1 The metabolism of (+)‐, (‐)‐ and (±)‐salbutamol by sulphoconjugation was determined in vitro using human lung cytosol and bronchial epithelial BEAS‐2B cell homogenate.
2 For the lungs the intrinsic clearance (Vmax/Km) value for the pharmacologically active (‐)‐salbutamol (0.49 ± 0.32 ml min‐‐1 g‐1 protein) exceeded that of (+)‐salbutamol (0.046 ± 0.028 ml min‐1 g‐1 protein) by 11‐fold. This was mainly due to a difference in Km value, which was 16 times higher for (+)‐salbutamol (1300 ± 170 μM) than for (‐)‐salbutamol (83 ± 12 μM).
3 The stereoselectivity of sulphoconjugation of salbutamol was very similar in the BEAS‐2B cells, although the absolute activity was considerably lower.
4 The enzyme catalyzing this reaction both in the lungs and in the BEAS‐2B cells was the monoamine (M) form phenolsulphotransferase.
5 These observations emphasize that the smooth muscle of the bronchi most likely are exposed to considerably higher concentrations of the potentially toxic (+)‐enantiomer than of the bronchodilating (‐)‐enantiomer during therapy with (±)‐salbutamol.
Saralasin, an angiotensin II antagonist, was infused into 49 patients with renal artery stenosis, 10 patients with essential hypertension and normal renal arteriograms, and five patients with "low-renin essential hypertension." Renal venous renin and differential renal function studies were used to assess the functional significance of arterial stenoses. "Response" to saralasin, evidenced by a fall in blood pressure during infusion, occurred in no patients with "low renin" hypertension and in only 20% of patients with normal renal arteriograms. In contrast, saralasin "response" occurred in more than 80% of patients with renal artery stenosis and lateralizing functional studies and 100% of cases of "proven" renovascular hypertension (cure or improvement of hypertension after operative treatment). We suggest that saralasin infusion might be a valuable screening test for the recognition of renovascular hypertension.
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