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Biomedical subjects

H Valtin

Publications and source records attributed to H Valtin.

At least 55 records · Page 3Linked to original sources
PubMed1974

Cellular action of antidiuretic hormone in mice with inherited vasopressin-resistant urinary concentrating defects.

Previous work has suggested that resistance to vasopressin in two strains of mice with nephrogenic deficiency of urinary concentration may entail a defect in the action of vasopressin at the cellular level. Several components involved in this action were therefore examined in vitro in renal medullary tissues from control mice (genotype VII +/+) and two genotypes with mild diabetes insipidus (DI +/+ nonsevere) and marked (DI +/+ severe) vasopressin-resistant concentrating defects. No significant differences were found in the affinity of adenylate cyclase for [8-arginine]-vasopressin (AVP), tested over a range of hormone concentration from 10(-10) to 10(-5) M. However, maximal stimulation of adenylate cyclase by saturating concentrations of AVP (intrinsic activity) was markedly decreased from control values in DI +/+ severe mice, and decreased to a lesser extent in DI +/+ nonsevere animals. A significant correlation was found between the activity of adenylate cyclase maximally stimulated by AVP in a given genotype, and the urine osmolality in the same animals. There were no significant differences in maximal stimulation of renal medullary adenylate cyclase in control experiments: not when stimulated nonspecifically by sodium fluoride, nor when stimulated by AVP in tissues from rats with induced water diuresis as compared to antidiuretic rats. Nor were there significant differences between VII +/+ and DI +/+ severe mice in the activity of renal cortical adenylate cyclase, either basal or when stimulated by parathyroid hormone. Furthermore, the abnormal genotypes did not differ significantly from control mice in the renal medullary activities of cyclic AMP phosphodiesterase or cyclic AMP-dependent protein kinase, nor in the content of microtubular subunits (assessed as colchicinebinding protein). The results are compatible with the view that impaired stimulation of renal medullary adenylate cyclase by vasopressin might be the sole or contributing cause of the vasopressin-resistant concentrating defect in the diseased mice; however, a causal relationship has not yet been proved.

Adenylyl Cyclases↗
PubMed1971

ostnatal development of renal function: micropuncture and clearance studies in the dog.

Postnatal renal development was studied in dogs between 2 and 77 days. Single, superficial nephrons were evaluated by micropuncture, concurrently with measurements of total renal function and morphometric analyses in the same animals. Glomerular filtration rate for the entire kidney increased linearly from 0.13 ml/min per g kidney weight at 2 days to 0.91 at 77 days. Extraction of p-aminohippurate increased from about 20 to 80%, and renal plasma flow per g kidney weight, measured as Cpah/Epah, increased threefold during the same period. Filtration fraction increased to the mature value during the first half of the postnatal period studied. The clearance of urea per unit of renal mass increased with age, whereas the fraction of filtered urea reabsorbed declined during the early part of the postnatal period. The pattern of fractional urea reabsorption may be due mainly to increased medullary recycling of urea and to a rise in the reabsorption of water from the medullary collecting duct. Urine osmolality was higher than plasma from birth onward and rose with age. Osmolal equality of collecting duct fluid and medullary interstitium reflected mature vasopressin (ADH)-induced water permeability. The rise in urinary concentration was predominantly due to increasing medullary sequestration of urea. Glomerular filtration rate of the superficial nephron increased from 3.2 nl/min at 21 days, when subcapsular nephrons were uniformly patent, to 23.1 at 77 days. Despite this rise in filtered load, fractional reabsorption of sodium and water in superficial proximal tubules was constant and at the mature level from the onset of intratubular perfusion. Changes in arterial plasma protein concentration, in filtration fraction, and in the hydrostatic pressure gradient between proximal tubule and peritubular capillary may interact to maintain glomerulotubular balance. The data, together with results of an accompanying morphological study, demonstrate a sequence of coordinated changes during postnatal renal maturation.

Absorption↗
PubMed1971

Intracortical distribution of number and volume of glomeruli during postnatal maturation in the dog.

Morphometric analysis was carried out on kidneys of neonatal dogs in which function of the entire kidney and of single nephrons had been evaluated. Measurements were begun after neogenesis of nephrons had been completed, i.e., at the end of the 3rd postnatal wk. They were continued to 74 days by which time glomerular function, expressed per unit of renal weight, had reached the mature level. For statistical analysis, the cortical histogram at each age was divided into eight zones of equal depth between the capsule and corticomedullary junction. The mean total number of glomeruli in this beagle strain was 589 x 10(3) per kidney. The fraction of the total number of glomeruli was lowest in the subcapsular layer (3.9%) and highest (24.5%) in the zone immediately beneath from where it decreased almost linearly to a value of 4.5% in the juxtamedullary region. This numerical distribution did not change with age, which suggests that growth of nonglomerular structures proceeded at the same rate in all cortical layers. Volume of the glomerular tuft rose slightly between the subcapsular and next layer and remained constant down to the juxtamedullary region where it increased sharply. The juxtamedullary glomerulus was about 45% larger in volume than the other glomeruli. This intracortical distribution of glomerular volume did not vary between 23 and 74 days, although the volume of an individual glomerulus at each level increased slightly with age. Total glomerular volume increased by 33% during the postnatal period studied, whereas simultaneously nonglomerular cortical volume rose by 235%. On the assumption that nonglomerular tissue consists mainly of tubules, the data suggest that the rate of tubular growth far exceeded that of glomerular growth. Despite this difference in glomerular and tubular growth rates, analysis of single nephrons in these dogs demonstrates constant and mature proximal fractional reabsorption of sodium and water.

Absorption↗
PubMed1970

On the role of antidiuretic hormone in the inhibition of acute water diuresis in adrenal insufficiency and the effects of gluco- and mineralocorticoids in reversing the inhibition.

In order to determine whether or not antidiuretic hormone (ADH) is essential to the inhibition of an acute water diuresis in adrenal insufficiency, the response to oral water loads was tested in rats with hereditary hypothalamic diabetes insipidus (DI) which lack ADH. It was found that 60 min after water loads of 3 or 5% of body weight urine flow was significantly lower and urine osmolality significantly higher in adrenalectomized DI rats than in the same DI rats before removal of their adrenal glands. The efficacy of gluco- and mineralocorticoids in reversing the inhibition was then determined in the same adrenalectomized DI rats. Prednisolone alone, administered either acutely or chronically, restored the response in urine flow to that seen in the same rats before adrenalectomy, but failed to correct the defect in urinary dilution. Aldosterone when given alone tended to correct the diluting ability but not the response in urine flow. When these two adrenal cortical hormones were given simultaneously, both the urine flow and urine osmolality were nearly identical to what they had been in the same DI rats before adrenalectomy. These studies strongly suggest (a) that ADH is not essential to the inhibition of an acute water diuresis in adrenal insufficiency, although it may abet the inhibition in individuals without diabetes insipidus, which can elaborate ADH; and (b) that both gluco- and mineralocorticoids are required in adrenal insufficiency in order to fully restore the water diuresis as judged by the dual criteria of urine flow and urine osmolality.

Adrenal Glands↗
PubMed1968

Kidney.

Explore the source record for details and available documents.

Acid-Base Equilibrium↗
PubMed1968

Impaired urinary concentration after vasopressin and its gradual correction in hypothalamic diabetes insipidus.

This study utilized rates with hereditary hypothalamic diabetes insipidus (D.I.) in order to explore possible mechanisms which prevent full urinary concentration after acute administration of vasopressin in hypothalamic D.I. and which correct this concentrating defect with prolonged therapy.IT WAS FOUND: (a) that the concentrating defect persisted even when the urinary osmolal excretion of D. I. rats was reduced to that of normal animals; (b) that the defect was not corrected more rapidly if larger doses of vasopressin were given; (c) that it persisted even when the D.I. rats were deprived of drinking water after vasopressin was given; (d) that there was osmotic equilibration between urine and renal papilla at a time when the concentrating defect was still evident; and (e) that the correction of the defect was associated with progressive and significant rise of the papillary osmolality. These studies appear to rule out osmotic diuresis, accumulation of exogenous vasopressin, persistent primary polydipsia, or delay in the induction of membrane permeability as causes for the concentrating defect. Rather, subnormal osmolality of the renal papilla, which can be corrected only gradually, accounts for the initial concentrating defect and the long time required for its correction. Reduction of water content and increase of urea content are primarily responsible for restoration of papillary osmolality to normal.

Animals↗