Browsing by Author "LOPEZMORENO, JM"

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    FEVER OF UNEXPLAINED ORIGIN, BIOCHEMICAL CUSHINGS-DISEASE AND CEREBRAL DYSRHYTHMIA CORRECTED BY VALPROATE SODIUM
    (1985) LOPEZMORENO, JM; RODRIGUEZPORTALES, JA; MAHANA, D
    A patient with cerebral dysrhythmia and fever of unexplained origin for 2 yr is described. She had elevated and nonsuppressible levels of urinary 17-hydroxycorticosteroids but no clinical features of hypercortisolism. Treatment with valproate sodium corrected all the abnormalities. Cerebral dysrhythmia may affect the hypothalamic mechanisms of body temperature and regulation of adrenocorticotropic hormone levels.
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    INHIBITION OF THE KALLIKREIN-KININ SYSTEM AND VASCULAR REACTIVITY IN BARTTERS-SYNDROME
    (1985) RODRIGUEZPORTALES, JA; LOPEZMORENO, JM; MAHANA, D
    To study the significance of the increased activity of the kallikrein-kinin system described in patients with Bartter''s syndrome, we investigated the pressor response to infused angiotensin II in four patients with the syndrome receiving no treatment and during the administration of aprotinin and of indomethacin. Five normal subjects served as controls. Aprotinin is a proteolytic enzyme that inhibits the formation of kinins by inhibiting plasma and glandular kallikrein. Indomethacin, a prostaglandin-synthesis inhibitor, can also inhibit the kallikrein-kinin system and normalizes vascular responsiveness to angiotensin II in Bartter''s syndrome. All patients had increased urinary kallikrein and prostaglandin E2 concentrations. Aprotinin significantly decreased the dose of infused angiotensin II required to induce a 20 mm Hg increase in diastolic blood pressure, from 11 .+-. 4 ng/kg per min to 7.0 .+-. 2.0 ng/kg per min (mean .+-. SD; p < 0.05) in normal subjects and from 135 .+-. 57 ng/kg per min to 70 .+-. 26 ng/kg per min (p < 0.05) in the patients with Bartter''s syndrome, without significantly changing plasma renin activity, mean control blood pressure, or urinary prostaglandin E2 concentration. Indomethacin normalized the pressor response to angiotensin II in three patients who had been pretreated for 4 days (pressor dose, 10 ng/kg per min) but not in one patient who received a single oral dose of indomethacin 5 hours before the test. Our results suggest that inhibition of the kallikrein-kinin system alone accounts for approximately a 50% decrease in vascular resistance to the pressor effect of angiotensin II in Bartter''s syndrome, while additional suppression of prostaglandins entirely normalizes the vascular response to angiotensin II. These observations underscore the importance of the kallikrein-kinin system as a vasodilator in Bartter''s syndrome and support the concept that this system may contribute to the regulation of blood pressure in human beings.