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PubMed1992

Common aspects of the cerebral regulation of thirst and renal sodium excretion.

It has been shown that several mammalian species increase the excretion of sodium in urine as they become dehydrated. This dehydration-induced natriuresis occurs despite simultaneous hypovolemia, and it can be blocked by an experimentally-induced reduction in the sodium concentration of CSF, or by ablation of the periventricular tissue in the vicinity of the lamina terminalis. These two experimental procedures also disrupt thirst and vasopressin secretion. There may therefore be common features involved in the central control of osmoregulatory thirst, vasopressin secretion and sodium excretion. Experimental evidence in sheep suggests that whenever the tonicity of body fluids increases, a centrally mediated natriuretic mechanism is engaged. This cerebral natriuretic mechanism may contribute along with other influences such as the extracellular fluid volume, aldosterone and atrial natriuretic peptide, to determine the rate of sodium excretion by kidneys. The efferent pathway from brain to kidney mediating osmoregulatory natriuresis is not known. It is probably hormonal, because renal denervation does not disrupt such natriuresis.

Animals↗

PubMed1991

Sodium retention and hepatic function after two-thirds hepatectomy in the rat.

Recently it was suggested that the onset of sodium retention in experimental cirrhosis in rats is related to a critical threshold of hepatic function, as assessed by the aminopyrine breath test. The aim of this study was to evaluate whether sodium retention occurred after two-thirds hepatectomy in rats and to investigate the relationship between sodium retention and changes in hepatic function associated with liver regeneration in this model. Sodium balance, creatinine clearance, serum sodium and the aminopyrine rate constant of elimination were evaluated daily for 4 days after surgery in partially hepatectomized (n = 6) and sham-operated rats (n = 6). All rats in the partial hepatectomy group exhibited sodium retention (sodium balance greater than 0.7 mmol/day) 24 hr after surgery. This was associated with a 62% reduction of the aminopyrine rate constant of elimination. Spontaneous natriuresis which occurred between 2 and 4 days after surgery, was associated with an increase in the aminopyrine rate constant of elimination (from 0.73 +/- 0.02 x 10(-2) min-1 on the last day of sodium retention to 0.95 +/- 0.04 x 10(-2) min-1 on the first day of natriuresis [p less than 0.05]). In contrast, no change in creatinine clearance occurred over the same period. A negative curvilinear association was found between sodium balance and the aminopyrine rate constant of elimination in all animals (r = -0.72, p less than 0.001). These observations indicate that natriuresis is related to the recovery of liver function, not to changes in creatinine clearance. In conclusion, the concept of a critical threshold of liver function below which sodium retention occurs has been substantiated in this model of hepatic dysfunction.

Analysis of Variance↗

PubMed1990

[Renal, hemodynamic and hormonal effects of repeated water immersion in liver cirrhosis].

In patients with cirrhosis of the liver sodium retention plays an important role in fluid and salt disturbances. We performed a study in 3 groups of 12 compensated and 7 decompensated cirrhotic patients and 11 controls to determine the renal, hemodynamic and hormonal effect of repeated water immersion (6 immersions in 3 weeks). In all groups immersion resulted in a marked acute natriuresis and diuresis combined with acute reduction of blood pressure. In both cirrhotic groups we found decreased salt excretion except the acute effect of immersion in comparison with controls. The natriuresis of the immersion day were in decompensated patients significantly elevated in comparison with a control day. This was not due to the acute, but the prolonged immersion effect on renal excretion. During the study the immersion effects increased in both groups of cirrhotic subjects. The controls showed decreased responses. The immersion response shall be caused at least, in part by the Atrial Natriuretic Peptide (ANP): all groups had a significant elevation of ANP during the immersion which was like the renal natriuresis prolonged in the 6th immersion in cirrhotics. A repeated water immersion may improve the natriuretic responsiveness of cirrhotics, especially those of decompensated patients.

Adult↗

PubMed1990

[The effect of moderate oxygen deficiency on volume regulation in man].

In acute hypoxia or at pharmacological stimulation of the peripheral arterial chemoreceptors by almitrine, a transient natriuresis and diuresis occurs. Depending on the starting level, e.g. on the state of water diuresis or the osmotic diuresis, the renal excretion responded differently in our examinations. In water diuresis the water excretion increased isolatedly. In the opposite to the osmotic diuresis, the natriuresis did not increase. This response might be based on the proximal inhibition of the sodium and water reabsorption at following augmented distal sodium reabsorption and suppressed distal water reabsorption. In this way the organism is able to respond with increased water excretion at sodium excretion kept constant or with diuresis and natriuresis when arterial chemoreceptors are stimulated.

Adult↗

PubMed1989

Evidence from functional and autoradiographic studies for the presence of tubular dopamine-1 receptors and their involvement in the renal effects of fenoldopam.

Evidence from receptor-ligand binding and biochemical studies seems to suggest the possible existence of tubular dopamine DA-1 receptors in the rat kidney. However, it is not yet clear whether these putative tubular DA-1 receptors are involved in the functional renal responses elicited during the administration of DA and DA receptor agonists. In the present study we have examined the renal effects of several doses of selective DA-1 receptor agonist fenoldopam in pentobarbital-anesthetized rats in an attempt to unmask a direct tubular DA-1 receptor-mediated diuresis and natriuresis. Additionally, we have performed receptor-ligand binding and autoradiographic studies to examine the presence and localization of DA-1 receptors in various regions of the rat kidney. At the highest dose studied (2 micrograms/kg/min), fenoldopam produced diuresis and natriuresis, which was accompanied by a significant decrease in blood pressure and also a significant increase in glomerular filtration rate. At 1 micrograms/kg/min, the diuretic and natriuretic effects of fenoldopam were observed in the absence of any changes in blood pressure and glomerular filtration rate, but there was a significant increase in renal blood flow. However, at 0.5 micrograms/kg/min, fenoldopam-induced natriuresis and diuresis was not accompanied by any changes in blood pressure, renal blood flow or glomerular filtration rate, implying a direct tubular effect. These effects of fenoldopam appear to be mediated via activation of DA-1 receptors, because they were antagonized by the selective DA-1 antagonist SCH 23390.(ABSTRACT TRUNCATED AT 250 WORDS)

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

PubMed1986

Observations on the natriuretic response to intravenous infusions of atrial natriuretic factor in water-loaded anaesthetized rats.

Natriuresis induced by infusions of atrial natriuretic factor (ANF) in water-loaded rats typically occurred in time sequences ('peak-and-shoulder' patterns) with an overlap of two different natriuretic responses. The first response was abrupt, short-lived and potentiated by angiotensin converting enzyme (ACE) inhibition. The second response was a gradual onset of natriuresis which lasted only as long as the ANF infusion and was directly correlated to the level of arterial blood pressure. This phenomenon explains the apparent loss of responsiveness to ANF bolus injections during a late phase. Atrial natriuretic factor facilitated excretion of intravenous salt loads, and the effect was also observed with low salt doses (1 microgram/h) which were below threshold for natriuresis when given alone. The data available so far suggest that ANF, apart from its effect on collecting-duct permeability, interferes with several control and feedback systems involved in sodium input into the collecting-duct system.

Animals↗

PubMed1987

Evidence for an involvement of dopamine receptors in the natriuretic response to atrial natriuretic peptide.

Intravenous injection of atrial natriuretic peptides (ANP) induces a preferential vasodilatation of the renal resistance vessels. A similar effect is exerted by dopamine. Exogenous administration of this catecholamine induces, like the atrial peptides, diuresis and natriuresis, an effect prevented by dopamine receptor antagonists. In view of these parallels, the influence of dopamine antagonists on the diuretic response of anaesthetized rats to ANP was tested. The unselective dopamine antagonists haloperidol (50 micrograms, i.v.) and chlorpromazine (50 micrograms, i.v.) prevented the diuretic and natriuretic effect of a partially purified atrial extract, and significantly blunted that of alpha-hANP (1 microgram). Dopamine receptors are classified as DA-1 and DA-2. The DA-2 receptor antagonists metoclopramide (50 micrograms, i.v.) and sulpiride (50 micrograms, i.v.) did not affect ANP induced natriuresis. The DA-1 receptor antagonists SCH 23390 and SK&F 83566 dose-dependently counteracted the renal response to the intravenous administration of ANP. The administration of haloperidol (25, 50 and 100 micrograms, i.v.) to rats undergoing a putative ANP dependent natriuresis (isotonic saline loading) dose-dependently reduced both urine volume and sodium excretion. Atriopeptin II (10(-9)-10(-10) M) displaced tritiated spiperone, a dopamine antagonist, from specific binding sites in homogenates of renal medulla, papilla and cortex. These results suggest that dopamine receptors, most probably of the DA-1 subclass, are involved in the natriuretic response to ANP. The present experiments do not allow the conclusion as to whether ANP directly interacts with the dopamine receptors or whether it affects these receptors by releasing dopamine.

Animals↗

PubMed1987

[Hyponatremia with high plasma ANP level--report of two cases with emphasis on the pathophysiology of cerebral salt wasting].

Two cases of hyponatremia with intracranial lesions are reported with emphasis on diagnostic value of measurement of antidiuretic hormone (ADH) and atrial natriuretic polypeptide (ANP). Case 1. A 77-year-old female was transferred to our hospital for further care of vegetative state after subarachnoid bleeding on May 23, 1986. She was operated by neck clipping of rt-IC bifurcation aneurysm and lt-internal carotid-posterior communicating aneurysm at another hospital. On admission, computed tomography showed diffuse low density at bilateral thalamus and centrum semiovale. Biochemical analysis revealed hyponatremia (120 mEq/t) with increased natriuresis. Endocrinological date revealed normal plasma ADH and high plasma ANP levels. Patient was treated with infusion of 1% NaCl. Case 2. A 65-year-old male was admitted to our department because of gradual impairment of consciousness and generalized convulsion. Computed tomography showed small low density area at rt-thalamus and lt-cerebellar hemisphere. Biochemical date revealed severe hyponatremia (91 mEq/t) with normal plasma level of ADH and high plasma ANP. He was treated with infusion of 3% NaCl and hyponatremia was improved. The hyponatremia is frequently associated with intracranial disorders such as brain tumor, subarachnoid hemorrhage and head injury. Originally, hyponatremia with natriuresis was thought to be caused by salt wasting. This syndrome was defined as the inability to prevent salt loss in the urine due to undefined natriuretic factor in the brain. However, since 1957, because of introduction of concept of SIADH, it has generally become accepted that patients with natriuresis had SIADH. (ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1988

[Plasma levels of atrial natriuretic peptide (ANP) in patients with paroxysmal supraventricular tachycardia and concomitant polyuria (urina spastica)].

A concomitant diuresis and natriuresis has been reported to occur in 30-50% of patients with paroxysmal supraventricular tachycardia. While the increase of the diuresis may be secondary to an inhibition of vasopressin, the etiology of the natriuresis is presently not well understood. To determine the role of atrial natriuretic peptide (ANP) in the pathogenesis of tachycardia-induced polyuria, we measured ANP levels in two female patients (aged 59 and 68 years) with recurrent episodes of paroxysmal supraventricular tachycardia during such attacks, as well as after conversion to a normal sinus rhythm. In both patients, episodes of supraventricular tachycardia were associated with both a large increase in ANP plasma levels (560 resp. 1.208 pg/ml; normal range: 50 +/- 10 pg/ml) and polyuria. Despite elevated ANP plasma levels, no diuretic and natriuretic response to tachycardia could be observed during episodes of shorter duration, some of which occurred in the older patient studied. After restoration of a normal sinus rhythm, ANP plasma levels decreased to baseline levels (107 resp. 32 pg/ml). The results of this study show that the secretion of ANP is increased during episodes of paroxysmal supraventricular tachycardia, suggesting that ANP might contribute to the pathogenesis of natriuresis and diuresis frequently associated with supraventricular tachycardia.

Aged↗

PubMed1988

The handling of NaCl load in rats during DOCA-salt and Goldblatt 2 kidney-1 clip hypertension development.

The handling of an intraperitoneal NaCl load (2% body weight, 0.9% NaCl) administered twice a week during DOCA-salt and Goldblatt 2K-1C hypertension development has been evaluated. An exaggerated natriuresis was observed in DS-hypertensive rats since blood pressure became higher with respect to normal (C), Doca (D) and uninephrectomized-salt (NS) rats that served as controls. However, this phenomenon was not observed in Goldblatt 2K-1C hypertensive rats (2K-1C) when compared to the response obtained in sham-operated (SO) rats. These results suggest that: 1) An increased blood pressure, per se, is not a determinating factor for exaggerated natriuresis. 2) Rise in blood pressure and exaggerated natriuresis may be related through a common mechanism in Doca-salt hypertension.

Animals↗

PubMed1987

Amiloride, frusemide and urinary kallikrein excretion.

Intravenous administration of the loop diuretic frusemide caused a rapid but short-lived increase in the urinary excretion of kallikrein-like activity in healthy volunteers. Indomethacin alone did not alter urinary electrolyte or kallikrein excretion, but when given concurrently with frusemide it blunted the natriuresis without altering the urinary kallikrein excretion. A single oral dose of amiloride, a distal tubular diuretic, caused a natriuresis but no significant change in urinary kallikrein excretion. The results do not support a direct role for the renal kallikrein-kinin system in mediating the natriuresis induced by diuretics.

Adult↗

PubMed1987

Brain involvement in the regulation of renal sodium excretion.

The aim of the present work was to study some aspects of the brain involvement in renal sodium excretion from the point of view of renal regulation of the extracellular fluid volume and composition. It was found on the basis of experiments on conscious sheep that sodium concentration in the cerebrospinal fluid may be of importance for the mechanism of the extracellular fluid volume regulation. Higher concentrations potentiate a homeostatically effective natriuresis during extracellular fluid volume expansion and lower concentrations impair natriuresis. It was also found in sheep with lesions of the anterior third cerebral ventricle that this brain region is of crucial importance for the mechanism of natriuresis evoked by an i.v. hypertonic saline load but the regulation of the extracellular fluid volume is undisturbed provided the sheep is kept in water balance. Finally it was demonstrated in anesthetized dogs that the heart atrial natriuretic system may be under control of both the extracellular fluid volume and plasma osmolality (and/or plasma sodium concentration) and a circumstantial evidence was provided that it may also be under the control of a cerebral function.

Animals↗

PubMed1978

Sodium excretion in volume-expanded dogs. I. Comparison of the effects of physiological saline and 5% glucose solution.

Dogs were subjected to volume expansion with physiological saline and 5% glucose solution. During the infusion Na excretion was significantly increased only when saline was given. Maintenance of the volume expansion with 5% glucose solution immediately following saline infusion was ineffective in preventing the decline of Na excretion rate after the cessation of saline loading. Although the indices of hemodilution such as plasma total protein concentration and peripheral venous hematocrit were reduced along with natriuresis, these values also correlated with the total amount of Na retained during saline infusion. And this amount of retained Na has also a good correlation with the natriuresis. It is concluded that hemodilution is not the essential cause of natriuresis in the present volume expansion experiments, and that the amount of Na retained during saline loading determines the Na excretion rate in some unknown manner. The implication of regression coefficient between Na retention and Na excretion is discussed as a characteristic value in the Na homeostatic mechanism of the organism.

Animals↗

PubMed1984

[Effect of diuretics on the humoral system of kidney prostaglandins in hypertension patients].

Sixty-four patients with stage IIB essential hypertension were examined for the urinary excretion of prostaglandins E2 and F2 alpha, natriuresis and diuresis in the control period and then on the 3rd, and the 12th-14th day of the treatment with diuretics (furosemid, hypotiazid, oxodolin, brinaldix). All diuretics were found to alter the urinary PG excretion, with the degree of their effect depending on the type of the drug, the route and duration of its administration. Furosemid, to a greater degree than other diuretics, increased the urinary excretion of PGE2 thus bringing down the PGF2 alpha/PGE2 ratio, brinaldix increased PGF2 alpha excretion whereas hypotiazid, in cases of its prolonged employment, reduced the excretion of both PGs, the PGF2 alpha decrease being more prominent. PGE2 contributed to a decrease in BP and to the development of natriuresis. The physiological effect of PGF2 alpha depended on the status of the water-electrolyte balance in the body: in patients with IIB stage essential hypertension it facilitated the development of natriuresis and BP decrease. When following the administration of the diuretics the balance of sodium and water in the body lowered, PGF2 alpha caused the retention of sodium and water in the body and did not affect the BP.

Adult↗

PubMedDate not supplied

[Effect of verapamil (isoptin) on kidney function].

In experiments on conscious dogs intravenous administration of verapamil (3-4 mg/kg) reduced diuresis, natriuresis and glomerular filtration. After that the filtration returned to normal and diuresis and natriuresis increased. Following infusion into the renal artery verapamil enhanced diuresis and natriuresis because of the inhibition of tubular reabsorption. In rats verapamil (5-10 mg/kg) also induced a rise in diuresis and sodium excretion, but water diuresis is reduced at first.

Animals↗

PubMedDate not supplied

[Role of vasopressin and aldosterone in the mechanism of osmoregulating reaction].

Possible mechanisms responsible for a natriuretic response to NaCl hypertonic solution (515 mmol/l) digestively administered were studied in chronic experiments on Wistar and Brattleboro rats with continuously implanted urinary bladder catheters. The administration of the solution resulted in rapid antidiuresis and marked natriuresis though the plasma levels of N+ remained unchanged throughout the experiment. Natriuresis did not differ in the Brattleboro and Wistar rats. The time course of blood aldosterone was examined in experiments on Wistar rats. There was its double statistically significant decrease. It is suggested that in addition to secretion of hypophyseal neuropeptides there are additional reflex mechanisms that modulate natriuresis in osmotic irritation of the liver and that these mechanisms may trigger a decrease in plasma aldosterone levels.

Aldosterone↗

PubMed1995

High plasma levels of atrial natriuretic peptide in preascitic cirrhosis: indirect evidence of reduced natriuretic effectiveness of the peptide.

Controversial results come from spot measurements of plasma atrial natriuretic peptide (ANP) in compensated cirrhotic patients. Moreover, either blunted or exaggerated natriuresis has been described after maneuvers increasing plasma ANP. This does not make it possible to delineate the ANP effectiveness. Plasma ANP, renin activity (PRA) and aldosterone and hematocrit were serially measured (7 AM, 9 AM, 6 PM, and 11 PM) in nine preascitic cirrhotic outpatients and in nine healthy subjects on normal sodium diet (150 mmol/day) and carrying on their usual activities (mobile from 7 AM to 10 PM). Daily natriuresis was monitored the day before and during the study. In both groups, ANP peaked at the end of the recumbence period (7 AM) and declined on the assumption of the upright position, so that both ANP values of the standing period were significantly lower than the mean daily level. These fluctuations were reciprocal to PRA and hematocrit changes. Patients showed steadily elevated plasma ANP and reduced PRA (ANP mean daily level: 33.3 +/- 3.8 vs. 15.5 +/- 3.2 pg/mL, P = .004; PRA: 0.76 +/- 0.23 vs. 1.66 +/- 0.21 ng/mL/hr, P = .003). Aldosterone fluctuations and mean daily level were similar in the two groups (mean daily level: 122 +/- 11 vs. 119 +/- 9 pg/mL). Natriuresis was well adapted to the sodium intake and similar in healthy subjects (day 1: 152 +/- 11 mmol; day 2: 138 +/- 12.5 mmol) and patients (143 +/- 15 mmol; 148 +/- 29 mmol). Preascitic cirrhotic patients on a normal salt intake and carrying on their usual activities develop a new steady state requiring increased ANP levels to maintain a sodium balance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

[New classification of hypertension based on renal mechanisms].

The renal mechanisms of hypertension were reviewed, and new way to classify hypertension based on renal mechanisms was proposed. Theoretically, the pressurenatriuresis relationship can be affected in two different ways; either a parallel shift along the blood pressure axis toward a higher blood pressure level or a depression in the slope. The parallel shift of the pressure-natriuresis relationship induces non-sodium sensitive hypertension, while the depressed slope induces sodium sensitive hypertension. Since the degree of the shift of the pressure-natriuresis relationship is determined by the preglomerular vascular resistance from heart to glomeruli, non-sodium sensitive hypertension should be based on the increased preglomerular vascular resistance. On the other hand, the slope of the pressure-natriuresis relationship is determined by glomerulo-tubular balance of sodium, which is mainly controlled by the difference between the whole kidney ultrafiltration coefficient and the rate of tubule sodium reabsorption. Therefore, sodium sensitivity of blood pressure is based on a decrease in the whole kidney ultrafiltration coefficient (due to a decrease in either filtration surface area per glomerulus, hydraulic permeability of glomerular filtration barrier or the number of glomeruli) and/or an increase in tubule sodium reabsorption. In sodium sensitive states, whether whole kidney ultrafiltration coefficient is reduced or tubule sodium reabsorption is enhanced, the glomerular capillary hydraulic pressure rises to compensate for the impairments in sodium excretory capability. If there is a linkage between sodium sensitivity of blood pressure and glomerular hypertension as proposed, renal failure may be expected to be more common in sodium sensitive types of hypertension than in non-sodium sensitive types.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗