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Biomedical subjects

H Sonnenberg

Publications and source records attributed to H Sonnenberg.

108 records · Page 6Linked to original sources
PubMed1975

Secretion of salt and water into the medullary collecting duct of Ringer-infused rats.

Using a microcatheterization technique, the contribution of the collecting duct to the renal response to extracellular fluid volume expansion was studied in anesthetized rats. During intravenous infusion of Ringer solution (0.25 ml/min per 100 g body wt), urinary excretion of fluid, sodium, and potassium was 365 mul/min per g kidney wt (V), 52.6 mueq/min per g kidney wt (UNaV), and 3.86 mueq/min per g kidney wt (UKV), representing 23, 24, and 65% of filtered load, respectively. Analysis of collecting duct fluid from cortex and outer medulla indicated continued net reabsorption of ions and water in these nephron segments; in contrast, in inner medulla net secretion of Na, K, and fluid into the collecting duct was demonstrated. Addition of sodium and water was equivalent to approximately 10% of filtered load. It is concluded that under the stress of extreme intravenous fluid loading tubular secretion of salt and water into the inner medullary collecting duct contributes importantly to diuresis and natriuresis. The mechanism of such secretion remains undetermined.

Animals↗
PubMed1973

Proximal and distal tubular function in salt-deprived and in salt-loaded deoxycorticosterone acetate-escaped rats.

Proximal and distal tubular function was compared with urinary excretion in rats after chronic administration of salt and deoxycorticosterone acetate (DOCA) or during salt deprivation. DOCA rats excreted significantly more sodium than did salt-deprived rats. Measurements of tubular fluid to plasma (TF/P) inulin ratios and concentrations of sodium and potassium in quantitative, timed collections, related to measured tubular length, allowed calculation of absolute reabsorption of fluid and ions in the different nephron segments. Proximal transport was not reduced in DOCA-treated rats compared with salt-deprived animals; in distal tubule the former group reabsorbed more sodium and secreted less potassium than the latter. Calculation of sodium transport in loop of Henle as the difference in flow between the end of the proximal convolution and the beginnings of the distal tubule indicated no inhibition of reabsorption in DOCA animals. Comparison of end-distal tubular flow with simultaneous urinary excretion suggested that sodium load was not the determining factor of enhanced natriuresis in DOCA-treated animals. The data are interpreted as indicating that DOCA-escape in the rat is associated with specific alteration of sodium transport in the collecting duct system.

Animals↗
PubMed1972

A humoral component of the natriuretic mechanism in sustained blood volume expansion.

A natriuretic and diuretic response to whole blood infusion in the rat, exaggerated and sustained by intravenous reinfusion of excreted urine, was shown to be associated with increased glomerular filtration and reduced tubular reabsorption. Cross-circulation of animals so responding (donor rats) with isovolemic recipients led to a modest natriuretic and diuretic response in the latter, not accounted for by altered physical composition of the blood nor by observed changes in filtration rate or arterial blood pressure. The recipient natriuresis was unchanged when nephrectomized donors were used and it occurred in experiments in which donor urine was simultaneously replaced by intravenously infused Ringer-Locke solution; the natriuretic property of the cross-circulating blood could therefore not have been due to reinfusion of urinary constituents, nor to accumulation of metabolites, nor to a factor of renal origin. A recipient natriuresis was also observed when the expanded and urine reinfused donor had been acutely adrenalectomized, ruling out an altered secretion of adrenal cortical or medullary hormones as a principal cause of this natriuresis; the data, however, do not exclude participation of reduced aldosterone secretion in the normal effector mechanism. In control experiments in which whole blood was exchanged for donor blood, a small delayed natriuresis did occur in the recipient; this could be completely prevented by administration of aldosterone. In similar exchange experiments with adrenalectomized donors, a small natriuresis developed in the recipient before blood administration but declined afterwards. These minor natriuretic effects probably resulted from altered mineralocorticoid content of the cross-circulating blood due to factors other than blood volume change. The larger natriuretic response seen in all recipients when the donor was volume expanded must have been due largely to a humoral natriuretic factor of other than renal or adrenal origin.

Adrenal Glands↗
PubMedDate not supplied

Regulation of sodium, calcium and vitamin D metabolism in Dahl rats on a high-salt/low-potassium diet: genetic and neural influences.

1. A dietary combination of high salt and low potassium (HSLK) exacerbates hypertension in Dahl salt-sensitive (DS) rats and renders previously normotensive Dahl salt-resistant (DR) rats hypertensive. In both strains, the severity of hypertension correlates with urinary calcium loss. However, the magnitude of excretory calcium losses is significantly greater in DS rats and is potentiated by chemical sympathectomy in both strains. 2. We hypothesized that a defect in vitamin D metabolism may underlie the observed strain-dependent differences in calcium balance. 3. Arterial blood pressure (ABP), water and mineral balance and serum concentrations of 1,25-dihydroxyvitamin D3 (1,25(OH)2 D3) and 25-hydroxyvitamin D3 (25(OH)D3) were measured in intact and chemically sympathectomized (6-hydroxydopamine; 6-OHDA) DS and DR rats after 8 weeks on a HSLK diet. 4. Chronic ingestion of this diet resulted in marked and moderate levels of hypertension in DS and DR rats, respectively. The hypertension was abated and eliminated by 6-OHDA in the DS and DR strains, respectively. Independent of treatment, DS rats had significantly higher urinary excretion of calcium and reduced intestinal absorption of the ion compared with DR rats. The DS rats had significantly higher serum levels of 1,25(OH)2 D3 and markedly lower serum levels of 25(OH)D3 than DR rats. Chemical sympathectomy tended to increase 1,25(OH)2 D3 and to decrease 25(OH)D3 levels in both strains. 5. These data indicate a genetic difference in vitamin D metabolism between DS and DR rats. The abnormally elevated levels of 1,25(OH)2 D3 in DS rats may be an appropriate compensatory response to excessive excretory calcium loss and reduced target organ sensitivity to the hormone and may, maladaptively, directly contribute to hypertension, by stimulating vascular smooth muscle contractility.

Adrenergic Agents↗
PubMedDate not supplied

Atrial natriuretic factor: reduced cardiac content in spontaneously hypertensive rats.

We recently discovered a potent natriuretic factor in cardiac atrial tissue. The present experiments were designed to determine whether hypertension was associated with altered tissue content of this atrial natriuretic factor. Extracts were prepared using fresh atria from spontaneously hypertensive rats of the Okamoto strain and from their Wistar-Kyoto controls. Two groups of anesthetized, normovolemic rats (Sprague-Dawley) were used to measure the renal natriuretic and chloriuretic effect of each type of extract. Results indicate that atrial content of natriuretic factor is reduced in hypertensive rats compared to control animals. We speculate that chronic release of the factor could have depleted atrial stores, and that increased blood levels of atrial natriuretic factor may be involved in the generation and maintenance of hypertension in this model.

Animals↗