Abstract
Hypokalemia in Bartter's syndrome or when experimentally induced is associated with an increase in synthesis of prostaglandin E2 which is a vasodilator. If hypokalemia mediates the vascular resistance to All in Bartter's syndrome, then resistance to AII should also be present in other hypokalemic states. To examine this possibility, seven patients with Bartter's syndrome (3 children, 9-17yrs old and 4 adults) and six patients with other hypokalemic states were studied under similar conditions. Serum K(SK), supine PRA and the blood pressure response to AII were determined, before and during treatment with indomethacin, in patients with Bartter's syndrome, and before and after correction of hypokalemia in other patients. In Bartter's syndrome treatment with indomethacin did not change mean BP(104/69 mmHg), but increased mean SK from 2.3 ± 0.1 (SE) to 3.1 ± 0.2 meq/1, decreased mean supine PRA from 29.4 ± 10 to 3.1 ± 1.1 ng/ml/hr, and decreased mean pressor dose of AII (a dose capable of increasing basal diastolic BP by 20 mmHg) from 26 ± 5.4 to 9.6 ± 2.3 ng/Kg/min. In other hypokalemic states, correction of hypokalemia did not change mean BP(92/50), but increased mean SK from 2.3 ± 0.3 to 3.5 ± 0.2 meq/l, decreased mean supine PRA from 27.6 ± 9.8 to 2.4 ± 0.4 ng/ml/hr and decreased mean pressor dose of AII from 102 ± 34 to 12 ± 2.5 ng/Kg/min. These data suggest: 1.Hypokalemia may be responsible for the vascular resistance to AII in hypokalemic states. 2.The effect of hypokalemia on vascular resistance to AII may be mediated by prostaglandin E2.
Article PDF
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Radfar, N., Gill, J., Taylor, A. et al. ROLE OF HYPOKALEMIA IN VASCULAR RESISTANCE TO ANGIOTENSIN II (AII). Pediatr Res 11, 430 (1977). https://doi.org/10.1203/00006450-197704000-00364
Issue Date:
DOI: https://doi.org/10.1203/00006450-197704000-00364