In the steady state of work on a bicycle ergometer repeated i.v. injections of (+) tubocurarine produced a decrease in handgrip strength. In spite of this the intensity of work was maintained constant for 20 to 30 min. During this time pulse rate and blood pressure increased slightly and irregularity but the ventilation increased, both absolutely and in relation to the oxygen uptake, by up to about 50 %. The cardiac output was uninfluenced by the curarization. By adding CO2 to the inspired air the alveolar PCO2 was maintained at the normal exercise level. It is therefore assumed that all the known humoral factors controlling respiration in exercise must have been normal. The greatly increased ventilation must consequently have been caused by some nervous factors. The origin of these factors, whether central or peripheral, is discussed on the background of earlier experimental findings. A tentative explanation, based on the assumption that bicycle‐work is performed by the mediation of the gamma‐loop, is suggested. According to this the“nervous factor” of respiratory regulation in exercise may be the feed‐back to the reticular formation of afferent impulses from the muscle spindles.

No abstract

A simple procedure for a reproducible preparation of radioiodinated angiotensin analogues is described. The iodination is performed at a low level of radioactivity – 200 μCi per 10 μg peptide – with low concentrations of chloramine-T and sodium metabisulphite. No destruction of the peptide occurs during the iodination. The yield is high, and the only purification step needed is a separation of iodinated peptide from non-labelled peptide. This separation is performed by means of column chromatography on DEAE-Sephadex A 25. The specific activity of labelled angiotensin I or II prepared by this method was about 500 μCi/μg. The homogeneity of the radioiodinated angiotensin analogues was established by means of paper chromatography and enzymatic degradation studies, including experiments on the enzymatic conversion of 125I-angiotensin I to 125I-angiotensin II. Radiochromatograms obtained after storage for various periods showed perfect stability of the labelled compounds. Immunological characteristics, as evaluated by standard displacement curves with selected antisera and maximal binding to excess antibody, were reproducible from batch to batch.

Since 1931, when Perla & Marmorston-Gottesman demonstrated the presence of an adrenocortical-like substances in benzene extracts of human urine, numerous biological and chemical methods for the quantitative assay of adrenocortical hormones in the blood and for their metabolites in the urine have been used. The chemical assays are based on widely different principles, e. g. the reducing properties of the compounds, the liberation of 1 7-ketosteroids or formaldehyde by oxidation and the reaction with phenylhydrazin. The methods used for the assay of adrenocortical steroids and their urinary excretion products are often designated as 'corticoid analyses'.Although more than 50 per cent of the total neutral 17-ketosteroids (17-KS) in the urine of normal males and a still higher percentage in the urine of females are metabolites of the adrenocortical hormones, the 17-KS test is of limited value as a means of evaluating the adrenocortical function. Thus it is well-known that patients suffering from Cushing's disease may have a normal excretion of 17-KS together with a markedly increased output of adrenocortical metabolites as measured by other procedures. The Chromatographie. 17-KS analyses, allowing of separate assays for dehydroepiandrosterone, androsterone, etiocholanolone and 1 l-oxy-17-KS, give additional information on the adrenal function, but several investigations have shown that only a small fraction of administered corticosteroids are excreted as 17-KS.An evaluation of the methods for the assay of adrenocortical metabolites in urine is given in the comprehensive and critical reviews by Diczfalusy et al. (1955 b) and Borth (1956 a).From the Hormone Department, Statens Seruminstitut, Copenhagen Excretion in normal subjects and after the administration of corticotrophin