The Effect of Bromocriptine on Circulating Vasopressin

1982 ◽  
Vol 63 (4) ◽  
pp. 367-372 ◽  
Author(s):  
Bruce G. Robinson ◽  
Phillip Clifton-Bligh ◽  
Solomon Posen ◽  
Brian J. Morris

1. The oral administration of 2·5 mg of the dopamine (3,4-dihydroxyphenethylamine) agonist bromoergocriptine enhanced the osmotically stimulated rise in plasma [arginine]vasopressin ([Arg]VP) concentrations in five normal human subjects. 2. This finding lends support to the suggestion that the osmotically induced release of [Arg]VP is under dopaminergic control in man.

1956 ◽  
Vol 34 (4) ◽  
pp. 683-688 ◽  
Author(s):  
Marion H. Ferguson ◽  
A. Naimark ◽  
J. A. Hildes

Parotid juice from normal human subjects was collected by means of suction cups over the parotid papillae. The iodide content of the secretion was determined at various flow rates with and without the oral administration of potassium iodide, ammonium thiocyanate, and methimazole (Tapazole, Lilly), as these drugs are known to influence iodide metabolism in the thyroid gland. An inverse curvilinear relationship was found between the concentration of iodide and the rate of parotid secretion. Potassium iodide by mouth increased the concentration of parotid juice iodide in the same proportion as the increase in blood level of iodide. The amount of iodide secreted by the parotid glands was depressed by the administration of thiocyanate but was not influenced by the administration of methimazole.


Science ◽  
1944 ◽  
Vol 100 (2602) ◽  
pp. 431-432 ◽  
Author(s):  
A. H. FREE ◽  
J. R. LEONARDS ◽  
D. R. MCCULLAGH ◽  
B. E. BIRO

1977 ◽  
Vol 53 (4) ◽  
pp. 401-404
Author(s):  
P. H. Baylis ◽  
R. A. Stockley ◽  
D. A. Heath

1. Acute hypoxaemia has been reported to stimulate vasopressin release in animals. 2. Hypoxaemia induced by breathing 9·3% oxygen for 15–20 min failed to produce a rise in plasma arginine vasopressin concentration in six out of eight healthy human subjects. The two subjects who developed an increase in plasma arginine vasopressin concentration had a significant rise in serum cortisol. 3. Breathing 100% nitrogen until impairment of consciousness caused no rise in plasma arginine vasopressin concentration.


1956 ◽  
Vol 34 (1) ◽  
pp. 683-688 ◽  
Author(s):  
Marion H. Ferguson ◽  
A. Naimark ◽  
J. A. Hildes

Parotid juice from normal human subjects was collected by means of suction cups over the parotid papillae. The iodide content of the secretion was determined at various flow rates with and without the oral administration of potassium iodide, ammonium thiocyanate, and methimazole (Tapazole, Lilly), as these drugs are known to influence iodide metabolism in the thyroid gland. An inverse curvilinear relationship was found between the concentration of iodide and the rate of parotid secretion. Potassium iodide by mouth increased the concentration of parotid juice iodide in the same proportion as the increase in blood level of iodide. The amount of iodide secreted by the parotid glands was depressed by the administration of thiocyanate but was not influenced by the administration of methimazole.


1983 ◽  
Vol 64 (4) ◽  
pp. 395-398 ◽  
Author(s):  
P. B. B. Jones ◽  
R. G. G. Russell

1. We studied the effect of oral administration of acetylsalicylic acid (1200 mg/day for 3 days) on the urinary excretion of 6-ketoprostaglandin F1α in normal human subjects as an index of prostacyclin production in vivo. 2. The concentrations and excretion rate in urine fell to 45% of pretreatment levels in 3 days, but returned to pretreatment values after 7 days. 3. These results suggest that production of prostacyclin in vivo is only partially inhibited by high doses of aspirin and that there are sites of production of prostacyclin which are protected from inhibition by aspirin and which contribute to urinary 6-ketoprostaglandin F1α. The measurement of 6-ketoprostaglandin F1α in urine may therefore be of only limited value as an index of the metabolism of vascular tissue in vivo.


1963 ◽  
Vol 10 (02) ◽  
pp. 400-405 ◽  
Author(s):  
B. A Amundson ◽  
L. O Pilgeram

SummaryEnovid (5 mg norethynodrel and 0.075 mg ethynylestradiol-3-methyl ether) therapy in young normal human subjects causes an increase in plasma fibrinogen of 32.4% (P >C 0.001). Consideration of this effect together with other effects of Enovid on the activity of specific blood coagulatory factors suggests that the steroids are exerting their effect at a specific site of the blood coagulation and/or fibrinolytic system. The broad spectrum of changes which are induced by the steroids may be attributed to a combination of a chain reaction and feed-back control.


1979 ◽  
Vol 42 (02) ◽  
pp. 694-704 ◽  
Author(s):  
F Rendu ◽  
A T Nurden ◽  
M Lebret ◽  
J P Caen

SummaryWe have used the mepacrine-labelling procedure to measure the dense body (serotonin storage organelle) content of the platelets of 2 hereditary disorders where abnormalities in dense body number were suspected. The platelets were incubated with mepacrine and examined by fluorescence microscopy. A mean number of 5.4 ± 0.8 (SD) dense bodies per platelet was calculated from the data obtained using platelets isolated from 40 normal human subjects. In contrast the platelets of 2 patients with the Bernard-Soulier syndrome contained an average of 14 and 17 labelled granules. This increase was associated with a much greater capacity of the platelets to accumulate 14C-5-HT. The opposite result was obtained using the platelets from 2 patients with the Hermansky-Pudlak syndrome which contained few granules labelled by mepacrine and took up less 14C-5-HT than normal human platelets. Centrifugation of the patients’ platelets on discontinuous sucrose gradients showed that the platelets of the 2 Bemard-Soulier patients were much denser than normal whereas a high proportion of low density platelets was observed in the Hermansky-Pudlak syndrome. These results further define the platelet abnormalities in the two syndromes and suggest that dense body number may be one of the factors governing platelet density.


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