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PubMed1976

Prostaglandins and renal function in acute extracellular volume expansion.

Mechanisms determining the natriuresis in ECV-expansion are not yet completely understood. The present study was therefore undertaken to investigate if prostaglandins (PG) are involved in the natriuresis of acute ECV-expansion and by which mechanisms PG may affect renal Na-absorption. In non-expanded rats the PG synthetase inhibitor indomethacin (INDO) had no effect on renal function. In 37 Sprague-Dawley rats ECV-expansion with isotonic saline corresponding to an increase in b.wt. of 10% was induced. Twenty-one animals received an oral dose of 10 mg/kg b.wt. of INDO prior to ECV-expansion. Sixteen animals served as ECV-expanded controls (C). GFR (INDO: 12.5 +/- 1.0; C: 10.5 +/- 0.9 ml/min/kg b.wt.) did not significantly differ in both groups. However, total renal plasma flow (RPF) (INDO: 22.9 +/- 1.8; C: 30.1 +/- 2.7 ml/min/kg b.wt.), urinary flow rate (INDO: 1.11 +/- 0.20; C: 1.93 +/- 0.21 ml/min/kg b.wt.) and urinary excretion of sodium (INDO: 141 +/- 26; C: 267 +/- 46 muEq/min/kg b.wt.) and potassium (INDO: 13.0 +/- 0.9; C: 19.8 +/- 1.7 muEq/min/kg b.wt.) markedly decreased in animals pretreated with INDO. The results indicate that PG are involved in the natriuresis of acute ECV-expansion and suggest, that PG may inhibit the intrinsic capacity for Na-absorption in more proximal parts of the nephron possibly via intrarenal physical factors.

Animals↗

PubMed2002

Renal medullary blood flow and salt load in Lyon hypertensive rats.

The present work studied renal medullary blood flow (MBF) and its response to salt load in Lyon hypertensive (LH) rats to understand the mechanisms underlying the abnormal renal sodium excretion exhibited by LH rats. Experiments were conducted in uninephrectomized, anesthetized, and volume-expanded 15-week-old male LH and their normotensive (LL) controls. Under standard diet, LH rats exhibited a blunted pressure diuresis and natriuresis associated with an absence of pressure-induced increase in MBF compared to LL rats. One week of salt load (2% NaCl as drinking water) induced a significant increase in blood pressure (BP) in LH (+11 mm Hg) than in LL (+6 mm Hg) rats associated with a decrease in MBF in LH rats only (from 182 +/- 25 to 122 +/- 20 perfusion units, P < .001). Finally, despite the salt load-induced increase in pressure natriuresis, it remained significantly lower in LH than in LL rats. The results show an alteration in MBF regulation in LH rats and suggest that this abnormality may be involved in their blunted pressure natriuresis and their enhanced salt sensitivity.

Animals↗

PubMed1982

Effect of acute unilateral renal denervation on intrarenal haemodynamics and urinary excretion in rats before and during hypervolaemia.

1. The possible involvement of renal nerves in the diuresis and natriuresis of blood volume expansion was studied in anaesthetized rats. Acute unilateral renal denervation caused increased excretion of fluid, sodium and potassium. 2. Renal blood and plasma flows were elevated without change in filtration rate. Intracortical blood flow distribution was not affected by the denervation. 3. Blood infusion caused diuresis, natriuresis and kaliuresis in both denervated and sham-denervated kidneys, associated with comparable initial increases in filtration and decreases in renal blood flow. No change in flow distribution was found, whether or not renal nerves were intact. 4. Although the magnitude of the excretory response to hypervolaemia was greater in denervated kidneys, the temporal pattern was identical with that of sham-operated kidneys. Our data thus do not show an effect of efferent renal nerve activity on volume natriuresis.

Animals↗

PubMed1991

How important are suppression of aldosterone and stimulation of atrial natriuretic peptide secretion in the natriuretic response to an acute sodium load in man?

1. Aldosterone is suppressed by sodium loading. We studied the contribution of this decrease in plasma aldosterone to the natriuresis after acute sodium loading in healthy volunteers. 2. Two litres of saline [0.9% (w/v) NaCl] were infused during the second hour of a 6 h infusion of aldosterone (3 pmol min-1 kg-1) or placebo in eight healthy young men. On the placebo day, plasma aldosterone decreased by 30 min after the start of saline infusion and remained suppressed. During aldosterone infusion, plasma aldosterone was maintained at around 400 pmol/l. 3. Urinary sodium excretion, lithium clearance and plasma atrial natriuretic peptide increased and plasma renin activity decreased after saline infusion, whether or not aldosterone was infused. However, from 60 to 240 min after saline infusion, natriuresis was significantly less during aldosterone infusion than on the placebo day. In addition, saline loading led to a progressive increase in the ratio of sodium clearance to lithium clearance, used as an index of the fractional distal tubular rejection of sodium, and in the ratio of urinary sodium to potassium. These increases were prevented by the infusion of aldosterone. 4. This study suggests that there are differences in the mechanisms determining the early and the later responses to an acute sodium load. Suppression of aldosterone may explain much of the later increase in natriuresis after saline infusion. In addition, the results are consistent with a role for atrial natriuretic peptide in the immediate increase in sodium excretion after saline loading.

Adult↗

PubMed1999

Role of androgens in mediating hypertension and renal injury.

1. Men are generally at greater risk for cardiovascular disease than are women, particularly with regard to enhanced progression of hypertension and loss of renal function. Despite these gender differences in the progression of hypertension and renal disease in humans and animals, the mechanisms responsible are unknown. 2. Castration in males has been shown to slow the progression of hypertension and ameliorate the loss in renal function. When serum testosterone was measured in the developing male spontaneously hypertensive rat (SHR), the peak serum testosterone level at 12 weeks coincided with the time when differences in systolic blood pressure could be measured between intact male SHR and females or castrated male SHR. Ovariectomy does not affect blood pressure in female SHR but testosterone treatment of ovariectomized females for 5 weeks results in exacerbation of hypertension almost to the level found in intact male SHR. These data strongly suggest a role for androgens in mediating the gender differences in hypertension. 3. The mechanisms by which androgens could increase blood pressure are not known. We have recently shown that, at comparable renal perfusion pressures, there is a hypertensive shift in the pressure-natriuresis relationship in male SHR compared with females or castrated male SHR. Testosterone treatment of ovariectomized female SHR also causes a rightward shift in the pressure-natriuresis relationship. 4. We hypothesize that androgens increase arterial pressure by causing a hypertensive shift in the pressure-natriuresis relationship, either by having a direct effect to increase proximal tubular reabsorption or by activation of the renin-angiotensin system. We also hypothesize that the enhanced proximal tubular reabsorption leads to a tubuloglomerular feedback-mediated afferent vasodilation, which, in combination with the increase in arterial pressure, results in glomerular hypertension and renal injury.

Androgens↗

PubMed1999

Renal nerve and alpha 2-adrenergic action during acute volume expansion in the anaesthetized rat.

1. The effects of renal denervation and alpha 2-adrenoceptor blockade on diuresis and natriuresis in response to acute volume expansion (VE) were investigated in anaesthetized rats. 2. In normal rats, a 30 min intravascular VE of up to 7.5% of bodyweight caused a significant diuresis and natriuresis. 3. Denervation enhanced the diuretic effect of VE by 39%, while alpha 2 blockade by 12 mumol/kg per h rauwolscine significantly inhibited the response by 61% in innervated kidneys and 43% in denervated kidneys. 4. Similar results were found for natriuresis in both innervated and denervated kidneys. 5. The results demonstrate that renal sympathetic nerve activity inhibits part of the increase in sodium and water excretion caused by VE, since denervation increased excretion under these conditions. The contribution of renal nerves to the control of renal function, however, decreases during the response to VE. 6. alpha 2-Adrenoceptor action enhanced the diuretic and natriuretic effects of VE by mechanisms otherwise unrelated to renal nerve activity.

Anesthesia↗

PubMed2001

Effects of L-arginine and furosemide on blood pressure and renal function in volume-expanded rats.

1. The aim of the present study was to investigate the effects of L-arginine (L-Arg) on blood pressure and water and electrolyte excretion in control and extracellular fluid volume-expanded rats (10% bodyweight with 0.9% NaCl) and to determine whether diuretic treatment with furosemide (FUR) can be optimized by the administration of L-Arg in this model. 2. Both groups of animals were anaesthetized, divided into groups and treated with either 7.5 mg/kg FUR, 250 mg/kg L-Arg, 1 mg/kg NG-nitro-L-arginine methyl ester (L-NAME), FUR + L-NAME or FUR + L-Arg. Mean arterial pressure (MAP), diuresis, natriuresis and kaliuresis were determined. 3. Extracellular fluid volume expansion induced no changes in MAP in control and volume-expanded rats (92+/-6 vs 100+/-8 mmHg, respectively). The hypotension induced by FUR in control and volume-expanded rats (69+/-7 and 76+/-5 mmHg, respectively) was significantly (P < 0.01) enhanced by the administration of L-Arg (54+/-3 and 64+/-3 mmHg, respectively). 4. Injection of L-NAME increased MAP and diminished diuresis, natriuresis and kaliuresis in both groups. 5. Furosemide-induced water and electrolyte excretion was blunted by the administration of L-NAME. 6. The combination of L-Arg + FUR increased diuresis induced by FUR alone (control rats: 29.33+/-1.68 vs 12.91+/- 0.41 microL/min per 100 g, respectively; volume-expanded rats: 248.5+/-25.4 vs 112,6+/-8.3 microL/min per 100 g, respectively; P < 0.01). 7. The administration of the combination of L-Arg + FUR promoted a decrease in the sodium/water excretion ratio compared with the administration of FUR alone (control rats: 0.230+/-0.018 vs 0.45+/-0.03, respectively, P < 0.001; volume-expanded rats: 0.091+/-0.010 vs 0.22+/-0.03, respectively, P < 0.01). 8. The potassium/water excretion rate induced by FUR alone and in the presence of L-Arg followed a pattern similar to that seen for natriuresis (control rats: 0.35+/-0.05 vs 0.20+/-0.05 microEq/min per 100 g, respectively; volume-expanded rats: 0.045+/-0.008 vs 0.014+/-0.003 microEq/min per 100 g, respectively; P < 0.01). 9. The decrease in the electrolyte/water excretion ratio observed with FUR + L-Arg in volume-expanded rats was greater than in control animals. 10. The results of the present study show that the administration of FUR with L-Arg contributes to enhanced hypotensive and diuretic effects of FUR, thus diminishing the relative electrolyte excretion in normal conditions and in extracellular fluid volume expansion.

Animals↗

PubMed2001

Level of hydration and renal function in healthy humans.

BACKGROUND: High hydration is commonly used in renal studies to improve the completeness of urine collection. The renal effects of hydration are not well defined. METHODS: Renal function was studied under fasting conditions (baseline) and after a meat meal (2 g of protein/kg body weight) in 12 healthy adults on a low and high hydration regimen of 0.5 and 4 mL of oral water per kg body weight/30 min, respectively. RESULTS: Urine flow, urinary and plasma Na, K, urea, and osmolality were stably different on low and high hydration regimens. At baseline, there were significant or borderline significant correlations of plasma and urine osmolality with glomerular filtration rate (GFR; inulin clearance) only in the low hydration regimen. GFR was higher in the low than the high hydration regimen at all time points. The difference was significant at baseline (19.2%) and at 90 to 180 minutes after the meal (14.4%). After the meal, GFR increased significantly over baseline values only in the high hydration regimen (30.0% at peak time). Urinary excretion of Na, urea, and osmoles was lower in the low than the high hydration regimen at all time points: The difference was significant for Na (at baseline) and osmoles (all time points). Urinary K excretion was not different in the two regimens. After the meal, there were significant increases in urinary excretion of Na (in the low hydration regimen) and urea (90 to 180 min after the meal). CONCLUSIONS: In fasting adults, high hydration lowered GFR and increased natriuresis. After a meat meal, GFR increased only in the high hydration regimen and natriuresis only in the low hydration regimen. Hydration affects GFR and natriuresis under fasting conditions and after a meat meal.

Adult↗

PubMed1997

[Low dosage dopamine improves kidney function: current status of knowledge and evaluation of a controversial topic].

The ability of low dose dopamine (1-3 micrograms x kg-1 x min-1) to cause selective renal vasodilation, to increase glomerular filtration rate, urine output, and natriuresis, is intuitively considered favourable. Dopamine, therefore, continues to be used in critically ill patients to preserve or improve renal function. Despite its application in a wide variety of disease states and in patients at risk of acute renal failure or with already decreased renal function, there is no conclusive evidence that "renal doses" of dopamine prevented acute renal failure or had any positive effect on patient outcome although it increased urine output and natriuresis consistently. Data from many clinical studies, however, are difficult to interpret due to small numbers of patients, the absence of control groups, the inability to exclude changes in cardiac output or to separate a diuretic effect of dopamine in the tubulus system from specific increases of glomerular filtration rate, and because of the variability of methods to determine renal performance (i.e. creatinine clearance, urine output, natriuresis, fractional excretion of sodium). Moreover, the routine use of dopamine is not innovous, since it may worsen gut ischaemia and suppress certain hormonal systems. Those who believe in the clinical benefits of "renal dose" dopamine argue that, even in the absence of an improvement in renal function, the maintenance of urine output could be useful in patients unresponsive to diuretics. Again, the clinical benefit of this diuretic action still needs to be shown. In conclusion, there is little justification for the routine administration of low-dose dopamine in patients at risk of renal failure. Large controlled clinical studies are urgently needed to determine whether dopamine improves renal function or prevents acute renal failure in patients at risk.

Acute Kidney Injury↗

PubMed1990

Renal responses to immersion and exercise in pregnancy.

Twelve healthy pregnant women were studied at 15, 25, and 35 weeks' gestation and at 8 to 12 weeks postpartum. Women were immersed for 20 minutes at 30 degrees C. They then exercised at 60% maximum oxygen capacity on a modified ergometer. Substantial diuresis and natriuresis occurred without changes in osmolarity or serum sodium. The diuresis was significantly greater during pregnancy than postpartum. The natriuresis was similar. Diuresis and natriuresis were greater than would be expected from investigations in nonpregnant subjects. This study suggests that immersion may be a beneficial therapy for edema without decreasing plasma volume.

Diuresis↗

PubMed2000

The role of intrarenal nitric oxide in the natriuretic response to dopamine-receptor activation.

Dopamine and dopamine-1 receptor agonists produce diuresis and natriuresis by causing changes in renal hemodynamics and by the activation of dopamine-1 receptors located within the various regions of the nephron. Nitric oxide plays an important role in the maintenance of systemic and regional hemodynamics. The present study was undertaken to investigate the effect of locally generated nitric oxide on renal function and its potential influence on the renal responses to dopamine-1 receptor agonists. The intrarenal infusion of a nitric oxide synthase inhibitor, L-NAME, (50 microg/kg min for 90 min) in anesthetized rats produced significant decreases in urine volume, urinary sodium excretion, glomerular filtration rate and fractional sodium excretion. These changes in renal function were associated with a concomitant decrease in urinary nitrate excretion, an indicator of nitric oxide release. However, L-NAME at this dose did not produce any significant changes in mean arterial pressure or heart rate. Intravenous infusion of fenoldopam (1 microg/kg min for 30 min), a selective dopamine-1 receptor agonist, produced diuresis and natriuresis without causing any changes in mean arterial pressure and heart rate. These renal effects of fenoldopam were significantly attenuated in animals that received the simultaneous infusion of L-NAME (intrarenal). Similar results were obtained with dopamine in that the natriuretic and diuretic response to dopamine was also attenuated during simultaneous infusion of dopamine with L-NAME. In addition, the diuresis and natriuresis produced by fenoldopam and dopamine was associated with increases in urinary nitrate excretion. Interestingly, these increases in the nitrate levels seen with fenoldopam and dopamine were also significantly reduced in the presence of L-NAME. These results indicate that intrarenal nitric oxide plays an important role in regulating renal sodium excretion and that an intact renal nitric oxide system is required for the full expression of diuretic and natriuretic response seen during dopamine-1 receptor activation.

Animals↗

PubMed1993

Natriuretic and kaliuretic response to potassium load: modulation by sodium intake.

Potassium (K) loading is followed by a rapid increase in sodium (Na) and K excretion. To evaluate the influence of Na intake on this effect, we studied the acute natriuretic and kaliuretic response to a single oral K load (100 mmol) in six healthy volunteers equilibrated on a 10-, 100-, and 400-mmol Na intake. Compared to the 100-mmol Na intake, the 400-mmol Na intake greatly enhanced the natriuretic effect of the K load; during the 10-mmol Na intake no natriuresis but even some Na retention occurred. The kaliuretic effect was not significantly changed and occurred at similar values of plasma K. Plasma aldosterone was suppressed during the 400-mmol Na diet and stimulated during the 10-mmol Na diet, but the relative increments after the KCl load did not differ among the three diets. In conclusion, whereas the effect of a K load on kaliuresis is relatively independent of Na intake, its effect on Na excretion varies from marked natriuresis to slight Na retention. The Na retention is probably due to acute K-induced aldosterone stimulation, and the natriuresis to K-induced increase in distal Na delivery not utilized to promote K excretion. Apparently, the integration of renal Na and K handling after a K load is such that K balance is maintained at the cost of Na balance.

Adolescent↗

PubMed1988

Role of vasopressin in regulation of sodium excretion.

It has been proposed that arginine vasopressin (AVP) contributes to the regulation of renal sodium excretion by direct intrarenal actions, by neural-hormonal interactions, and via secondary effects of fluid volume retention. The present studies were designed to determine the extent to which the natriuretic effects of AVP are secondary to volume expansion. Three groups of dogs were studied: the first was infused with AVP for 2 weeks in amounts that increased plasma levels from 3 to 15 pg/mL, while water intake was maintained constant by intravenous (iv) water infusion. The second group received the same amount of AVP and was permitted to drink ad libitum. The third group was infused with the same amount of AVP, while total body weight and volume were maintained at a constant level by use of an electronically servo-controlled water infusion system. The results showed a large increase in total body weight (+1.5 kg) and arterial pressure (mean arterial pressure (MAP); +40 mm Hg) in dogs receiving a fixed water intake. This was accompanied by a continuing natriuresis over a 2-week period and severe hyponatremia (115 mEq/L). Dogs allowed ad libitum drinking retained much less fluid (+0.5 kg). MAP was not significantly elevated, and natriuresis did not occur in this group, but hyponatremia was observed (130 mEq/L), and plasma renin activity (PRA) was suppressed. Servo-controlled dogs exhibited no change in MAP, plasma sodium, or PRA, and only a small (-15 mEq) natriuresis occurred on day 1 of AVP infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Diuretic and natriuretic properties of fenoldopam in chronic renal failure.

The effect of intravenously administered fenoldopam on diuresis and natriuresis was investigated in a group of 10 patients with advanced chronic renal failure. After an initial basal period of 1 h, a fenoldopam infusion was started and maintained for 12 h at rates varying between 0.025 and 0.1 microgram/kg per min. During the study, blood pressure was measured every 10 min and urine volume, natriuresis and creatinine clearance were measured hourly. Fenoldopam induced a significant increase in urine volume, natriuresis and creatinine clearance (P less than 0.05-0.001) accompanied by a small but significant drop in blood pressure (P less than 0.05-0.01). These results show that for advanced chronic renal failure, fenoldopam has diuretic and natriuretic properties that could be of clinical relevance.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1993

The relationship between blood pressure and sodium and potassium excretion during the day and at night.

OBJECTIVE: The relationships between blood pressure and the urinary excretion rates of sodium and potassium during the day and at night were investigated. METHODS: A total of 160 participants (135 normotensive subjects and 25 untreated patients with essential hypertension) were examined using ambulatory blood pressure monitoring and timed urine collections during waking and sleeping hours. RESULTS: Blood pressure averaged 126/79 mmHg during waking hours and 107/62 mmHg during sleep. More sodium, potassium and aldosterone were excreted during the daytime, but the natriuretic substance kallikrein was excreted at a fixed rate throughout the 24 h. During waking hours there was poor correlation between blood pressure and urinary sodium and potassium excretion. By contrast, at night when the aldosterone: kallikrein ratio fell, the sodium and potassium excretion rates were positively correlated with blood pressure. CONCLUSIONS: Pressure natriuresis, not apparent during waking hours, may be unmasked at night when the balance between sodium-retaining and sodium-losing mechanisms favours natriuresis. Thus, the relationship between blood pressure and 24-h sodium excretion, usually considered to show the influence of salt intake on blood pressure, may also reflect pressure-induced natriuresis, if urine is more completely collected at night than during the day, and in circumstances favouring sodium retention during the day and sodium loss during sleep.

Adult↗

PubMed1993

Angiotensin converting enzyme inhibition does not prevent the natriuretic effect of felodipine.

The mechanism of natriuresis with calcium entry blockers such as felodipine is largely unexplained. As these drugs prevent sodium retention following exogenous angiotensin II, the natriuretic effect of felodipine might be due to a similar interaction with endogenous angiotensin II. In such a case, angiotensin converting enzyme inhibition with ramipril should prevent natriuresis with felodipine. We tested this hypothesis in a randomized, double-blind, crossover study in 12 male volunteers by comparing intravenous felodipine after 1 week of oral ramipril with felodipine after placebo and with solvent after ramipril. Ramipril pretreatment reduced ACE activity to 11 +/- 1%, lowered the blood pressure, and increased renal blood flow. However, ramipril pretreatment did not prevent the pronounced increase in natriuresis and diuresis with felodipine. Fractional sodium excretion only tended to increase less during felodipine after ramipril than during felodipine after placebo (absolute changes of + 1.2 +/- 0.2 and + 1.7 +/- 0.2%, respectively; p = 0.07). Ramipril did not influence the felodipine-mediated blood pressure reduction and renal vasodilation. In conclusion, ACE inhibition has no significant effect on the natriuretic and hemodynamic effects of felodipine, suggesting that mechanisms other than interaction with endogenous angiotensin II are involved in these effects of calcium entry blockers.

Adult↗

PubMed1993

Digitalis-like factor and ouabain-like compound in plasma of volume-expanded dogs.

Previous studies demonstrated that ouabain-like compound (OLC) is widely distributed in mammalian species and is found in a variety of different tissues. Although much evidence suggests that OLC is endogenous to mammals, little information is available concerning physiological and/or pathophysiological roles for OLC. In this study, generic endogenous digitalis-like factor (E-DLF) was measured using an enzyme bioassay and the more specific OLC was determined using ouabain antisera in plasma drawn from dogs before and 30 and 120 min after massive volume expansion with isotonic saline. Plasma OLC was not changed by the saline load, whereas Na excretion was significantly elevated at the 30-min blood draw and remained elevated at the 120-min blood draw. Because renal exposure to OLC did not change with saline loading, it is unlikely that any portion of the profuse natriuresis in these animals could be attributed to OLC. In contrast, plasma E-DLF was higher after the saline load than before in each of four dogs at 30 and 120 min after the infusion. What portion of the profuse natriuresis can be attributed to E-DLF is unknown, although it is reasonable to assume that nanomolar levels of pump inhibitor contributed to the natriuresis to some degree.

Animals↗

PubMed1996

Interactions between arterial pressure and sodium excretion.

Recent developments have led to renewed interest in the mechanisms that mediate the changes in sodium excretion in response to changes in arterial pressure, a phenomenon termed pressure-natriuresis. Pressure-natriuresis occurs in the absence of changes in filtered load and thus, the changes in sodium excretion are caused by changes in net tubular sodium reabsorption. Both proximal and distal nephron segments have been implicated as the sites of altered reabsorption. The specific mechanism responsible for pressure-natriuresis remains unresolved. One proposal suggests that changes in renal interstitial fluid pressure which may be due, in part, to a less efficient autoregulation of the renal medullary circulation than of the cortex, alter sodium reabsorption. Alternatively, recent studies indicate that increases in arterial pressure increase endothelial nitric oxide formation which inhibits sodium reabsorption via direct effects on the tubules as well as hemodynamically mediated effects.

Animals↗