot and ribonuclease protection assay, respectively, was not affected. Immunohistochemical analysis, however, revealed that nuclear distribution of TonEBP is generally increased throughout the medulla in dehydrated animals compared with water loaded animals. Increased nuclear localization was particularly dramatic in thin limbs. Notable exceptions were the middle to terminal portions of the inner medullary collecting ducts and blood vessels, where a change in TonEBP distribution was not evident. Immunohistochemical detection of SMIT mRNA revealed that the changes in nuclear distribution of TonEBP correlate with expression of SMIT. It is concluded that under physiologic conditions, nucleocytoplasmic distribution is the dominant mode of regulation of TonEBP in the renal medulla.

Cisplatin nephrotoxicity in rats: defect in papillary hypertonicity

1981 ◽  
Vol 241 (2) ◽  
pp. F175-F185 ◽  
Author(s):  
R. Safirstein ◽  
P. Miller ◽  
S. Dikman ◽  
N. Lyman ◽  
C. Shapiro
Keyword(s):  
Glomerular Filtration Rate ◽  
Proximal Tubule ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Collecting Duct ◽  
Urine Volume ◽  
Distal Tubule ◽  
Urine Osmolality ◽  
Solute Content ◽  
Cisplatin Nephrotoxicity

We examined the effects of cisplatin (5 mg/kg BW) on renal function in rats. Three days after administration of cisplatin whole kidney clearance of inulin fell and 24-h urine volume increased. Maximal urine osmolality and papillary solute content were reduced. Superficial nephron glomerular filtration rate measured along the proximal tubule, where no leak of inulin could be demonstrated, was reduced in cisplatin-treated animals. Differences between superficial nephron glomerular filtration rate determined in proximal and distal tubules were greater in cisplatin-treated rats than in control rats. Neither a change in fluid or sodium movement along superficial nephrons nor a reduced early distal tubule transepithelial sodium gradient explain the polyuria. Urea was reabsorbed from, not added to, the loop fluid in cisplatin-treated animals. Morphologic changes were evident in the S3 segment of the proximal tubule in cisplatin-treated animals but the glomeruli were normal. Polyuria occurred despite diminished glomerular filtration rate in cisplatin nephrotoxicity. The diminished concentration of salt and urea in the papilla as a result of abnormal function of the collecting duct or pars recta portion of the proximal tubule contributed to the defect in concentrating ability.

Genetic AVP deficiency abolishes cold-induced diuresis but does not attenuate cold-induced hypertension

2006 ◽  
Vol 290 (6) ◽  
pp. F1472-F1477 ◽  
Author(s):  
Zhongjie Sun
Keyword(s):  
Cold Exposure ◽  
Urine Output ◽  
Room Temperature ◽  
Control Period ◽  
Free Water ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Free Water Clearance ◽  
Receptor Mrna ◽  
Induced Hypertension

Chronic cold exposure causes hypertension and diuresis. The aim of this study was to determine whether vasopressin (AVP) plays a role in cold-induced hypertension and diuresis. Two groups of Long-Evans (LE) and two groups of homozygous AVP-deficient Brattleboro (VD) rats were used. Blood pressure (BP) was not different among the four groups during a 2-wk control period at room temperature (25°C, warm). After the control period, one LE group and one VD group were exposed to cold (5°C); the remaining groups were kept at room temperature. BP and body weight were measured weekly during exposure to cold. Food intake, water intake, urine output, and urine osmolality were measured during weeks 1, 3, and 5 of cold exposure. At the end of week 5, all animals were killed and blood was collected for measurement of plasma AVP. Kidneys were removed for measurement of renal medulla V2 receptor mRNA and aquaporin-2 (AQP-2) protein expression. BP of LE and VD rats increased significantly by week 2 of cold exposure and reached a high level by week 5. BP elevations developed at approximately the same rate and to the same degree in LE and VD rats. AVP deficiency significantly increased urine output and solute-free water clearance and decreased urine osmolality. Chronic cold exposure increased urine output and solute-free water clearance and decreased urine osmolality in LE rats, indicating that cold exposure caused diuresis in LE rats. Cold exposure failed to affect these parameters in VD rats, suggesting that the AVP system is responsible for cold-induced diuresis. Cold exposure did not alter plasma AVP in LE rats. Renal medulla V2 receptor mRNA and AQP-2 protein expression levels were decreased significantly in the cold-exposed LE rats, suggesting that cold exposure inhibited renal V2 receptors and AVP-inducible AQP-2 water channels. We conclude that 1) AVP may not be involved in the pathogenesis of cold-induced hypertension, 2) the AVP system plays a critical role in cold-induced diuresis, and 3) cold-induced diuresis is due to suppression of renal V2 receptors and the associated AQP-2 water channels, rather than inhibition of AVP release.

Acute regulation of the predominant organic solutes of the rabbit renal inner medulla

1989 ◽  
Vol 257 (4) ◽  
pp. F676-F681 ◽  
Author(s):  
S. D. Wolff ◽  
T. S. Stanton ◽  
S. L. James ◽  
R. S. Balaban
Keyword(s):  
High Performance Liquid Chromatography ◽  
High Performance ◽  
Renal Medulla ◽  
Organic Solutes ◽  
Solute Content ◽  
Organic Solute ◽  
Renal Inner Medulla ◽  
High Concentrations ◽  
Acute Changes ◽  
Functioning Kidney

High concentrations of organic solutes are present in the medulla of the antidiuretic kidney. However, their role in and response to acute changes in the diuretic state are unknown. In this study the organic solute content of the renal medulla was determined from extracts with the use of high-performance liquid chromatography following the acute dilution of the medullary interstitium during various forms of diuresis. After acute infusion of saline and furosemide, inner medullary urea, sodium, inositol, sorbitol, and betaine decrease significantly with no change in glycerophosphorylcholine (GPC) content. After diuresis, inner medullary urea and sodium contents eventually returned to control levels, although inositol, sorbitol, and betaine contents still remained low. Addition of antidiuretic hormone to the saline/furosemide infusion gave similar results. In contrast, induction of diuresis from mannitol infusion caused an acute decrease in all 4 organic solutes, whereas glucose infusion caused an acute decrease in all organic solutes except sorbitol. These data demonstrate that a decrease in all four organic solutes can accompany medullary dilution. However, GPC and sorbitol do not decrease when diuresis is induced by furosemide or glucose, respectively. In addition, the recovery of these compounds in a normally functioning kidney after diuresis is much slower than the regeneration of the sodium chloride and urea gradients.

scholarly journals mPGES-1 deletion potentiates urine concentrating capability after water deprivation

2012 ◽  
Vol 302 (8) ◽  
pp. F1005-F1012 ◽  
Author(s):  
Zhanjun Jia ◽  
Gang Liu ◽  
Maicy Downton ◽  
Zheng Dong ◽  
Aihua Zhang ◽  
...  
Keyword(s):  
Water Deprivation ◽  
Potential Role ◽  
Urine Volume ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Protein Abundance ◽  
Wild Type ◽  
Control Groups ◽  
Urine Concentrating Ability

PGE2 plays an important role in the regulation of fluid metabolism chiefly via antagonizing vasopressin-induced osmotic permeability in the distal nephron, but its enzymatic sources remain uncertain. The present study was undertaken to investigate the potential role of microsomal PGE synthase (mPGES)-1 in the regulation of urine concentrating ability after water deprivation (WD). Following 24-h WD, wild-type (WT) mice exhibited a significant reduction in urine volume, accompanied by a significant elevation in urine osmolality compared with control groups. In contrast, in response to WD, mPGES-1 knockout (KO) mice had much less urine volume and higher urine osmolality. Analysis of plasma volume by measurement of hematocrit and by using a nanoparticle-based method consistently demonstrated that dehydrated WT mice were volume depleted, which was significantly improved in the KO mice. WD induced a twofold increase in urinary PGE2 output in WT mice, which was completely blocked by mPGES-1 deletion. At baseline, the KO mice had a 20% increase in V2 receptor mRNA expression in the renal medulla but not the cortex compared with WT controls; the expression was unaffected by WD irrespective of the genotype. In response to WD, renal medullary aquaporin-2 (AQP2) mRNA exhibited a 60% increase in WT mice, and this increase was greater in the KO mice. Immunoblotting demonstrated increased renal medullary AQP2 protein abundance in both genotypes following WD, with a greater increase in the KO mice. Similar results were obtained by using immunohistochemistry. Paradoxically, plasma AVP response to WD seen in WT mice was absent in the KO mice. Taken together, these results suggest that mPGES-1-derived PGE2 reduces urine concentrating ability through suppression of renal medullary expression of V2 receptors and AQP2 but may enhance it by mediating the central AVP response.

The Effect of Papillectomy on Renal Function in the Rat during Hydropenia and after an Acute Saline Load

1972 ◽  
Vol 50 (7) ◽  
pp. 662-673 ◽  
Author(s):  
D. R. Wilson
Keyword(s):  
Renal Function ◽  
Partial Nephrectomy ◽  
Sodium Excretion ◽  
Free Water ◽  
Renal Medulla ◽  
Fractional Excretion ◽  
Urine Osmolality ◽  
Renal Handling ◽  
Water Excretion ◽  
Fractional Excretion Of Sodium

The effect of unilateral papillectomy on renal function in the rat was compared with the effect of partial nephrectomy which produced a similar decrease in glomerular filtration rate (G.F.R.) in the presence of an intact papilla. Under hydropenic conditions the kidney with papillectomy had a higher urine flow rate, sodium excretion rate, fractional sodium excretion, and osmolar clearance, while urine osmolality was lower. After an acute saline load the differences in sodium and water excretion disappeared, and fractional excretion of sodium and water were significantly higher in both types of kidney damage than in the contralateral control kidney. Free water reabsorption was lower in the papillectomized kidney after saline loading. Thus removal of the papilla resulted in abnormalities in the renal handling of salt and water which varied with the state of hydration of the animal and which were distinct from the effects of a reduction in G.F.R. by partial nephrectomy. It was concluded that the site of nephron loss, whether mainly in the renal medulla or in the cortex, may be another factor, in addition to G.F.R. and tubular reabsorption, which influences sodium and water excretion by the moderately damaged kidney.

Characterization of organic osmolytes in avian renal medulla: a nonurea osmotic gradient system

1993 ◽  
Vol 264 (6) ◽  
pp. R1045-R1049
Author(s):  
Y. H. Lien ◽  
M. M. Pacelli ◽  
E. J. Braun
Keyword(s):  
Water Deprivation ◽  
Renal Cortex ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Gradient System ◽  
Osmotic Gradient ◽  
Organic Osmolytes ◽  
Before And After ◽  
Avian Kidney

We measured the organic osmolytes present in the renal cortex and medullary cones of adult female domestic fowl before and after 48 h of water deprivation. Urine osmolality increased from 198 +/- 82 to 569 +/- 42 mosmol/kgH2O after water deprivation. In water-deprived birds, the major organic osmolytes, myoinositol, betaine, and taurine, in the medullary cones increased by 40, 100, and 24%, respectively, compared with control birds. No sorbitol was detected, and glycerophosphorylcholine (GPC) content was not affected by water deprivation. In the renal cortex, only betaine content increased significantly (4.8 +/- 0.6 vs. 3.1 +/- 0.3 mmol/kg wet wt) after water deprivation. In this study, we demonstrated that birds, like mammals, accumulate organic osmolytes in response to the increased interstitial osmolality that occurs during antidiuresis. Because urea is nearly absent in the avian medullary interstitium, our observation that GPC is not osmoregulated in the avian kidney supports the idea that GPC is the “counteracting osmolyte” for urea in the mammalian kidney. Furthermore, the organic osmolytes present in avian medullary cones are remarkably similar to those of the mammalian outer medulla. This similarity may be relevant to the morphological analogy of the two regions.

Lithium-induced diuretic effect of antidiuretic hormone in rats

1976 ◽  
Vol 231 (6) ◽  
pp. 1754-1759 ◽  
Author(s):  
TP Dousa ◽  
LD Barnes
Keyword(s):  
Antidiuretic Hormone ◽  
Low Dose ◽  
Free Water ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Urinary Volume ◽  
Free Water Clearance ◽  
Sodium Potassium ◽  
Collecting Ducts

The effect of a low dose of lithium (1 meq/kg per day) on renal function and its response to antidiuretic hormone (ADH) was studied in unanesthetized rats. This dose of lithium itself had no influence on renal water and electrolyte excretion, but lithium-treated rats responded paradoxically to exogenous ADH by increases in urinary volume, excretion of total solutes, sodium, potassium, and phosphate. Administration of ADH in the presence of lithium led to a lowering of urine osmolality, but free water clearance was not significantly reduced. Adenylate cyclase from the renal medulla of animals treated with ADH and lithium had a lower response to synthetic vasopressin in vitro than in animals treated with lithium alone. The results suggest that exogenous ADHis diuretic in the presence of a low concentration of lithilm. The predominant mechanism for this diuresis is probably inhibition of electrolyte and isomotic water reabbsorption in various nephron segments, including those proximal to the collecting ducts. ADH also markedly increased urinary excretion of lithium and appears to promote accumulation of lithium in the renal medulla.

Abstract P328: Angiotensin II Inhibits the High Salt-induced Production of Sphigosine-1-phosphate in the Renal Medulla

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Weili Wang ◽  
Junping Hu ◽  
Pin-Lan Li ◽  
Justin L Poklis ◽  
Ningjun Li
Keyword(s):  
Angiotensin Ii ◽  
Renal Medulla ◽  
High Salt ◽  
Ang Ii ◽  
Male Adult ◽  
High Salt Diet ◽  
Salt Diet ◽  
Protein Levels ◽  
Medullary Tissue ◽  
Natriuretic Effect

We have previously shown that sphigosine-1-phosphate (S1P) produces natriuretic effects via activation of S1P receptor 1 in the renal medulla and that this natriuretic effect may be through inhibition of epithelial sodium channel. The present study examined the expression of the enzymes that produce S1P in the renal medullary tissue and tested the hypothesis that angiotensin II (ANG II) reduces the expression of S1P-producing enzyme and thereby the levels of S1P in the renal medulla. Male adult C56BL/6 mice, 10-12 weeks old, were treated with a low salt diet (LS, 0.4%), high salt diet (HS, 4% NaCl) or HS + ANG II (600ng/kg/min, S.C.) for 10 days. A high salt diet increased the level of S1P, whereas ANG II significantly inhibited the HS-induced increase of S1P levels in the renal medullary tissue. The levels of S1P were 6.6 ± 0.34, 11.4 ± 1.33 and 3.5 ± 0.49 pmol/mg of tissue in LS, HS and HS + ANG II group, respectively. There were no difference in the levels of sphingosine kinase 1 (SPHK1), the enzyme that produces S1P by phosphorylating sphingosine, among the different groups of mice by Western blot analysis. However, a high salt diet increased the protein levels of acid ceramidase (ACDase), an upstream enzyme that produces sphingosine, the substrate for SPHK1. This HS-induced increase in ACDase was inhibited by ANG II. The relative protein levels of ACDase were 1.0 ± 0.07, 1.4 ± 0.07 and 0.17 ± 0.11 in LS, HS and HS + ANG II group, respectively. These results demonstrated that a high salt diet increased the levels of S1P in the renal medulla, probably by increasing the level of one of the S1P-producing enzymes ACDase, and that ANG II reduced the levels of ACDase and S1P in the renal medulla. Given the diuretic effect of S1P, ANG II-induced reduction of S1P production in the renal medulla may be a mechanism contributing to the sodium retention and hypertension associated with excessive ANG II. (Support: NIH grant HL89563)

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