Influence of different sources of injected selenium on certain enzymes, glutathione and adenosylmethionine concentration in buffalo (Bubalus bubalis) calves.

Sodium selenite and selenomethionine were investigated as possible causative factors for the induction of Degnala disease syndrome in twelve buffalo (Bubalus bubalis) calves divided into three groups of four. Group 1 was the control group and received no additional selenium. Sodium selenite and selenomethionine were given daily as intramuscular injections on a selenium-equivalent basis, with a weekly increment in the dose of 0.05 mg Se/kg live weight from 0.05 to 0.20 mg Se/kg live weight per day, in groups 2 and 3 respectively. Only one animal from group 3 manifested the lesions of Degnala disease. The blood Se concentration and erythrocyte glutathione peroxidase (EC 1.11.1.9; GSH-Px) activity were both greater in groups 2 and 3 than in control group 1. The overall blood Se concentration was 0.22 (SE 0.01), 0.38 (SE 0.12) and 0.77 (SE 0.20) micrograms Se/ml in groups 1 to 3 respectively with corresponding GSH-Px activities of 63.84 (SE 7.38), 88.37 (SE 12.38) and 165.32 (SE 40.62) enzyme units/mg protein. Erythrocyte glutathione reductase (NAD(P)H) (EC 1.6.4.2) activity was not affected by treatment but reduced glutathione content was lower in groups 2 and 3. Liver adenosylmethionine, estimated at autopsy, was lowest (22.87 (SE 6.17) mumol/g) in group 3, and greatest (102.63 (SE 9.39) mumol/g) in group 1 (P less than 0.01). Organic Se sources seemed to accumulate in tissues more than inorganic sources, and might be the causative toxic factors of Degnala disease.

Adrenocorticotropin release by tryptophan in man.

Previous work from this laboratory indicated significant elevations of cortisol after the administration of tryptophan. The current investigation was designed to confirm this observation and study the effect of this agent on ACTH. Cortisol rose 12.4 +/- 5.2 microgram/dl (mean +/- SD) in 10 of 12 tests (P less than 0.02). Responding patients had rises of ACTH averaging 101.8 +/- 45.8% (range, 40-159 pg/ml) above baseline. The time course of the ACTH change closely paralleled that of cortisol, and there were significant correlations between the rises of the two substances (r = 0.81; P less than 0.01). The current data strongly suggest that tryptophan administration stimulates ACTH release, possibly through activation of the central serotonergic nervous system. Review of the literature suggests the possibility that ACTH stimulation only occurs at high plasma tryptophan (and presumably brain serotonin) concentrations, with ACTH inhibition occuring at lower levels.

Stimulation of aldosterone, renin, and cortisol by tryptophan.

Tryptophan administration was used to evaluate the possibility that serotonergic neurons are involved in regulating the release of cortisol, renin, and aldosterone. Eleven studies were undertaken using 2 or 10 g tryptophan administered to fasting patients in continued supine posture. Aldosterone rose significantly to 208% (range, 128-329%) of baseline in all seven studies using 10 g and in one of the four studies using 2 g. Renin rose significantly to 189% (range, 116-340%) of baseline in four of the seven studies using 10 g and in two of the four studies using 2 g. Cortisol rose from 10.1 +/- 3.3 to 20.0 +/- 3.7 micrograms/100 ml (P less than 0.001 by t test) in six of the seven studies using 10 g and three of the four studies using 2 g. In eight studies, there was a significant rise of more than one substance after tryptophan administration. In six of these, peak values of the responding hormones occurred at the same time or within a single 30-min sampling interval despite the absence of a constant relationship between their rises. The results suggest participation of the central serotonergic nervous system in the control of renin and aldosterone in addition to its previously postulated role in cortisol release.

Evaluation of surgical response in renovascular hypertension using angiotensin II blockade.

The mechanisms involved in residual or recurrent hypertension following operation to correct renal artery stenosis were studied in 10 patients by performing angiotensin II blockade with Saralasin (Sarcosine, alanine, angiotensin II) before and after operation. Peripheral renin and renal vein renin determinations, angiography, and renography were done as well. The limitations of renin determinations are cited and the application of angiotensin II blockade as a specific method of detecting renin-dependent hypertension before and after operation are presented. Saralasin infusion under the controlled conditions of our study proved to be a sensitive method for detection of renin-dependent hypertension. The results of Saralasin infusion correlated closely with peripheral and renal vein renin determinations. Thus angiotensin II blockade before and after operation may supercede more invasive and less specific diagnostic methods.