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PubMed1995

Relation between pressure natriuresis and urinary excretion of nitrate/nitrite in anesthetized dogs.

Alterations in intrarenal nitric oxide (NO) formation during changes in renal arterial pressure (RAP) have been suggested as a mechanism mediating pressure natriuresis. To test this hypothesis further, we examined the relation between RAP and the urinary excretion rate of nitrate/nitrite (NO3-/NO2-; NO metabolites) in anesthetized sodium-replete dogs before (n = 9) and during (n = 6) intrarenal infusion of the NO synthesis inhibitor nitro-L-arginine (NLA; 50 micrograms.kg-1.min-1). Urinary NO3-/NO2- concentrations were measured with the Griess reaction and spectrophotometry methods after enzymatic reduction of NO3- to NO2- in the samples. During control conditions, there were decreases in the urinary NO3-/NO2- excretion rate in response to reductions in RAP (150 to 75 mm Hg; slope, 0.04 +/- 0.01 nmol.min-1.g-1.mm Hg-1) in association with decreases in urinary sodium excretion (UNaV). There was a positive correlation between changes in NO3-/NO2- excretion rate and changes in RAP (r = .48; P < .005) or UNaV (r = .59; P < .001). NLA infusion resulted in decreases in NO3-/NO2- excretion rate (4.8 +/- 1.4 to 1.0 +/- 0.3 nmol.min-1.g-1) in association with reductions in UNaV (4.3 +/- 0.3 to 0.7 +/- 0.2 microL.min-1.g-1), fractional excretion of sodium (2.9 +/- 0.2% to 0.5 +/- 0.1%), and renal blood flow (4.8 +/- 0.3 to 3.3 +/- 0.2 mL.min-1.g-1), without changes in glomerular filtration rate. Furthermore, there was a marked attenuation of the NO3-/NO2- and sodium excretory responses to alterations in RAP during NO synthesis inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗
PubMed1998

Current and birth weights exert independent influences on nocturnal pressure-natriuresis relationships in normotensive children.

The objective was to study the impact of birth weight on the relationship between ambulatory blood pressure and urinary sodium excretion in children and adolescents. The study included 134 healthy children (61 boys), all Caucasians, who were born at term after a normotensive pregnancy. For each subject, a 24-hour ambulatory blood pressure monitoring and a complete urine collection were simultaneously performed according to the protocols designed. Average ambulatory blood pressure (BP) and the urinary excretion rates for sodium, potassium, and creatinine were calculated separately for 24-hour, awake, and sleep periods defined by a mini-diary. The excretion rate of sodium during sleep time was positively correlated with ambulatory systolic BP; such a positive relationship was not found for waking hours. Consequently, the impact of birth weight on the relationship between blood pressure and the urinary sodium excretion rate was analyzed during sleeping hours. Stepwise multiple regression analysis shows that although current weight was the strongest predictor for the sodium excretion rate during sleep (P<.001), there was also an independent significant direct relationship for birth weight (P<.04) after controlling for age, sex, and the average of systolic BP during sleep. Adjusted for current weight, a significant difference in the regression slopes relating urinary sodium excretion rate and systolic BP during sleep exists between children in the lowest (<3.100 kg) and the highest tertiles (>3.500 kg) of birth weight (P<.02). Differences in sodium excretion rates, adjusted for current weight, between the two extreme tertiles of birth weight became significant at the highest systolic BP (P<.04). The children who had the lowest birth weight tended to excrete less sodium during sleep. The results of the present study show a blunted pressure natriuresis curve in children and adolescents with the lowest birth weight. Whether this abnormal renal sodium handling may be present as an initial or as an intermediate mechanism leading to higher BP values must be assessed in additional studies.

Adolescent↗
PubMed2001

Renal interstitial cGMP mediates natriuresis by direct tubule mechanism.

The objective of this study was to test the hypothesis that renal interstitial (RI) cGMP is natriuretic in vivo. In conscious rats (n=8), urinary sodium excretion (U(Na)V) was significantly greater on days 3 and 4 of RI infusion of cGMP (1.17+/-0.14 and 1.61+/-0.11 mmol/24 h, respectively) than during vehicle infusion (0.56+/-0.15 and 0.70+/-0.17 mmol/24 h, respectively) (P<0.01). Similarly, U(Na)V was greater on days 3 and 4 of RI infusion of 8-bromo-cGMP (2.15+/-0.42 and 2.16+/-0.1 mmol/24 h, respectively). Protein kinase G inhibitor Rp-8-pCPT-cGMPS reduced cGMP-induced and 8-bromo-cGMP-induced U(Na)V to control levels. Acute RI infusion of L-arginine (L-Arg, 40 mg. kg(-1). min(-1)), but not D-arginine, caused an increase in U(Na)V from 1.65+/-0.11 to 4.07+/-0.1 micromol/30 min (P<0.01). This increase was blocked by RI infusion of N(G)-nitro-L-arginine methyl ester (100 ng. kg(-1). min(-1)) by the phosphodiesterase (PDE II) activator 5,6DMcBIMP (0.01 micromol/microL), by PDE II (0.03 U. kg(-1). min(-1)) itself, or by the soluble guanylyl cyclase inhibitor 1-H-[1,2,4]oxadiazolo-[4,2-alpha]quinoxalin-1-one (ODQ, 0.12 mg. kg(-1). min(-1)). The PDE II activator also blocked L-Arg-stimulated cGMP levels. The NO donor S-nitroso-N-acetylpenicillamine (SNAP, 0.12 micromol. L(-1). kg(-1). min(-1)) increased U(Na)V from 1.65+/-0.11 to 2.93+/-0.08 micromol/30 min (P<0.01), and this response was blocked completely by ODQ. Renal arterial but not RI administration of the heat-stable enterotoxin of Escherichia coli induced natriuresis. RA infusion of cGMP (3 microg/min) increased U(Na)V, renal blood flow (RBF), and glomerular filtration rate (GFR). Renal cortical interstitial cGMP infusion increased U(Na)V with no effect on total RBF, renal cortical blood flow, or GFR. Similarly, the natriuretic actions of renal interstitial L-Arg or SNAP were not accompanied by any change in RBF or GFR. Medullary cGMP infusion had no effect on U(Na)V, total RBF, or medullary blood flow. Texas red-labeled cGMP infused via the RI space was distributed exclusively to cortical renal tubular cells. The results demonstrate that RI cGMP inhibits renal tubular sodium absorption via protein kinase G independently of hemodynamic changes. These observations indicate that the cortical interstitial compartment provides a potentially important domain for cell-to-cell signaling within the kidney.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1987

Altered pressure-natriuresis relationship in young spontaneously hypertensive rats.

In the present study, the pressure-natriuretic responses of 3- to 5- and 6- to 9-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were characterized to determine whether the relationship between sodium excretion and renal perfusion pressure is altered during the development of hypertension. Differences in the neural tone and renal hormone levels in SHR and WKY were minimized by denervating the kidney and fixing plasma concentrations of aldosterone, vasopressin, norepinephrine, and cortisol by intravenous infusion. Renal perfusion pressure was varied using adjustable occluders on the lower aorta. The slopes of the relationships between sodium excretion and renal perfusion pressure were not significantly different in 3- to 5-week-old SHR and WKY (0.31 +/- 0.05 vs 0.42 +/- 0.06 microEq/min/g kidney weight); however, the x-intercept of this relationship was significantly shifted to the right by 15 mm Hg in SHR compared to WKY. Blood pressure was moderately elevated even in the 3- to 5-week-old SHR in comparison to WKY (98 +/- 5 vs 81 +/- 6 mm Hg). As the degree of hypertension became more severe, the slope of the pressure-natriuresis relationship became significantly lower in 6- to 9-week-old SHR compared to the corresponding slope observed in age-matched WKY (0.16 +/- 0.02 vs 0.31 +/- 0.04 microEq/min/g kidney weight). These results indicate that the relationship between sodium excretion and renal perfusion pressure is altered even in very young SHR. Thus, the resetting of kidney function occurs very early and may be necessary for the development of hypertension in SHR.

Aging↗
PubMed1992

Relation between vasa recta blood flow and renal interstitial hydrostatic pressure during pressure natriuresis.

Pressure natriuresis may be mediated through increases in inner medullary vasa recta blood flow (QVR). By means of acute renal decapsulation to prevent increases in renal interstitial hydrostatic pressure (RIHP), the effect of increases in QVR in the presence and absence of changes in RIHP in the natriuretic and diuretic responses to increases in renal perfusion pressure (RPP) was evaluated. Blood flow in descending (QDVR) and ascending (QAVR) vasa recta was determined in the exposed papilla by fluorescence videomicroscopy in anesthetized euvolemic Munich Wistar rats. In rats with intact renal capsules (n = 12), increases in RPP from 101 +/- 0.5 to 132 +/- 2.9 mm Hg caused significant increases in QDVR (from 4.7 +/- 0.9 to 5.5 +/- 0.9 nl/min, p < 0.001) and QAVR (from 2.8 +/- 0.2 to 3.5 +/- 0.2 nl/min, p < 0.001) in association with increases in RIHP (from 4.6 +/- 1.3 to 7.6 +/- 1.3 mm Hg, p < 0.001), urine flow (from 16.2 +/- 2.6 to 20.2 +/- 3.2 microliters.min-1 x g kidney wt-1, p < 0.01), and urinary sodium excretion (from 2.10 +/- 0.38 to 3.36 +/- 0.62 mu eq.min-1 x g kidney wt-1, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1973

Mechanism of natriuresis after closure of chronic arteriovenous shunts.

Animals subjected to certain cardiovascular manipulations, such as arteriovenous fistulas, diminish their urinary sodium excretion. It has been shown that closure of such fistulas results in a prompt increase in the rate of sodium excretion. However, the nature of the renal mechanisms increasing the excretion of sodium when the initial cardiovascular abnormality is corrected has remained unclear. Since the elucidation of such mechanisms might provide information pertinent to other sodium-retaining states, the effect of closure of chronic Teflon-Silastic arteriovenous shunts was studied in desoxycorticosterone acetate (DOCA)-treated dogs by utilizing micropuncture techniques.Nephron filtration rates were measured first during a control period with open arteriovenous shunts and then again after closure of the shunts in 12 dogs. Nephron filtration rate rose 32% while total glomerular filtration rate (GFR) decreased 8%. After closure of the arteriovenous shunt, fractional reabsorption increased 6%, while total kidney filtration fraction increased from 0.31 to 0.35. Renal plasma flow decreased from a mean of 111 ml/min to 90 ml/min. Closure of the arteriovenous shunts increased sodium excretion from a mean of 21 mueq/min to 45 mueq/min. Concomitantly, a redistribution of filtrate to superficial nephrons occurred. Since pharmacological doses of DOCA were being administered while total GFR was not increased and fractional reabsorption of sodium in the proximal tubule was not inhibited, it was concluded that filtrate distribution to superficial nephrons may have contributed to the observed natriuresis, although alternate explanations were also deemed possible.

Animals↗
PubMed1989

Dissociation of natriuresis and diuresis and heterogeneity of the effector system of atrial natriuretic factor in rats.

The hypotensive, natriuretic, and diuretic actions of human atrial natriuretic factor-(99-126) (hANF) are accompanied by an elevation of cyclic guanosine monophosphate (cGMP) in plasma and urine. However, the oxidized hANF analogue, human [Met-O110]ANF-(99-126) (Met-O-ANF), has been reported to be unable to increase cGMP (Biochem. Biophys. Res. Commun. 128: 538-546). We employed this oxidized peptide to evaluate the relationship between its biological effects and cGMP generation, with cGMP serving as a marker of the recognized property of ANF to stimulate particulate guanylate cyclase. Met-O-ANF appeared to be a partial agonist, exhibiting a decreasing order of relative potency of hypotensive, vasorelaxant, diuretic, and natriuretic functions compared to hANF. A lower degree of cGMP increases was achieved by this analogue in cultured smooth muscle and endothelial cells. Met-O-ANF doses, which led to a significant increase in diuresis, were neither natriuretic nor accompanied by an increase of urinary cGMP. We were thus able to dissociate the diuretic and natriuretic effects of ANF. High doses of the oxidized analogue were required to elevate cGMP levels in plasma and urine. In isolated kidney fractions, Met-O-ANF's action on cGMP was significantly lower in glomeruli (fivefold less), virtually absent in the collecting duct, yet only slightly different (20% less) in thick ascending limb. Our results indicate that the diuretic and natriuretic effects are exerted at distinct sites, with only the natriuresis being related to an increase of extracellular cGMP. The variability of differential potency of biological and biochemical effects from tissue to tissue of these two forms of human ANF support the notion of the heterogeneity of the ANF effector system.

Animals↗
PubMed1992

Cellular basis for blunted volume expansion natriuresis in experimental nephrotic syndrome.

Experimental nephrotic syndrome results in sodium retention, reflecting, at least in part, an intrinsic defect in renal sodium handling in the distal nephron. We studied the relationships among plasma atrial natriuretic peptide (ANP) concentration, sodium excretion (UNaV), and urinary cyclic GMP excretion (UcGMPV) in vivo, and the responsiveness of isolated glomeruli and inner medullary collecting duct (IMCD) cells to ANP in vitro, in rats with adriamycin nephrosis (6-7 mg/kg body weight, intravenously). 3-5 wk after injection, rats were proteinuric and had a blunted natriuretic response to intravenous infusion of isotonic saline, 2% body weight given over 5 min. 30 min after onset of the infusion, plasma ANP concentrations were elevated in normals and were even higher in nephrotics. Despite this, nephrotic animals had a reduced rate of UcGMPV after the saline infusion, and accumulation of cGMP by isolated glomeruli and IMCD cells from nephrotic rats after incubation with ANP was significantly reduced compared to normals. This difference was not related to differences in binding of 125I-ANP to IMCD cells, but was abolished when cGMP accumulation was measured in the presence of 10(-3) M isobutylmethylxanthine or zaprinast (M&B 22,948), two different inhibitors of cyclic nucleotide phosphodiesterases (PDEs). Infusion of zaprinast (10 micrograms/min) into one renal artery of nephrotic rats normalized both the natriuretic response to volume expansion and the increase in UcGMPV from the infused, but not the contralateral, kidney. These results show that, in adriamycin nephrosis, blunted volume expansion natriuresis is associated with renal resistance to ANP, demonstrated both in vivo and in target tissues in vitro. The resistance does not appear related to a defect in binding of the peptide, but is blocked by PDE inhibitors, suggesting that enhanced cGMP-PDE activity may account for resistance to the natriuretic actions of ANP observed in vivo. This defect may represent the intrinsic sodium transport abnormality linked to sodium retention in nephrotic syndrome.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1982

The relationship between intravascular volume expansion and natriuresis in developing puppies.

The role played by the relative degree of expansion of the intravascular and extravascular compartments in limiting the natriuretic response of fluid-loaded developing animals was determined in 1-, 2-, 3- and 6-wk-old puppies. Volume expansion was induced by infusing either isotonic saline, 10% body weight or isoncotic albumin in saline 5% body weight, and measurements of glomerular filtration rate, sodium excretion, fractional excretion of sodium, and plasma volume were made. Each expansion procedure resulted in an increase in the absolute excretion of sodium at all ages (P less than 0.001). The greatest natriuretic effect was observed in the 3-wk-old puppies, the average of the two solutions being 19, 30, 70, and 28 muEq/min/kg in the 1, 2, 3, and 6-wk-old animals, respectively. The difference in natriuresis among the age groups was due predominantly to differences in the magnitude of the increase in fractional excretion of sodium. At all ages, a greater absolute excretion of sodium was encountered during volume expansion with saline than observed with albumin (P less than 0.05). The intravascular volume increased by a similar % at all ages (P greater than 0.1), and saline and albumin yielded equivalent degrees of intravascular expansion (approximately 50%). The results demonstrate that age-related changes in natriuretic response to volume expansion cannot be attributed to differences in either the degree of expansion or the distribution of the load. In addition, the observations indicate that the mechanism underlying the difference between the response to isotonic saline and isoncotic albumin in saline is already operative at birth, and that it is independent of nephron heterogeneity since the proportion of superficial nephrons must have changed during the period of nephrogenesis. The collecting duct, which is sensitive to both isotonic saline and isoncotic albumin, is likely to be responsible for the parallel development of the renal response to these two methods of intravascular volume expansion.

Albumins↗
PubMed1983

Role of sympathetic nerve activity and natriuresis in the antihypertensive actions of potassium in NaCl hypertension.

Although the precise mechanism of the antihypertensive action of potassium remains controversial, the natriuretic property of potassium is thought to play an important role. Since the renal nerves have been shown to control urinary sodium excretion, the present study was performed to clarify the role of the sympathetic nervous system in the antihypertensive effect of potassium supplements in DOCA-salt hypertensive rats and in salt-sensitive hypertensive patients. Supplements of a 0.2% or a 1% KCl were able to moderate the development of the DOCA-salt hypertension dose-dependently, in combination with natriuresis. Renal norepinephrine turnover was markedly accelerated in the DOCA-salt rats as compared with the control rats, but the potassium supplements normalized it. Eleven patients, who had taken the potassium supplement (96 mEq/day) on a high-sodium diet, showed a lesser increase in mean blood pressure with sodium loading than 12 patients who did not take the potassium supplement. With a high-sodium diet, the potassium-supplemented patients retained less sodium and showed a lesser increase of plasma volume and cardiac output, and their adrenergic nervous activity was relatively lower during the early period of salt loading. Moreover, in salt-sensitive patients the potassium supplement was more effective for preventing a rise in blood pressure with sodium loading than in non-salt-sensitive ones. These results suggest that potassium may attenuate the rise in blood pressure during the DOCA-salt treatment in the rat and during sodium loading in salt-sensitive patients, mainly as a result of inhibiting sodium retention due to increased renal sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effects of renal denervation on pressure-natriuresis in spontaneously hypertensive rats.

To investigate the role of renal sympathetic nerve activity (RSNA) under developing and established hypertension, renal function was studied in chronically renal-denervated and sham-operated male spontaneously hypertensive rats (SHR) and control Wistar Kyoto rats (WKY) at 8 (early hypertensive) and 22 (established hypertensive) weeks of age. To further characterize the renal pressure-natriuresis-diuresis relationship in SHR, renal perfusion pressure (RPP) was reduced by aortic constriction to the level seen in age-matched WKY and the same studies were repeated. After denervation, urinary sodium excretion (UNaV), fractional excretion of sodium (FENa) and urine flow (UF) were increased in 8-week-old SHR (p < 0.01). With the exceptions of UNaV and FENa in denervated 8-week-old SHR, renal cortical blood flow, glomerular filtration rate, UF, UNaV and FENa decreased with the reduction of RPP in all of the SHR groups. These results suggest that RSNA significantly influences renal sodium and fluid handling, thus contributing to the shifting of the arterial pressure-renal sodium excretion curve to the right along the pressure axis and/or to an increase in the steepness of the relationship in 8-week-old SHR. There appeared to be a marked difference in renal sodium handling between 8- and 22-week-old SHR.

Animals↗
PubMed1992

Importance of atrial natriuretic hormone in an exaggerated natriuresis during acute sodium load in primary aldosteronism.

To elucidate the factors which contribute to the exaggerated natriuresis in primary aldosteronism, hemodynamic and hormonal changes induced by saline infusion (at a rate of 0.5 l/h for 3 h) were examined in 6 patients with primary aldosteronism, 13 with essential hypertension, and 8 normotensive subjects. After saline infusion, increases in urinary sodium excretion, glomerular filtration rate, atrial natriuretic hormone, and urinary dopamine excretion along with suppression of plasma renin activity and aldosterone were compared in the three groups. All three groups demonstrated similar increases in glomerular filtration rate, but patients with primary aldosteronism did not show changes in urinary dopamine excretion, plasma renin activity, and aldosterone, despite their increased excretion of sodium. The increase in plasma atrial natriuretic hormone was significantly greater in primary aldosteronism than in essential hypertension or normotensive subjects. No changes in blood pressure or heart rate were seen. These findings suggest that atrial natriuretic hormone might play a role in the exaggerated excretion of sodium in patients with primary aldosteronism.

Aldosterone↗
PubMed1999

Pressure natriuresis in nitric oxide-deficient hypertensive rats: effect of antihypertensive treatments.

Chronic inhibition of nitric oxide (NO) synthesis has been shown to result in arterial hypertension and an important blunting of the pressure diuresis and natriuresis response (PDN). The mechanisms mediating these abnormalities are not completely understood. In the present study, the role of several antihypertensive drugs to ameliorate these alterations was evaluated. The PDN relationships have been evaluated in rats chronically (8 wk) treated with the NO synthesis inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME; 40 mg/kg per d in the drinking water). Appropriate groups of rats were simultaneously treated with the angiotensin II receptor blocker candesartan at a low (1.5 mg/kg per d) and high (2.5 mg/kg per d) dose, with the converting enzyme inhibitor captopril (60 mg/kg per d) and with the calcium channel blocker verapamil (100 mg/kg per d). Chronic treatment with L-NAME significantly elevated mean BP (163.6 +/- 6.5 mmHg versus 105.1 +/- 3.6 in controls), reduced GFR and renal blood flow (RBF), and shifted to the right the PDN responses. Chronic administration of low-dose candesartan, captopril, or verapamil prevented the arterial hypertension and improved renal hemodynamics, but these levels were not completely normalized. High-dose administration also improved renal hemodynamics but induced reduced BP below the levels of control animals. Despite the normalization of the elevated BP, the PDN responses of these hypertensive treated groups were not normalized, and the slopes of the respective diuretic or natriuretic responses were very similar to those of the hypertensive untreated rats. The results indicate that interruption or blockade of the renin-angiotensin system and calcium channel blockade are effective treatments for the NO-deficient arterial hypertension and renal vasoconstriction. However, the PDN responses are not normalized, and this finding suggests that the antihypertensive treatment is not enough to overcome the renal alterations associated with the chronic deficiency of NO.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Adenosine and renal sodium handling: direct natriuresis and renal nerve-mediated antinatriuresis.

Adenosine infusion is associated with natriuresis as well as antinatriuresis. The physiologic significance of these opposite effects is unknown but may have to do with different conditions of ischemia, in which adenosine accumulates. These effects were characterized in the rat. First, intrarenal and systemic infusions within one animal were performed. Infusing 10 micrograms/min into the left renal artery increased sodium by approximately 50%; however, the subsequent infusion of 50 micrograms/min into the thoracic aorta decreased sodium excretion by approximately 60%, in association with a small reduction of blood pressure. Second, to explore the effect of intrarenal adenosine in tubular sodium handling, free-flow micropuncture experiments were performed. The intrarenal infusion of 10 micrograms/min again caused sodium excretion, but no change in GFR, volume, and sodium deliveries up to the early distal tubule was found. Apparently, the direct effect of adenosine in the kidney is sodium excretion, by a tubular action beyond the early distal tubule. Third, to further characterize the indirect effect, which apparently is sodium retention, adenosine was infused systemically at low rates, in order to avoid a decrease in blood pressure. A 25 micrograms/min infusion again caused sodium retention, in the absence of a fall in blood pressure. After acute left renal denervation, the antinatriuretic effect disappeared in the denervated kidney but remained in the right kidney. These data suggest that increased intrarenal adenosine suppresses sodium reabsorption at some distal nephron site, appropriately decreasing the workload of the kidney. On the other hand, systemic adenosine stimulates sodium reabsorption, an effect that is appropriate to improve systemic circulation and depends on the renal nerves.

Adenosine↗
PubMed1998

A possible molecular basis of natriuresis during ischemic-reperfusion injury in the kidney.

Ischemic renal injury is associated with increased fractional excretion of sodium, suggesting a Na+ reabsorption deficiency in renal tubules. To determine whether alterations in expression of the major Na+ transporter genes might contribute to the natriuresis that follows ischemic acute renal failure, the expression of these genes was analyzed in renal cortex and medulla after ischemic-reperfusion injury. Rats were subjected to 30 min of renal pedicle clamping and then sacrificed at 12, 24, or 48 h after reperfusion. Serum creatinine increased significantly at 12 and 24 h, indicative of acute renal failure, but decreased substantially by 48 h. mRNA levels for the NHE-3 Na/H exchanger of the proximal tubule, the apical Na-K-2Cl cotransporter of the thick ascending limb of Henle, the Na-Cl cotransporter of the distal convoluted tubule, the epithelial Na+ channel of the collecting duct, and the basolateral Na(+)-K(+)-ATPase were measured by Northern hybridization. NHE-3 mRNA decreased by approximately 75% at 12 h and remained suppressed at 24 and 48 h after reperfusion. Na-K-2Cl cotransporter mRNA decreased by approximately 88% at 12 h and remained suppressed at 24 and 48 h. Na-Cl cotransporter mRNA remained unchanged at 12 h, decreased by approximately 60% at 24 h, and returned to almost control levels at 48 h. mRNA levels for sodium channels (beta subunit) remained unchanged. Na(+)-K(+)-ATPase mRNA in the medulla decreased by approximately 35 to 40% at 12 and 24 h and by 70% at 48 h, whereas in cortex it decreased by only < 15% at 12 or 48 h after reperfusion. These results suggest that sharp reductions in expression of the NHE-3 Na/H exchanger and the apical Na-K-2Cl cotransporter are major factors in the natriuresis/diuresis that is one of the hallmarks of ischemic acute renal failure. Lasting suppression of these transporters, despite improvement in renal function, could contribute to the deranged NaCl and water excretion that often leads to volume depletion during recovery from ischemic acute renal failure.

Analysis of Variance↗
PubMed1984

Renin-angiotensin-aldosterone system in exaggerated natriuresis of chronic glomerulonephritis.

Angiotensin II (AII) and aldosterone (Aldo) in plasma, blood pressure (BP) and urinary excretion of sodium were studied before, during and in two periods after intravenous sodium loading with 500 ml of sodium chloride solution (50 g/l) in 11 normotensive and 10 hypertensive patients with histologically verified chronic glomerulonephritis and creatinine clearance in the range from 11 to 167 ml/min, and in 10 normotensive control subjects. The absolute increase of sodium excretion during loading was higher in the patients grouped together and in the hypertensives alone, but not in the normotensive patients when compared with the control subjects. No correlation was found between sodium excretion and control mean BP or change in mean BP during loading. AII and Aldo were suppressed during loading in both patients and control subjects. In the patients but not in the control subjects the increase of sodium excretion correlated positively with pre-infusion value of AII and negatively with change in AII during the sodium loading. No correlation was found between sodium excretion and Aldo and changes of Aldo. In conclusion, the results might suggest that the renin-angiotensin system is involved in the regulation of exaggerated natriuresis in chronic glomerulonephritis.

Adult↗
PubMed1993

Proximal renal tubular pressure-natriuresis-relation in essential hypertensives following acute vasodilatation.

Blood pressure (BP) and excretory function including lithium clearance were investigated during water-loading and constant infusion of 131I-hippuran and 125I-iothalamate for measurement of renal haemodynamics in 8 untreated essential hypertensives (mean BP +/- SD: 169 +/- 14/107 +/- 6 mmHg) before and after vasodilatation with an i.v. bolus of the potassium-channel opener, pinacidil, 0.01 mg/kg. Systolic BP (-7 +/- 4%; p < 0.05) and diastolic BP (-13 +/- 8%; p < 0.01) decreased significantly and heart rate increased (11 +/- 8%; p < 0.01). Clearance (C) of lithium, sodium, urinary flow rate, potassium and absolute distal reabsorption of sodium all fell significantly. The changes of these variables were significantly correlated with the fall in BP (CLi:r = 0.92, CNa: r = 0.85, V: r = 0.81, CK:r = 0.84), despite no significant changes in renal haemodynamic parameters: glomerular filtration rate, renal plasma flow and renal vascular resistance. A proximal tubular effect was also indicated by a fall in Curic acid and fractional Curic acid. In conclusion, vasodilatation in essential hypertensives following administration of the potassium channel opener, pinacidil, induces a fall in blood pressure with a corresponding fall in fractional proximal tubular excretion of sodium and output of sodium and water from proximal to distal tubular segments, proposing an acute proximal tubular pressure-natriuresis relation.

Adult↗
PubMed1995

Partial purification of a factor from the feline small intestine causing natriuresis in vivo and inhibiting rubidium uptake into renal cells in vitro.

Small intestine of cat was homogenized under denaturing condition (6.0 M guanidinium chloride) in the presence of protease inhibitors and molecules in the 500 to 10,000 Da mass range were obtained by sequential ultrafiltrations. This material was separated by gel chromatography (Sephadex G-25), where fractions eluted in the mass range of 500-1000 Da inhibited 86Rb uptake into kidney slices in vitro. Furthermore, the same fractions exhibited a natriuretic effect when given intravenously to anesthetized rats. The gel chromatography fractions were further purified by cation exchange chromatography (CM-Sephadex C-25). Fractions eluted with a NaCl solution of around 250 mM inhibited 86Rb uptake into renal cortical tissue in vitro and showed natriuretic activity when tested in vivo in rats. It is proposed that intestine contains a water soluble natriuretic factor with an apparent molecular mass of 500-1000 Da. This material evokes a natriuresis in vivo and inhibits 86Rb uptake in vitro.

Animals↗