Autor: |
Wood AJ; University Department of Clinical Pharmacology, Radcliffe Infirmary, Oxford, UK., Brearley CJ, Aronson JK, Grahame-Smith DG |
Jazyk: |
angličtina |
Zdroj: |
British journal of clinical pharmacology [Br J Clin Pharmacol] 1990 Sep; Vol. 30 (3), pp. 383-90. |
DOI: |
10.1111/j.1365-2125.1990.tb03788.x |
Abstrakt: |
1. We have measured the effect of oral salbutamol on cation transport in vivo by studying the disposition of an oral load of rubidium chloride in healthy treated volunteers and in untreated matched controls. 2. During the administration of salbutamol there was a significantly lower plasma rubidium concentration 5 h after the administration of the oral load of rubidium chloride, reflecting an increase in the net clearance of rubidium from the plasma into at least some tissues in vivo. 3. There was no difference in either intraerythrocytic rubidium concentrations or the pseudo-rate constant for erythrocyte rubidium uptake in vivo after salbutamol. 4. Ex vivo incubation of whole blood preloaded in vivo with rubidium showed that the clearance of rubidium from the plasma was inhibited by 95% in the presence of the Na+,K(+)-ATPase inhibitor digoxin. 5. These data suggest that salbutamol stimulates cation transport via Na+,K(+)-ATPase in vivo into some tissues but not into the erythrocyte. 6. This pattern of change in rubidium disposition after salbutamol is completely different from the patterns of change we have seen in patients with essential hypertension or acute manic illness. We therefore suggest that the changes in erythrocyte rubidium uptake which we have previously described in vivo in patients with essential hypertension or acute manic illness do not result from beta 2-adrenoceptor-mediated catecholamine stimulation of Na+,K(+)-ATPase. |
Databáze: |
MEDLINE |
Externí odkaz: |
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