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PubMed2001

[Postprandial natriuresis].

Of the common responses elicited by differences in the composition of the meal, specific effects on renal fluid-electrolyte excretion that manifest themselves as postprandial natriuresis have attracted significant interest. Unfortunately, our understanding of their mechanisms remains incomplete. Hepatorenal reflexes, dopamin action, urodilatin secretion and NO synthesis have been the candidates most frequently cited to contribute to postprandial natriuresis. The recent identification of a novel class of natriuretic peptides named guanylins has brought a new impact on water-sodium homeostasis regulation studies. The elucidation of mechanisms of postprandial natriuresis can be of importance in the research of primary hypertension. The article briefly reviews work in this area.

Animals↗
PubMed2002

Human leptin administered intraperitoneally stimulates natriuresis and decreases renal medullary Na+, K+-ATPase activity in the rat -- impaired effect in dietary-induced obesity.

BACKGROUND: Leptin, produced by adipose tissue, apart from regulating food intake and energy expenditure, also has natriuretic activity. In this study we examined the effect of leptin on renal Na+, K+-ATPase responsible for active tubular sodium reabsorption, and compared the renal effects of leptin in lean and obese rats. MATERIAL/METHODS: Male Wistar rats were either kept on normal laboratory chow or made obese by a high-calorie diet. The animals were placed in metabolic cages and urine was collected in 2-hour periods. RESULTS: In lean animals, leptin (1 mg/kg i.p.) caused a 139.5% increase in urine output, a 112.4% increase in natriuresis, and a 57.2% increase in the fractional excretion of sodium, but had no effect on the glomerular filtration rate. Leptin at this dose decreased renal medullary Na+, K+-ATPase activity at 30 minutes, 1 hour and 2 hours by 31%, 34.3% and 21.2%, respectively. The effect of leptin on Na+, K+-ATPase at 1 hour was dose-dependent; the lowest dose inducing significant inhibition was 0.25 mg/kg. By contrast, leptin had no effect on either cortical Na+, K+-ATPase or the ouabain-resistant fraction of ATPase. In obese rats, leptin increased urine output by only 29.1% and natriuresis by 28.9%, and had no significant effect on medullary Na+, K+-ATPase. CONCLUSIONS: Leptin stimulates natriuresis primarily by inhibiting tubular sodium reabsorption. This effect is mediated, at least partially, by decreased Na+, K+-ATPase activity in the renal medulla, and is impaired in obese rats.

Animals↗
PubMed1992

[Massive natriuresis and polyuria after triple craniocervical subarachnoid hemorrhage: cerebral salt wasting syndrome?].

A thirty-year-old male patient suffered subarachnoidal haemorrhage from an angioma positioned in the cranio-cervical transition. After rebleeding twice the patient developed a hydrocephalus internus malresorptivus and excessive natriuresis and polyuria, accompanied by depressed renin activity and extremely low aldosterone plasma levels. Neither fluid restriction and sodium substitution, nor administration of hydro-chlorothiazide/indomethacin affected natriuresis and polyuria. It was only after treatment with fludrocortisone-acetate/hydrocortisone that hyponatraemia and polyuria were resolved. At the same time a ventriculo-peritoneal shunt was applied. Differential diagnosis excluded the syndromes of inadequate antidiuretic hormone secretion, renal and cerebral diabetes insipidus, osmotic receptor hypofunction, chronic renal dysfunction and tubular necrosis. Natriuresis and polyuria developed under dexamethasone therapy. Since patient history, physical examination and laboratory criteria could not explain the electrolyte and fluid imbalance, this might be attributed to the hydrocephalus. Similar disturbances have been reported from other patients with intracranial disorders. Mechanical pressure exercised on the hypothalamus might cause the disturbance of fluid and sodium balance. Assuming a cerebral salt wasting syndrome, a putative natriuretic factor coming from the brain or an imbalance in the cerebral renin-angiotensin-system, as described in rats and dogs, must be discussed.

Adult↗
PubMed1992

Is natriuresis on felodipine due to reversal of the renal effects of angiotensin II?

Felodipine induces natriuresis, possibly by renal hemodynamic and/or tubular effects. Theoretically, reversal of the sodium-retaining effect of angiotensin II (Ang II) could be involved. Therefore, we administered felodipine during Ang II infusion and during suppression of endogenous Ang II production in two double-blind studies in healthy volunteers. First, a gradually increasing dose of Ang II was infused during felodipine or solvent infusion. Before starting Ang II, felodipine had lowered renal vascular resistance (RVR) and filtration fraction (FF), and simultaneously increased CNa. The Ang II induced rise of mean arterial pressure (MAP) and renal vasoconstriction was partly antagonized and the falls in glomerular filtration rate (GFR) and CNa completely abolished by felodipine. The combination of felodipine and 3.0 ng/kg/min Ang II even enhanced natriuresis. Second, felodipine or solvent was infused after one week of pretreatment with placebo or the angiotensin converting enzyme (ACE) inhibitor ramipril, which reduced MAP and induced renal vasodilatation. Ramipril pretreatment did not influence significantly the blood pressure reduction, renal vasodilatation, and natriuresis caused by felodipine. In conclusion, it seems unlikely that the natriuretic effect of felodipine is due to interference with renal effects of endogenous Ang II. The fact that felodipine reverses sodium retention on exogenous Ang II may be explained by interference with systemic and renal hemodynamic effects of exogenous Ang II.

Adult↗
PubMed1991

Reduction of nocturnal diuresis and natriuresis during treatment of obstructive sleep apnea (OSA) with nasal continuous positive air pressure (nCPAP) correlates to cGMP excretion.

In ten patients with severe obstructive sleep apnea (OSA) profound changes in renal function could be demonstrated at night during nCPAP therapy. Natriuresis and diuresis decreased by about 50% while creatinine excretion rate and urinary osmolality did not change. We found parallel changes in the excretion of ANP's second messenger cyclic guanosine monophosphate (cGMP) in a dose-response-related manner to natriuresis respectively diuresis. These data are in agreement with recently demonstrated decrease of nocturnal plasma levels of atrial natriuretic peptide (ANP) during nCPAP therapy in apneic patients. This may be an indicator for an increased cardiac volume load during obstructive apnea. The decrease of diuresis, natriuresis and cGMP excretion demonstrate the beneficial effects of nCPAP treatment on the cardiovascular system. Therefore measurements of cGMP excretion may be a useful parameter to assess the cardiovascular function of apneic patients before and during treatment.

Adult↗
PubMed1991

Exaggerated natriuresis in primary aldosteronism.

Acute response in blood pressure (BP) and natriuresis to saline infusion was evaluated in 16 patients with primary aldosteronism caused by aldosteronoma (PA) and 12 patients with salt-sensitive essential hypertension (SSEH). Salt-sensitivity was defined by a decrease in mean BP exceeding 5% at the second hour after a 20 mg furosemide injection. Plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urine electrolytes in response to saline infusion were determined. During a 2-liter isotonic saline infusion, a similar degree of natriuresis and change in BP were observed in PA and SSEH patients. A significantly inverse correlation between the increase in mean BP and the degree of natriuresis at the end of the infusion was found in patients with SSEH (r = -0.80, p less than 0.01). No correlation was observed between these parameters in patients with PA (r = 0.28, p greater than 0.05). These results suggest that hypernatriuresis in SSEH may play a protective mechanism against abrupt increases in BP and volume during acute saline loading. This protective mechanism was not evident in patients with PA.

Adrenal Cortex Neoplasms↗
PubMed1991

[Role of brain cholinergic system on diuresis and natriuresis induced by volume expansion in rats].

The role of brain cholinergic system on diuresis and natriuresis induced by volume expansion was studied in conscious rats. In a series of experiments, the diuretic, natriuretic and kaliuretic responses induced by volume expansion were compared in three groups of conscious rats pretreated respectively with intracerebroventricular (icv) injection of artificial cerebrospinal fluid (ACSF), atropine and hexamethonium. The natriuretic, kaliuretic and diuretic responses induced by volume expansion were much less in the animals with icv injection of atropine than in the control group with injection of ACSF (P less than 0.01). While the group pretreated with icv injection of hexamethonium showed no significant decrease in these responses of volume expansion than that of the control (P greater than 0.05). Volume expansion produced no change in insulin and PAH clearance in both the atropine and the ACSF group. Thus the atropine suppressed diuresis, natriuresis and kaliuresis are independent of changes in GFR and RPF. It is inferred from the results of the present investigation that volume expansion induced diuresis and natriuresis appear to be due to inhibition of water and sodium reabsorption in the renal tubules and regulated by certain brain cholinergic system.

Animals↗
PubMedDate not supplied

[Studies of atrial natriuretic peptide, diuresis and natriuresis in patients with diabetes mellitus types 1 and 2 after water immersion].

In 30 diabetics (15 with type I and 15 with type II) and in 15 healthy controls the effect was studied of two-hour immersion in water on the concentration of atrial natriuretic peptide, sodium and potassium in serum, diuresis and natriuresis, mean arterial pressure and percent change of circulating plasma volume. Diabetics with either type of diabetes differed from the controls by a significantly lower concentration of the atrial natriuretic peptide under basal conditions, and lower rise of the peptide during immersion in water. Type I diabetics differed from type II diabetics and controls in that their natriuresis was lower under basal conditions and during immersion. On the basis of these results the authors conclude that in diabetics the reaction of atrial natriuretic peptide secretion to central hypervolaemia is preserved but weaker, and the role of this hormone in the pathogenesis of increased diuresis and natriuresis induced by water immersion is smaller in these patients than in controls.

Adult↗
PubMed1986

Enalapril and the kidney: renal vasodilation and natriuresis due to the inhibition of angiotensin II formation.

Essential hypertension is characterized by increased renal vascular resistance, which also has definite implications for renal sodium handling. We studied the possibility of correcting these abnormalities by inhibiting angiotensin-converting enzyme with enalapril. Enalaprilic acid produced renal vasodilation. This, particularly postglomerular, vasodilation was accompanied with an increase in sodium excretion. The natriuresis was positively correlated to initial plasma renin activity. During continuous treatment with enalapril up to 12 weeks, this vasodilation persisted in 22 patients with essential hypertension. We also showed that orally administered enalapril induces natriuresis, both during a 50-mmol and during a 200-mmol sodium intake a day. This natriuresis caused a net negative sodium balance of approximately 120-140 mmol Na after 1 week of enalapril therapy. This was accompanied with a fall in body weight. We conclude that enalapril in essential hypertension alleviates the angiotensin-II-mediated abnormalities in renal hemodynamics and sodium excretion.

Administration, Oral↗
PubMed1989

Natriuresis during and early after cardiopulmonary bypass: relationship to atrial natriuretic factor, aldosterone, and antidiuretic hormone.

Because neurohumoral responses to cardiopulmonary bypass (CPB) are similar to those seen in shock, CPB might be expected to decrease renal blood flow; yet diuresis is commonly observed during and early after routine cardiac procedures with CPB. To examine this apparent paradox, we studied 15 patients before, during, and after CPB for coronary artery bypass grafting. Plasma levels of atrial natriuretic factor (alpha-ANF), aldosterone, and antidiuretic hormone (ADH) and urinary sodium excretion were measured before anesthesia, after sternotomy but before CPB, at 15 and 30 minutes of CPB, and at 15 and 30 minutes after discontinuation of CPB. alpha-ANF increased only slightly during CPB, and the initial natriuresis during CPB occurred in the presence of a markedly increased ADH level. After CPB ended, urine flow and sodium excretion increased in conjunction with increased alpha-ANF and normal ADH. We conclude that the early natriuresis during CPB occurs in the presence of a high ADH concentration, with no significant increase in plasma alpha-ANF. This may be a paradoxic response to supraphysiologic levels of ADH. The natriuresis after CPB appears to be strongly associated with increased alpha-ANF, present for at least the first 30 minutes after CPB, which could reflect alpha-ANF release resulting from atrial distention during volume loading.

Aged↗
PubMed1987

On the brain involvement in saline loading natriuresis--an indirect evidence for the cerebral participation in the functional expression of the atrial natriuretic system.

The ablation of the anterior third cerebral ventricle region totally prevented the homeostatically effective natriuresis which should have followed hypertonic saline loading in conscious sheep. The increased cerebrospinal fluid (CSF) sodium concentration potentiated, and the decreased CSF[Na] prevented, natriuresis during isotonic saline loading. It is thus probable that a cerebral natriuretic system is involved in the functional expression of any other peripheral natriuretic system, e.g. the heart atrial natriuretic system which has been found to play a role in both hypertonic and isotonic saline loading natriuresis.

Animals↗
PubMed1988

Effects of felodipine on natriuresis, atrial natriuretic factor, the renin-angiotensin-aldosterone system, and blood pressure in essential hypertension.

The aim of this study was to evaluate the short-term and long-term effects of felodipine, a new dihydropiridine calcium antagonist, on arterial blood pressure (BP), the renin-angiotensin-aldosterone system, diuresis, natriuresis, and the atrial natriuretic factor (ANF). In 15 essential hypertensives (WHO class II) BP, venous BP at the posterior tibial vein (VBPTV), diuresis, natriuresis, plasma renin activity (PRA), and both plasma aldosterone and ANF levels were evaluated at the end of a washout period and after two and 24 hours and 30, 90, and 180 days of follow-up with felodipine, 5 mg twice daily. The first dose of felodipine induced a significant decrease in BP, which was associated with increases in both heart rate and VBPTV. An acute diuretic and natriuretic effect, increases in ANF and PRA, and a transient decrease in plasma aldosterone levels were also observed. Throughout the follow-up period, the antihypertensive efficacy remained unchanged, whereas variations in electrolyte balance and hormonal parameters quickly disappeared, except for the increase in PRA, which lasted until the 30th day of therapy. In our study, felodipine showed a great antihypertensive activity during both short-term and long-term treatment. Moreover, the effect of the first dose was characterized by transient increases in circulating ANF and decreases in plasma aldosterone concentrations, which were associated with marked diuresis and natriuresis.

Adult↗
PubMed1988

Effects of perindopril on renal haemodynamics and natriuresis in essential hypertension.

Renal haemodynamics and natriuresis were studied before and 6 h after oral intake of perindopril (8 mg) in eight hypertensive patients without renal failure. The patients were then treated with perindopril (8 mg per day) and renal haemodynamics were measured on the fifth day, 6 h after the morning intake. Sodium intake was controlled during the study (100 mmol sodium per day). Renal blood flow and the glomerular filtration rate were measured by the clearance method using 131I-hippuran and 125I-iothalamate, respectively. Mean blood pressure decreased from 135 to 110 after 6 h, and was 118 mmHg on the fifth day (P less than 0.001, respectively). Renal vascular resistance decreased significantly after acute drug intake from 0.19 to 0.15 arbitrary units (P less than 0.001) and on the fifth day to 0.16 arbitrary units (P less than 0.001). Renal blood flow rose from 708 to 723 after 6 h, and to 750 ml/min per 1.73 m2 on the fifth day but the change was no significant. There was no alteration in the glomerular filtration rate so that the filtration fraction decreased from 0.27 to 0.26 (after 6 h), and to 0.25 on the fifth day (P less than 0.02). Natriuresis increased after the first intake between the first and tenth hours. On the fifth day, maximum natriuresis was observed between the fourth and sixth hours. Perindopril caused strong renal vasodilation after the first intake and during the following days, with no change in the glomerular filtration rate. There was a significant decrease in the filtration fraction, indicating efferent, as well as afferent, arteriolar vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Hyponatremia due to excess natriuresis].

Nine cases with hyponatremia were precisely examined during the past 2 years. Seven of them showed normal plasma volume, serum aldosterone and pituitary function, although ADH was detected. Therefore, those seven cases were diagnosed without dilutional hyponatremia due to SIADH (a syndrome of inappropriate secretion of antidiuretic hormone). The mechanism of hyponatremia of such a type has not been yet explained definitely, but it may be referring to excess natriuresis. Only each one case of hyponatremia due to hypopituitarism and dilutional hyponatremia due to SIADH was verified in this series. SIADH showing high plasma volume value was thought to be rare. Differential diagnosis between SIADH and hyponatremia due to excess natriuresis is essential and simple. Non-invasive plasma volume measurement using RISA is significantly useful for it. For the hyponatremia due to excess natriuresis, water restriction is not necessary, but digestive supply of NaCl is needed.

Adult↗
PubMed1986

Regulation of arterial pressure: role of pressure natriuresis and diuresis.

The importance of the renal pressure natriuresis and diuresis mechanisms in long-term control of body fluid volumes and arterial pressure has been controversial and difficult to quantitate experimentally. Recent studies, however, have demonstrated that in several forms of chronic hypertension caused by aldosterone, angiotensin II (AngII), vasopressin, or norepinephrine and adrenocorticotropin, increased renal arterial pressure is essential for maintaining normal excretion of sodium and water in the face of reduced renal excretory capability. When renal arterial pressure was servo-controlled in these models of hypertension, sodium and water retention continued unabated, causing ascites, pulmonary edema, or even complete circulatory collapse within a few days. Apparently, other mechanisms for volume homeostasis, such as the various natriuretic and diuretic factors that have been postulated, are not sufficiently powerful to maintain fluid balance in the absence of increased renal arterial pressure when renal excretory function is reduced in these forms of hypertension. The intrarenal mechanisms responsible for pressure natriuresis and diuresis are not entirely clear, but they seem to involve small increases in glomerular filtration rate and filtered load as well as reductions in fractional reabsorption in proximal and distal tubules. During chronic disturbances of arterial pressure additional factors, especially changes in AngII and aldosterone formation, act to amplify the effectiveness of the basic renal pressure natriuresis and diuresis mechanisms in regulating arterial pressure and body fluid volumes.

Aldosterone↗
PubMed1987

Role of the natriuretic hormone in the specific natriuresis induced by intraportal infusion of hypertonic saline in dogs.

Previous experiments from our laboratory demonstrated that the infusion of a small amount of hypertonic saline into the portal vein induced higher diuresis and natriuresis than those induced by the infusion of the same amount of saline into a cubital vein. The purpose of the present experiment was to study the role of the so-called natriuretic hormone in this phenomenon. For this purpose, two groups of 5 dogs each were infused with 855 mM NaCl (0.05 ml X min-1 for 20 min), one group through the portal vein and the other through the cubital vein. Samples of peripheral, arterial and suprahepatic blood and urine were obtained, and the fraction described to contain the natriuretic hormone was purified by gel filtration chromatography. Its natriuretic activity was assayed by measuring the natriuresis induced by its infusion in conscious, unilaterally nephrectomized rats. The urine taken from the dogs infused with hypertonic saline into the porta showed higher natriuretic activity than that obtained before infusion or from the dogs infused into the cubital vein. Also, natriuretic activity was observed in the suprahepatic and arterial plasma samples obtained after portal infusion but not in those obtained before the infusion. There were no differences in natriuretic activity between suprahepatic and arterial samples. These results suggest that the natriuretic hormone plays an important role in the natriuresis induced by portal hypertonic saline infusion, and they do not support the hepatic origin of this substance.

Animals↗
PubMed1984

Effects of vasoactive drugs on the natriuresis of nephrotic rats.

Seven nephrotic rats with edema, massive proteinuria and reduced glomerular filtration rate and filtration fraction were compared with ten normal rats. The experiment consisted of three consecutive periods: C, control; Ach, in which acetylcholine (40-60 ng/min) was continuously infused directly into the left renal artery; and Ach-AN-NA, in which angiotensin II (AN, 0.025 ng/min) + noradrenaline (NA, 0.25 micrograms/min) was systemically infused to elevate blood pressure, without interrupting acetylcholine infusion. Mean arterial pressure (MAP) and renal function parameters were measured. In both groups, MAP remained unchanged from C to Ach (P greater than 0.05) and was increased (P less than 0.05) from Ach to Ach-AN-NA (136 +/- 3.3 to 148 +/- 2.9 mmHg in normal animals, and 132 +/- 5.8 to 148 +/- 4.9 mmHg in nephrotic animals). In the normal group, intrarenal acetylcholine infusion increased (P less than 0.05) natriuresis from 3.75 to 7.93 microEq min-1 kd-1 kg BW-1 and a further, but transitory, increment up to 10.20 microEq min-1 kd-1 kg BW-1 was observed (P less than 0.05) when MAP was elevated. These natriuretic changes occurred without alterations of glomerular filtration rate (P greater than 0.05). Therefore, as previously reported in the literature, normal rats were responsive to intrarenal infusion of acetylcholine (vasodilator) followed by increased blood pressure, a condition known as pressure natriuresis. However, no natriuretic response was observed in the nephrotic group either to intrarenal acetylcholine infusion or to blood pressure elevation. We assume that nephrotic rats are insensitive to pressure natriuresis.

Acetylcholine↗
PubMed1984

Resetting of pressure-natriuresis and frusemide sensitivity in spontaneously hypertensive rats.

We compared pressure-natriuresis in isolated perfused kidneys of spontaneously hypertensive rats (SHR), and age-matched controls, and studied the effect of frusemide on sodium excretion. Okamoto SHR and age-matched Wistar-Kyoto controls (WKY) were used. Conscious BP was measured in a tail artery cannulated before the experiment. Isolated kidneys were perfused at 37 degrees C and glomerular filtration rate, urinary sodium excretion (UNaV) and percentage sodium reabsorption (%TNa) were measured as mean perfusion pressure was increased in steps from 100 to 180 mmHg and repeated after addition of frusemide. At all perfusion pressures GFR and UNaV were lower in SHR and %TNa higher, consistent with a 50 mmHg rightward shift of the pressure-natriuresis relationship in SHR. However, at intrarenal perfusion pressure equal to MBP, sodium excretion was the same (2.9 microEq/min/g WKY; 2.7 microEq/min/g SHR). Subsequent response to frusemide was markedly reduced in SHR. We conclude that resetting of pressure-natriuresis in SHR compensates exactly for increased renal perfusion pressure. The mechanism by which these are so precisely linked is not known, nor is the reason for the blunted sensitivity to frusemide in SHR, but it is possible that Na-K-Cl cotransport in Henle's loop may be altered in this genetic model of hypertension.

Absorption↗