Browsing by Author "RODRIGUEZPORTALES, JA"

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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.
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    PRIMARY HYPERPARATHYROIDISM AND HYPERTENSION - PERSISTENTLY ABNORMAL PRESSOR SENSITIVITY IN NORMOTENSIVE PATIENTS AFTER SURGICAL CURE
    (1994) RODRIGUEZPORTALES, JA; FARDELLA, C
    To examine the effects of primary hyperparathyroidism separately from those of hypertension per se on blood pressure regulation in patients with primary hyperparathyroidism, we studied the presser response to infused angiotensin II (All) and to norepinephrine (NE) in 7 normotensive patients with primary hyperparathyroidism before and after surgical cure, and compared it to that observed in 10 subjects with idiopathic hypertension and 10 normal controls. While the subjects were on an ad libitum diet, we measured urinary and plasma electrolytes, creatinine, and plasma renin activity. Except for calcium, these values were not significantly different among the three groups. The blood pressure was measured basally and in response to graded doses of All or of NE until a 20-mmHg increase in the diastolic blood pressure was reached (''pressor dose''). The presser doses of All and of NE were lower in the normotensive patients with primary hyperparathyroidism than in normal controls [4.6 +/- 2.0 vs. 7.3 +/- 3.5 ng/kg/min (p<0.05) and 164 +/- 114 vs. 302 +/- 176 ng/kg/min (p<0.05) respectively] and not significantly different from those found in idiopathic hypertension (3.1 +/- 1.2 and 137 +/- 95 ng/kg/min). When the patients with primary hyperparathyroidism were studied again between 2-6 months after surgical cure, their presser doses of All and of NE remained unchanged from their preoperative values (5.4 +/- 2.9 and 137 +/- 80 mg/kg/min). We conclude that the hyperparathyroid condition can disrupt the normal responsiveness to presser agents even if the blood pressure remains within normal limits, and that this abnormality may persist after surgical cure.