دورية
Effects of salbutamol and metoprolol on plasma renin activity and plasma potassium of normal subjects and of hypertensive patients
| العنوان: | Effects of salbutamol and metoprolol on plasma renin activity and plasma potassium of normal subjects and of hypertensive patients |
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| المؤلفون: | Salvetti, Antonio, Poli, L., Arzilli, F., Sassano, L., Pedrinelli, R., Motolese, M. |
| المصدر: | Journal of Endocrinological Investigation; January 1978, Vol. 1 Issue: 1 p1-8, 8p |
| مستخلص: | The effect of β2-agonist salbutamol on plasma renin activity (PRA) and plasma potassium was investigated in seven normal subjects, in twenty-three patients with essential hypertension and in one patient with primary aldosteronism. The action of β1-antagonist metoprolol on PRA and plasma potassium changes induced by salbutamol was also studied in one normal subject and in seven patients with essential hypertension. Salbutamol significantly increased PRA in normal subjects and in patients with essential hypertension with normal (8 cases) or high (5 cases) PRA, while it did not modify PRA in patients with essential hypertension with low PRA (10 cases), and in the patient with primary aldosteronism. Plasma potassium was significantly decreased after salbutamol both in normal and hypertensive patients: no correlation was found between PRA and plasma potassium changes. Metoprolol inhibited both PRA increments and plasma potassium decrements induced by salbutamol. These data suggest the following conclusions. β-Adrenergic receptors mediating renin release in man cannot be clearly differentiated into β-subtypes. The PRA unresponsiveness observed in patients with essential hypertension with low PRA and in the patient with primary aldosteronism indicates a decreased renal response to adrenergic stimuli, probably due to a decreased renin storage. The hypokalemic action of salbutamol cannot be explained by changes of the renin angiotensin system. Moreover the β-receptors mediating the decrease of plasma potassium cannot be clearly differentiated into β-subtypes. |
| قاعدة البيانات: | Supplemental Index |
| تدمد: | 03914097 17208386 |
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| DOI: | 10.1007/BF03346764 |