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Biomedical subjects

B Lichardus

Publications and source records attributed to B Lichardus.

At least 55 records · Page 3Linked to original sources
PubMed1987

Effect of metoclopramide therapy on arginine vasopressin excretion and renal water handling in premature infants.

The role of endogenous dopamine (DA) in regulating arginine vasopressin (AVP) release and renal water excretion was studied in 10 premature infants with a mean birth weight of 1,341 g (range 1,150-1,660 g) and a mean gestational age of 30.2 weeks (28-33 weeks), who were given metoclopramide (MTC), a specific DA antagonist. It was demonstrated that in response to MTC urine flow rate increased significantly from a basal value of 0.90 +/- 0.07 to 1.27 +/- 0.09 ml/min/1.73 m2 (mean +/- SE; p less than 0.01), urinary sodium excretion from 6.10 +/- 1.47 to 11.7 +/- 2.24 microEq/min/1.73 m2 (p less than 0.025) and osmolar clearance from 0.38 +/- 0.044 to 0.600 +/- 0.075 ml/min/1.73 m2 (p less than 0.01). MTC administration did not cause any alterations in free water clearance, whereas urinary AVP excretion fell significantly from 49.38 +/- 10.13 to 32.66 +/- 6.53 ng/min/1.73 m2 (p less than 0.05) after MTC. It is concluded that, contrary to adults, in low birth weight premature infants endogenous DA is enhancing rather than inhibiting AVP release and the MTC-induced water diuresis is independent of the fall of AVP since free water clearance remained unaltered after MTC.

Arginine Vasopressin↗
PubMed1987

Heart atrial auriectomy reduces the diuretic and natriuretic responses to a hypertonic saline load.

Acute bilateral atrial auriectomy in anesthetized dogs reduced diuresis and natriuresis induced by both extracellular fluid volume expansion with isotonic saline and a hypertonic saline load. Since a hypertonic saline load, in contrast to isotonic saline infusion, was not accompanied by a significant increase in central venous pressure it is proposed that either increased plasma osmolality or plasma sodium concentration (or both) participate in the modulation of the atrial natriuretic mechanism.

Animals↗
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↗
PubMed1987

The effect of atrial natriuretic factor on natriuresis in acutely hypophysectomized saline-loaded rats.

Acute hypophysectomy (a.h.) (i.e. pituitary ablation 120 min prior to the experiment) abolished the ability of anaesthetized rats to excrete sodium following isotonic saline load (4% body weight). The diuretic response remained even slightly increased as compared to control sham-operated animals (s.o.) (maximal UNaV a.h. rats +/- SE: 0.65 +/- 0.10 mumol/min vs maximal UNaV in s.o. rats: 4.54 +/- 0.50 mumol/min). Alpha h-atrial natriuretic factor 1-28 (ANF) in a doses of 3.3 micrograms/animal.40 min restored natriuresis in a.h. rats following isotonic saline load to the level observed in s.o. rats (4.25 +/- 0.64 mumol/min), the change being transient. A decrease of blood pressure to 78.6 +/- 3.21 mm Hg during ANF infusion was followed by a reduction in the natriuretic effect of ANF, while the diuretic effect remained unchanged. Based on own results and literary data it could be suggested that impairment of ANF release or its renal effect are involved in the abolishment of homeostatically effective natriuresis in a.h. animals.

Animals↗
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↗
PubMed1986

Atrial natriuretic hormones--thirty years after the discovery of atrial volume receptors.

Twenty-five years after the discoveries of the existence of atrial granules and of volume receptors in the heart atria the search for natriuretic hormones has led to the isolation and identification of the atrial natriuretic factors (ANF) now considered as a hormonal system. These peptides are probably synthesized and stored in the Golgi apparatus of cardiac myocytes and are released in response to atrial wall stretch following acute plasma volume expansion and increased central blood volume, e.g., during head-out water immersion, in arterial hypertension, or increased left and/or right atrial pressure in cardiac failure, but also possibly in response to increased frequency of myocardial contractions, e.g. in paroxysmal tachycardia. The mechanisms of the renal action of these potent natriuretic hormones are not yet precisely known. Increased GFR may contribute to the initial rise in urinary sodium excretion and increased renal medullary blood flow to the later phase of natriuresis. The proximal tubule, the thin descending and the ascending limb of Henle's loop and especially the medullary collecting tubule were so far incriminated as tubular sites of action of ANF. Finally, recycling of sodium in medullary tissue and secretion of sodium via back-flux from the interstitium into the medullary collecting tubule are postulated to result in the hypernatric urine observed after ANF administration. Direct suppression of the secretion of renin, aldosterone, vasopressin, and vasopressin-stimulated cAMP synthesis may also contribute to its diuretic, natriuretic, and antihypertensive effects. The renal hemodynamic and tubular as well as the adrenal and systemic vascular effects are related to enhanced cGMP synthesis in medium-sized arterial vessels, in glomeruli and specific tubular segments, and in adrenal tissue, and may be calcium dependent. Specific ANF-binding sites were detected in these target organs. Although increased ANF release was observed in response to atrial distension in various disease states, which may contribute to renal sodium elimination in human hypertension and congestive heart failure, further studies are needed to identify its precise physiological and pathophysiological significance.

Amino Acid Sequence↗
PubMed1986

Renal response to arginine vasopressin in premature infants with late hyponatraemia.

To assess the influence of late hyponatraemia on the renal responsiveness to endogenous arginine vasopressin (AVP), urinary excretion and plasma concentration of sodium, plasma and urine osmolality, free water clearance, and urinary AVP concentration and excretion were measured in 11 healthy premature infants with a mean birth weight of 1360 g and mean gestational age of 31 weeks. Studies were performed on days 1, 5, and 19. The development of late hyponatraemia was associated with a pronounced decline in urine osmolality, whereas urine flow rate and free water clearance increased significantly. Mean (SEM) urine AVP concentration and excretion also rose significantly from 2.15 (0.31) pg/ml and 0.36 (0.55) pg/min/m2 on the first day to 6.5 (0.96) pg/ml and 3.85 (0.63) pg/min/m2 on the 19th day, respectively. When renal response to AVP was compared at different ages the highest urine osmolality and steepest response curve was observed on the first day. With development of hyponatraemia the renal response became blunted. It is concluded that the limited tubular sodium transport and hyponatraemia hinders the establishment of intrarenal osmotic gradient, impairs renal response to AVP, and prevents excessive water retention and further fall of plasma sodium.

Arginine Vasopressin↗
PubMed1985

Late hyponatremia in premature infants: role of aldosterone and arginine vasopressin.

To assess the possible involvement of arginine vasopressin in the pathogenesis of late hyponatremia in preterm infants, serial measurements of sodium balance, fractional sodium excretion, plasma and urine osmolality and sodium concentration, and urinary aldosterone and arginine vasopressin excretion were performed at weekly intervals in nine healthy preterm infants. During the course of late hyponatremia, there was a significant increase in urinary aldosterone and arginine vasopressin excretion, from 0.94 +/- 0.16 to 4.30 +/- 0.76 micrograms/day and from 0.38 +/- 0.08 to 1.19 +/- 0.26 ng/day, respectively, from the first to the fourth to fifth weeks. A significant negative correlation was found between fractional sodium excretion and urinary aldosterone excretion. Aldosterone excretion, however, correlated positively with urinary arginine vasopressin excretion in seven of the nine infants. The parallel increase in urinary aldosterone and arginine vasopressin excretion in salt-losing premature infants may occur in response to the protracted contraction of the extracellular fluid compartment, and may contribute to the restoration of volume in the body fluid compartments and to the development of late hyponatremia.

Aldosterone↗
PubMed1985

Simple diagnosis of diabetes insipidus and antidiuretic hormone excess.

The value of information that may be obtained by measuring osmolality of body fluids is not generally appreciated by clinicians. Osmolality determination by freezing point depression is technically simple to perform and requires only 0.2 ml fluid. The simultaneous measurement of plasma and urine osmolality may yield useful information concerning alterations in water homeostasis (diabetes insipidus and antidiuretic hormone excess) and avoid uncomfortable and sometimes hazardous investigations of patients.

Adolescent↗
PubMed1985

Analytical identity of an inhibitor of sodium transport isolated from human serum and urine.

Inhibitors of sodium transport purified from serum and urine of healthy and uremic subjects show the same elution pattern on columns of a weak anion exchanger (DEAE Sephadex A-25), reverse-phase chromatography (Separon SI C 18) and gel permeation chromatography (Separon Hema 300 Glc). Moreover, their thin-layer chromatographic mobility (DC-Alufolien Cellulose) in nine solvent systems is the same. These identical physicochemical properties document satisfactorily their identity, which permits the use of the urinary inhibitor of sodium transport for structure studies.

Biological Transport↗
PubMed1984

Effects of lysine-vasopressin (LVP) and 1-deamino-8-D-arginine-vasopressin (dDAVP) upon electrical potential, short-circuit current and transepithelial D.C. resistance of the frog skin.

The synthetic analogue of vasopressin, 1-deamino-8-D-arginine-vasopressin (dDAVP), possesses a protracted antidiuretic activity while having practically no pressoric activity as compared to arginine-vasopressin (AVP) or lysine-vasopressin (LVP). The effects of LVP and dDAVP were studied on the frog skin (Rana temporaria) sodium transport as reflected by the short-circuit current (SCC) level, on an Ussing apparatus. The application two different equimolar doses of LVP or dDAVP (approx. 9.4 X 10(-8) mol X l-1 and 18.8 X 10(-8) mol X l-1 to the inner surface of the skin resulted in identical maximal increases of sodium transport. However, the maximum transport stimulation after the application of dDAVP was delayed by about 30 min as compared to the stimulation by LVP (P less than 0.01). In addition, a protracted recovery of SCC towards its original levels was observed in experiments with dDAVP application after the hormone removal (P less than 0.01). It is concluded that dDAVP stimulates Na+ transport through the frog skin despite its lacking pressoric activity. Thus, the natriferic activity of vasopressin is related to its antidiuretic rather than pressoric activity. Maximum increase in the sodium transport following dDAVP application was delayed and more protracted as compared to the effect of LVP.

Animals↗