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PubMed1986

Dopamine receptor blockade does not affect the natriuresis accompanying sodium chloride infusion in dogs.

Intravenous (IV) saline infusions cause parallel increments in urinary excretion of dopamine (DA) and sodium. Exogenous administration of DA exerts a natriuretic effect by action on DA receptors. The possibility that DA mediates the natriuretic response to saline infusion was studied by infusing 0.9% saline solution IV (60 ml/kg) in conscious dogs with and without selective blockade of DA1 and DA2 receptors. With no antagonist, the total increase in sodium excretion during the 120-minute saline infusion and the 60 minutes after the saline infusion was 99.5 +/- 7.6 mmol. The increase in total sodium excretion was not affected by IV infusion of the selective DA1 antagonist SCH 23390 in doses of 0.5 micrograms/kg/min and 5 micrograms/kg/min. The total increment in sodium excretion produced by saline was also unaltered by large doses (1 micrograms/kg/min and 10 micrograms/kg/min) of the selective DA2 antagonist domperidone. Our results do not support a role of DA as a mediator of saline-induced natriuresis in the dog.

Animals↗

PubMed1986

The effects of selective and non-selective inhibition of cyclo-oxygenase on frusemide-stimulated natriuresis.

The relative potency of four non-steroidal anti-inflammatory drugs (NSAIDs) - indomethacin, flurbiprofen, sulindac and piroxicam - in inhibiting frusemide-stimulated natriuresis and creatinine clearance was investigated in a placebo controlled cross-over study using healthy volunteers. All four drugs tested significantly inhibited the action of frusemide and they were equipotent in their effects. If it is accepted that sulindac is renal sparing with respect to inhibition of prostaglandin synthesis, our observations raise two possibilities concerning the underlying mechanism of antagonism: a) that inhibition of renal prostaglandin synthesis is not important; b) that sulindac interacts with frusemide in a manner different from other NSAIDs.

Adult↗

PubMed1988

Dehydration natriuresis in Dahl S rats: no evidence for renal excretory deficit.

There is conflicting evidence for the existence of a renal sodium excretory deficit in the salt-sensitive hypertensive Dahl S (DS) rat strain. While presentation of acute sodium loads, in vivo or in vitro, suggests that DS kidneys cannot excrete sodium as efficiently as kidneys from the salt insensitive genetic control Dahl R (DR) rat strain, metabolic studies of Dahl rats on a high-sodium diet are unable to differentiate between DS and DR rats. The natriuretic response to acute sodium loads is dependent on the integrity of structures in or near the anteroventral 3rd ventricle (AV3V) region. Therefore, it was thought that an AV3V-dependent chronic sodium challenge might also uncover an excretory defect in DS rats. We have investigated the renal response of inbred Dahl S (SS/Jr) and Dahl R (SR/Jr), and Sprague-Dawley rats to 48 h of dehydration; a manoeuvre which produces hyperosmolality and hypernatremia, with its renal response dependent on the integrity of the AV3V. Inbred Dahl S, Dahl R and Sprague-Dawley rats showed identical renal electrolyte excretory responses to both dehydration and rehydration. These results are discussed in terms of the mechanism of salt-induced hypertension and dehydration natriuresis.

Animals↗

PubMed1987

The carotid body and natriuresis: effect of almitrine bismesylate.

Almitrine bismesylate is a peripheral chemoreceptor agonist. When given intravenously to anaesthetized rats it results in a reversible diuresis and natriuresis. The effect is abolished by denervation of the carotid bodies and is still present following vagotomy, when the animal is paralysed and artificially ventilated or following bilateral adrenalectomy. Denervation of the carotid bodies results in a lower resting sodium excretion. In chronically hypoxic rats which have enlarged carotid bodies the natriuretic response to almitrine is grossly diminished.

Adrenal Glands↗

PubMed1986

Tubular sites of furosemide natriuresis in volume-replaced and volume-depleted conscious rats.

There is accumulating evidence that the renal Li clearance reflects the delivery of Na and volume out of the proximal tubules. In the present study we used the Li clearance technique to evaluate the effects of submaximal furosemide (Fur) infusion (7.5 mg/kg/hr) on proximal and distal Na reabsorption in conscious rats with and without volume replacement with saline. Li was given as an p.o. test dose (0.5 mmol/kg) and [3H]inulin was infused in saline to measure the glomerular filtration rate (GFR). In control rats not infused with F, fractional Na excretion was about 1% and fractional Li excretion was about 30 to 35%. Infusion of F with constant rate and volume replacement increased fractional Na excretion to 22% and fractional Li excretion to 57% associated with a small decrease of the GFR. Without volume replacement F infusion caused a smaller and temporary diuretic and natriuretic response (maximum fractional Na excretion = 7.5%) followed by a decrease of urine flow and Na excretion almost to control levels, despite continued high excretion rates of F. The GFR decreased by 25% and fractional Li excretion showed an initial increase followed by return to baseline levels. The results suggest that in conscious rats submaximal doses of F cause major inhibition of proximal tubular Na reabsorption, which effect contributes substantially to the initial natriuresis. Along with diuretic-induced volume contraction, the natriuretic response is abolished due to a fall in GFR and particularly due to a secondary increase in fractional Na reabsorption, which occurs both in proximal distal tubular nephron segments.

Animals↗

PubMed1977

Influence of acute hypophysectomy on the natriuresis of dogs submitted to expansion of the extracellular fluid volume.

Three days after creating an access to the turcica on the sphenoid bone, twelve anesthetized mongrel dogs, after control collections, were submitted to extracellular volume expansion with saline. Thereafter, maintained constant the rate of saline infusion, the dura-mater covering the pituitary gland was incised in all dogs, the hypohysis being removed in seven and remaining untouched in the other five dogs. Pharmacological doses of pitressin, glycocorticoids and mineralocorticoids were administered to all dogs. It was shown, for the same filtered sodium load(p is greater than 0.05), that hypophysectomy produces a significant reduction (p is less than 0.05) in urinary sodium excretion previously elevated by the extracellular volume expansion, while durostomy only, without removal of th hypophysis, did not change (p is greater than 0.05) the rate of sodium excretion. Thus, the pituitary gland could be considered as contributing to natriuresis during extracellular volume expansion, all other factors related to this expansion remaining constant in both, hypophysectomized and sham operated dogs.

Animals↗

PubMed1982

Natriuresis and renal Na-K-ATPase activity in kidneys of normotensive and spontaneously hypertensive rats.

The isolated perfused kidneys of spontaneously hypertensive (SHR) rats aged 10-12 weeks (early hypertensive phase) exhibited pressure natriuresis curves already shifted to the right, as compared with kidneys of the normotensive Wistar rats and Wistar-Kyoto rats. Sodium excretion in relation to tubular sodium load was higher in kidneys of SHR rats as compared with those of the normotensive controls. Renal Na-K-ATPase activity was significantly lowered only in the cortex during chronic hypertension but not in the outer medulla. In both parts of the kidney no differences could be detected in the apparent Km value for sodium stimulation or the apparent activation energies. Mg-ATPase activity was lowered in SHR rats during chronic hypertension. Protein content was significantly decreased in the outer medulla of SHR rats in the early hypertensive phase as well as during chronic hypertension. The results suggest that the functional changes observed in kidneys of young SHR rats are not due to a genetically determined defect in renal Na-K-ATPase.

Adenosine Triphosphatases↗

PubMedDate not supplied

[Effect of cholagogic agents on volumetric natriuresis in rats with experimental dystrophy of the liver].

In experimental dystrophy of the liver in rats provoked by introduction of CCL4 the enlargement of the extracellular space is followed by a diminished excretion of sodium. Administration against this background of cholagogues--dehydrocholic acid (250 mg/kg), flaminum (50 mg/kg) and sodium selenite (30 mg/kg) for a space of 7 days helps restore the volumetric natriuresis. It may be assumed that in experimental dystrophy of the liver the process of formation of the natriuretic factor in the liver is deranged. Introduction of the cholagogues under study helps re-establish its formation. Under these circumstances the sensitivity of the rats' kidneys to the natriuretic factor remains practically unchanged.

Animals↗

PubMedDate not supplied

[Dilution hyponatremia and conserved natriuresis in pulmonary tuberculosis (author's transl)].

Association of dilution hyponatremia and normal natriuresis produce an inappropriate secretion of antidiuretic hormone. In this pulmonary tuberculosis case we report manifestations along with the other biological criteria of inappropriate secretion of antidiuretic hormone. All disturbances cease when pulmonary tuberculosis is cured. This syndrome may be due either to disturbance in the regulatory apparatus of antidiuretic hormone secretion or to the antidiuretic principle in tubercular lung tissue.

Aged↗

PubMed1983

Dopamine excretion during natriuresis of starvation.

Five obese subjects were studied when they were on a 3.35 MJ (800 kcal)-diet, 1.67 MJ (400 kcal) diet and during total starvation. Urine excretion of sodium and dopamine and plasma renin activity (PRA) and plasma aldosterone levels were measured. Urine sodium excretion increased from 88 +/- 9.8 mmol/d before starvation to 150 +/- 15.7 mmol/d on day 4 of starvation. Dopamine excretion increased from 0.92 +/- 0.23 mumol/d before starvation to 1.56 +/- 0.24 mumol/d on day 1 of starvation (P less than 0.01). These results suggest that dopamine excretion is increased in early starvation and may play a role in the natriuresis of starvation.

Adult↗

PubMedDate not supplied

[On the role of glucagon in natriuresis of fast (author's transl)].

Glucagon administered to fasting obeses enhanced natriuresis as well as ketonuria while devoid of influence on ketonemia. This suggest that glucagon reduces ketone body reabsorption by renal tubule cells, which accounts for the natriuretic properties of this hormone.

Fasting↗

PubMed1995

Intrarenal production of dopamine and natriuresis following DOPA and saline infusions in healthy human volunteers.

The interactions of intrarenal dopamine (DA) synthesis and natriuresis were studied in 11 healthy volunteers by giving a low and high sodium diet (LoSo, 50 mmol Na+; HiSo, 250 mmol Na+). On 2 days in both dietary phases an acute saline load was given, without or with an infusion of the DA precursor 3, 4-dihydroxyphenylalanine (DOPA) 0.15 microgram kg-1 min-1. Urinary excretion rates of sodium (UNa V), DOPA (UDOPA V), DA (UDA V) and noradrenaline (NA; UNA V), hormonal parameters, blood pressure (BP), glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured. On HiSo UDOPA V increased by 35% (P < 0.05) while UDA V remained unchanged. Only weak correlations were found between 24h UNa V and UDA V (r = 0.23) or UDOPA V (r = 0.39). On both diets and without the DOPA infusions, the saline infusions enhanced UNa V but did not increase UDA V. The DOPA infusions caused no significant change of UNa V, in spite of five- to eight-fold increases in UDA V. During LoSo the DOPA infusion only caused a slightly larger increase of UNa V after the saline infusion, when expressed as percentage change to the pre-saline UNa V (119 +/- 25% without DOPA infusion, 244 +/- 56%, P < 0.05 with DOPA infusion). On HiSo the DOPA infusion did not affect UNA V. The dietary sodium intake and the DOPA infusions did not influenced BP, GFR, or ERPF. In conclusion, dietary sodium intake or acute sodium loads did not clearly modulate UDA V.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Blood pressure response to angiotensin converting enzyme inhibitor in essential hypertension: its relation to the renin status and natriuresis during acute sodium loading.

We examined the antihypertensive response to enalapril and its relation to the changes of the renin-angiotensin-aldosterone axis (RAA) in essential hypertensive patients. The responders, whose blood pressure reduced after enalapril administration, had significant elevation of plasma renin activity after enalapril (7.5 +/- 4.0 to 31.9 +/- 10 ng/mL/h, p < 0.05). There was no significant change in the plasma renin activity of the nonresponders (3.0 +/- 1.0 to 5.6 +/- 1.9 ng/mL/h). Natriuretic response to acute salt loading was compared between the two subgroups. The natriuresis on acute salt loading of nonresponders was better than that of the responders (82.9 +/- 13.2 vs 44.5 +/- 5.7 mmol/4h, p < 0.05). These results imply that the RAA and extracellular fluid volume both contribute in different ways to the maintenance of high blood pressure in different subgroups of essential hypertension.

Adult↗

PubMed1996

Nocturnal polyuria and natriuresis in male patients with nocturia and lower urinary tract symptoms.

PURPOSE: We investigated the circadian variation in urine output, plasma angiotensin II, aldosterone, atrial natriuretic peptide, arginine vasopressin and blood pressure. MATERIALS AND METHODS: We studied 17 elderly men with nocturia and lower urinary tract symptoms, and 10 age matched controls without nocturia. RESULTS: Of the 17 patients studied 11 had a lack of diurnal variation in urine output and increased nocturnal urine production associated with increased nocturnal sodium excretion, and 6 had a diurnal variation in urine output comparable to controls. CONCLUSIONS: Nocturia in a large proportion of elderly men with lower urinary tract symptoms is caused by nocturnal polyuria and natriuresis.

Adult↗

PubMed1998

[Glucose in conjunction with peptides derived from kininogens might act from digestive tract as blockers of atrial natriuretic peptide mediated diuresis-natriuresis].

This paper describes long term research efforts which have lead: 1) to the identification of peptides present in pepsanurin, a peptidic fraction obtained by pepsin hydrolysis of plasma globulins that inhibits the renal excretory action of atrial natriuretic peptide (ANP) and 2) to the discovery of an unexpected role of glucose, as a requisite for these inhibitory effects. The active peptides identified in pepsanurin are derived from plasma kininogens, substrates of the kallikrein-kinin system. Pro-kinins of 15, 16 and 18 amino acids, and bradykinin itself, block ANP-induced diuresis and natriuresis when injected i.v., i.p. or into the duodenal lumen of anesthetized rats in picomol doses. Furthermore, a novel 20 amino acids fragment derived from kininogen dominium-1, named PU-D1, is the most potent and longer lasting blocker of ANP renal effects. The anti-ANP effects of those peptides are prevented by B2-kinin receptor antagonists. The inhibition of ANP by kinins and PU-D1 was evident only in rats infused with isotonic glucose; whereas the excretory effect of ANP was not affected in fasted rats not infused, or infused with saline. These findings provide evidence that glucose facilitates liquid retention through a kinin-mediated inhibition of ANP excretory action that may be related to the prandial cycle.

Animals↗

PubMed1998

Interactions between bradykinin and ANP in rat kidney in vitro: inhibition of natriuresis and modulation of medullary cyclic GMP.

In anesthetized rats, the renal excretory actions of atrial natriuretic peptide (ANP) are inhibited by intravenous or intraperitoneal injections of bradykinin. To elucidate the mechanisms underlying this inhibition, we evaluated bradykinin effects on: i- ANP-induced natriuresis and diuresis in isolated perfused rat kidneys, and ii- ANP-induced cGMP production in rat renal medulla in vitro. In perfused kidneys, 1 microgram bradykinin completely inhibited the diuretic and natriuretic responses elicited by 0.5 microgram ANP, without changes in perfusion pressure. The inhibitory effects of bradykinin were abolished by HOE-140, a kinin-B2 receptor antagonist. Bradykinin alone had no effect on urinary excretion or perfusion pressure. Incubation with ANP (0.1 nM to 1 microM) increased renal medullary cGMP content up to 30-fold, in a concentration-dependent fashion. Medullary cGMP was moderately increased by the nitric oxide donor, sodium nitroprusside (1 microM), but it was unchanged by bradykinin (0.1 nM-0.1 microM). Despite this, ANP-induced cGMP production was significantly enhanced by co-incubation with low concentrations of bradykinin (up to 0.1 nM). In contrast, ANP-induced cGMP accumulation was unchanged by concentrations of 1 nM bradykinin or higher. In the presence of 100 nM HOE-140, bradykinin (0.1-1 nM) did not affect ANP-induced cGMP production. These results demonstrate that bradykinin counteracts ANP-stimulated sodium and water excretion, by acting directly on the kidney. The interaction between both peptides is complex; our data suggest that renal medullary ANP receptors are subjected to an on/off modulation by fluctuating bradykinin concentrations.

Animals↗

PubMed1981

Dissociation of saline-induced natriuresis from urea washout in the rat.

Medullary urea washout has been postulated to play a major role in the natriuretic response to volume expansion (VE). To examine this hypothesis, renal tissue solute composition was measured in a natriuretic and nonnatriuretic model of VE. Renal tissue composition was analyzed during hydropenia, acute VE, acute VE with renal artery pressure reduced to 70 mmHg at the onset of saline loading (immediate clamping), and acute VE with renal artery pressure reduced to 70 mmHg after 45 min of saline loading (delayed clamping). Immediate clamping, a nonnatriuretic model of VE, prevented VE-induced urea washout and the increase in sodium and water content in the cortex and outer medulla. Delayed clamping, a natriuretic model of VE, produced a pattern of tissue composition very similar to immediate clamping. Tissue urea content was not significantly different in the two protocols and only minor differences in sodium and water content were noted. Thus, under these experimental conditions, VE-induced natriuresis can be dissociated from medullary urea washout, and other mechanisms must be invoked to explain the increased sodium excretion.

Animals↗

PubMed1980

Exaggerated natriuresis in normotensive subjects with a previous history of pregnancy-associated hypertension.

The effect of an isotonic saline infusion on urinary sodium excretion and plasma renin activity (PRA) has been studied in 11 normotensive patients with a previous history of pregnancy-associated hypertension. The results have been compared with a group of controls matched for age, sex and parity. The results demonstrate an exaggerated natriuresis and a suppressed PRA response in the patients with a previous history or pregnancy-associated hypertension which is similar to those reported in patients with established 'essential' hypertension.

Adolescent↗