PubMed Health⌕ Search

Biomedical subjects

D Haack

Publications and source records attributed to D Haack.

At least 73 records · Page 4Linked to original sources
PubMed1978

Effects of prolonged vasopressin treatment in Brattleboro rats with diabetes insipidus.

Normal Long-Evans rats (LE) exhibited diurnal variations of plasma arginine vasopressin (AVP) concentrations with peak values at 10 A.M. and minimum values at 1 P.M. Brattleboro rats heterozygous for hypothalamic diabetes insipidus (DI) had significantly reduced plasma AVP concentrations and increased plasma osmolalities when compared with LE rats. By prolonged injection of 100 mU/day of vasopressin tannate (VPT) into Brattleboro rats homozygous for DI, plasma AVP concentrations close to those of LE rats were achieved. Potassium was retained for 7 days until escape of vasopressin-induced potassium retention occurred. When 500 mU VPT were injected into DI rats, high plasma AVP levels were induced. Potassium was retained for 2-3 days. After initial sodium retention, periods of natriuresis occurred. During treatment with 100 mU VPT/day most of the alterations present in DI rats were corrected, which included increased water turnover and external water loss, increased hematocrit and plasma sodium concentrations (but not increased plasma osmolalities), hypokalemia, increased activity of the renin-angiotensin system, and reduced adrenocortical function.

Adrenal Glands↗
PubMed1978

Plasma vasopressin concentrations and effects of vasopressin antiserum on blood pressure in rats with malignant two-kidney Goldblatt hypertension.

Male Sprague-Dawley rats with unilateral renal artery stenosis and a contralateral untouched kidney develop a malignant hypertension (MH) which is characterized by high blood pressures, sodium and water depletion, and subsequent activation of the renin-angiotensin system. In the present studies we found plasma arginine vasopressin (AVP) concentrations-3-fold higher than those in rats with benign renal hypertension, and 4- to 5-fold higher than those in normotensive control rats. Analysis of individual values showed considerable scatter; about 50% of the values fell in the range of benign hypertensive or control rats. When a specific AVP antiserum was injected, iv, into eight conscious unrestrained MH rats, BP transiently fell toward control values in four; in one, BP fell by only 10 mm Hg, and three other MH rats showed no response. In the same rats, injection of a specific angiotensin II antiserum always induced a transient fall in BP. On the basis of these and previously reported observations, we conclude that, subsequent to sodium and water loss and activation of the renin-angiotensin system, vasopressin release is stimulated in a significant number of MH rats and that, in these rats, vasopressin may cause significant systemic vasoconstriction. Thereby vasopressin may contribute to the development of malignant renal hypertension in rats.

Animals↗
PubMed1977

Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension.

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.

Angiotensin II↗
PubMed1977

Comparative study on development of corticosterone and DOCA hypertension in rats.

The administration of corticosterone for 5 consecutive days to normal rats on a standard sodium intake induced negative sodium and water balance. These effects were opposite those observed under DOCA treatment. However, not only under DOCA but also under corticosterone treatment extracellular fluid volume (ECFV) and plasma volume (PV) increased, and blood pressure (BP) rose in parallel. Plasma renin and angiotensin II concentrations declined under the influence of both steroids. Plasma arginine vasopressin concentrations increased under DOCA, whereas they transiently decreased under corticosterone administration. These data suggest that the common mediator for BP elevation due to steroid excess would be an increase in ECFV and PV. The pathways by which this increase is achieved seem to be different. Under DOCA treatment ECFV and PV increased subsequent to renal sodium and water retention. Under corticosterone, however, sodium and water were shifted from intra- to extracellular compartments, and a fraction of this shifted sodium and water was conserved in extracellular space, most likely because corticosterone also affected renal sodium handling.

Animals↗
PubMed1976

Is vasopressin involved in the pathogenesis of malignant desoxycorticosterone hypertension in rats?

Rats with unilateral nephrectomy were offered 1% sodium chloride as drinking fluid and were injected with desoxycorticosterone trimethylacetate (D.O.C.-T.M.A.) at weekly intervals. During the fourth to seventh week after the start of the experiment, malignant hypertension developed in most of the animals: body weight fell, reflecting volume depletion; serum osmolality and serum sodium and urea concentrations increased; in the kidneys malignant nephrosclerosis occurred. In such animals, plasma concentrations of arginine-vasopressin were increased ten-fold in comparison with control animals; intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood-pressure (B.P.) to normal or subnormal levels, while the injection of an angiotensin-I or angiotensin-II antibody did not affect B.P. In control animals none of the antibodies had an effect on B.P. It is concluded that in the pathogenesis of malignant D.O.C. hypertension vasopressin plays a role similar to that of renin-angiotensin in malignant renal hypertension.

Angiotensin II↗
PubMed1976

Vasopressin and malignant deoxycorticosterone hypertension in rats.

1. The role of arginine-vasopressin in the pathogenesis of malignant deoxycorticosterone (DOC) hypertension of rats was investigated. 2. In rats with malignant DOC hypertension plasma arginine-vasopressin concentrations increased more than tenfold subsequent to volume depletion and a rise of serum osmolality. 3. The injection of a specific antibody serum for arginine-vasopressin caused a marked fall of blood pressure in rats with malignant DOC hypertension, whereas the injection of angiotensin II antiserum did not affect blood pressure. 4. In rats exhibiting a benign course of DOC hypertension plasma concentrations of arginine-vasopressin were increased threefold in comparison with normotensive control rats; the injection of an arginine-vasopressin antiserum induced a significant but small fall of blood pressure. 5. It is concluded that in the pathogenesis of malignant DOC hypertension arginine-vasopressin might play the role that the renin-angiotensin system plays in the pathogenesis of malignant renal hypertension.

Animals↗
PubMed1976

Effects of saline drinking on malignant course of renal hypertension in rats.

In rats with unilateral renal artery stenosis and an intact contralateral kidney, a malignant course of hypertension (MH) may develop, which is characterized by 1) high BP levels, 2) sodium and water loss and a polyuric-polydipsic syndrome, 3) marked activation of the renin-angiotensin system, 4) malignant nephrosclerosis in the contralateral kidney and high plasma urea concentrations, and 5) deterioration of the animals' general condition. (Some rats exhibit signs of a cerebral vascular crisis; some rats die). When such rats are offered in addition to water 0.9% NaCl, they compulsively drink the saline, BP falls for some days to levels found in the other hypertensive animals, and signs of MH nearly or completely disappear. It is concluded that high saline intake has, for a limited period, a beneficial effect on the malignant course of renal hypertension in rats. The observations made are consistent with the hypothesis that salt and water loss, which ensue subsequent to an increase of BP into a critical high range might trigger the onset of malignant hypertension.

Angiotensin II↗
PubMed1975

[Changes in the binding capacity of thyroxine-binding globulin (TBC), of total thyroxine (T4), of the free thyroxine index (FT4-I) and of thyrotropin (TSH) during normal pregnancy and in hydatidiform mole].

TBC-index and total serum thyroxine were measured in 100 healthy nonpregnant and in 163 pregnant women during the 8. and 41. weeks of gestation. The free thyroxine index was calculated. The TBC-index was found to be elevated in pregnant women and rose continously with duration of pregnancy. The amount of total serum thyroxine was greater in pregnant women (p less than 0,01) without difference between early and late pregnancy. The free thyroxine index decreased continously during pregnancy (p less than 0,01). Serum TSH level were elevated during the first two trimesters of pregnancy. At the third trimester the TSH level were found within the normal range. In patients with hydatidiform mole TSH, total thyroxine, FT4-index, ETR-index as well as TSH levels were increased.

Adult↗
PubMedDate not supplied

[Variability of corticosterone methyl oxidase (type II) deficiency. Presentation of three case reports].

We report on three cases of Corticosterone Methyl Oxidase Typ II deficiency in two siblings and one boy. All three children were presented with typical symptoms of a saltlosing syndrome (vomiting, poor drinking, weight loss, hypotonia). Hyponatremia and hyperkalemia, low plasma aldosterone concentrations when related to high plasma-renin-activities suggested deficiency in the final steps of aldosterone biosynthesis. Variable degrees of enzyme deficiency and no relation of biochemical findings to the clinical symptoms were observed. Clinical symptoms became less severe with age. Diagnosis of CMO II-deficiency was established by an abnormal high ratio of 18-hydroxycorticosterone to aldosterone, by measurement of their precursors and metabolites in plasma and urine. In one sibling negative values may have been caused by suppression of the renin-angiotensin-system due to high sodium replacement therapy.

Aldosterone↗
PubMedDate not supplied

Assessment of hypothalamic-pituitary-adrenocortical axis function in dexamethasone treated very low birth weight infants by a single dose metyrapone test and gas chromatographic mass spectrometric determination of urinary steroids.

In order to assess hypothalamic-pituitary-adrenocortical axis function, we conducted low and single oral dose metyrapone tests (35 mg/kg) in dexamethasone treated very low birth weight infants with bronchopulmonary dysplasia (n = 12). The responses to metyrapone of tetrahydro-11-deoxycortisol (THS) and cortisol metabolites were analyzed by gas chromatography and mass spectrometry in 24-h urinary specimens. For comparative reasons, morning plasma 11-deoxy-cortisol and cortisol were measured by radioimmunoassay before and after metyrapone. No side effects of metyrapone were observed in our patients. In 5 of 12 patients, no urinary THS could be stimulated after metyrapone and most of the other patients had small increases in urinary THS. These findings suggest suppressed or strongly impaired hypothalamic-pituitary-adrenocortical axis function in most patients. While the concentrations of plasma 11-deoxycortisol showed little variation, those of plasma cortisol were grossly different from the respective urinary values. We recommend steroid analysis in 24-h urinary specimens by gas chromatography and mass spectrometry, because urinary steroids provide more information and the highly specific analytical technique is independent of phenomena such as cross reactivity or matrix effects. The low and single oral dose metyrapone test in combination with urinary steroid analysis by gas chromatography and mass spectrometry therefore provides a noninvasive, convenient and safe means of evaluating the integrity of the hypothalamic-pituitary-adrenocortical axis in very low birth weight infants.

Adrenal Cortex↗
PubMedDate not supplied

Increased aldosterone-18-glucuronide/tetrahydroaldosterone ratios in pregnancy.

In the present study the aldosterone-18-glucuronide and tetrahydroaldosterone values in 24 hour urine collections of healthy nonpregnant women, women with normal pregnancies and women with pregnancy induced hypertension (PIH) were compared. In pregnancy an elevated excretion of both aldosterone metabolites was found. The Q-ratio (aldosterone-18-glucuronide/tetrahydro-aldosterone+aldosterone-18-glu cur onide) was also increased compared to healthy nonpregnant women. The elevated Q-ratios point out to increased formation of aldosterone-18-glucuronide. This predominantly renal metabolite may reflect greater availability of aldosterone molecules for interaction with mineralocorticoid receptor in the kidney.

Aldosterone↗