Long-Term Use of Propranolol, Ibuprofen, and Spironolactone in the Management of Bartter's Syndrome

PEDIATRICS ◽  
1979 ◽  
Vol 63 (5) ◽  
pp. 754-756
Author(s):  
Robert J. Cunningham ◽  
Ben H. Brouhard ◽  
Michael Berger ◽  
Tom Petrusick ◽  
Luther B. Travis

This report concerns two patients wter'sth Barter's syndrome who were treated with propranolol, spironolactone, and potassium supplements. When ibuprofen was added to this regimen, potassium supplements were no longer required. In both patients, plasma renin activity decreased, plasma volumes increased, and a "catch-up" in linear growth ensued. This report confirms others that indicate prostaglandin synthetase inhibitors are a useful adjunct in the therapy of Bartter's syndrome.

1970 ◽  
Vol 77 (6) ◽  
pp. 1071-1074 ◽  
Author(s):  
Ronald G. Strauss ◽  
Shakil Mohammed ◽  
Jennifer M.H. Loggie ◽  
William K. Schubert ◽  
Alfred F. Fasola ◽  
...  

1976 ◽  
Vol 51 (s3) ◽  
pp. 551s-554s
Author(s):  
H. M. Brecht ◽  
E. Werner ◽  
W. Schoeppe

1. The effect of long-term treatment with prindolol on blood pressure, total body potassium (Kt), exchangeable sodium (Nae) and plasma renin activity was investigated in twelve patients with essential hypertension. 2. Systolic and diastolic pressures were significantly reduced from 164/112 to 127/90 mmHg under basal conditions. 3. Before treatment Na. in patients with essential hypertension was significantly higher than in normotensive individuals. After an average of 16 weeks on prindolol Nae in patients with essential hypertension was significantly decreased, despite an average increase in body weight of 2 kg in the patients. 4. In contrast to the decrease in Nae, Kt was found to be significantly increased after long-term treatment with prindolol. Kt values of patients before and after prindolol, however, did not differ significantly from the corresponding sex- and age-dependent normal values. 5. Plasma renin activity was slightly diminished under basal and orthostatic conditions; the stimulatory effect of orthostasis was not abolished but reduced by prindolol. 6. It is suggested that the changes in sodium balance contribute to the anti-hypertensive effect of prindolol in patients with essential hypertension.


1995 ◽  
Vol 25 (4) ◽  
pp. 589-592 ◽  
Author(s):  
Genjiro Kimura ◽  
Naoyuki Takahashi ◽  
Yuhei Kawano ◽  
Takashi Inenaga ◽  
Takuya Inoue ◽  
...  

1984 ◽  
Vol 67 (3) ◽  
pp. 329-335 ◽  
Author(s):  
C. J. Kenyon ◽  
N. A. Saccoccio ◽  
D. J. Morris

1. The mineralocorticoid activity of corticosterone based on acute changes in urinary Na+/K+ ratios in adrenalectomized rats was 1000 times less than that of aldosterone. However, corticosterone had only kaliuretic actions whereas aldosterone had both antinatriuretic and kaliuretic properties. Corticosterone inhibited the antinatriuretic actions of aldosterone. 2. Adrenalectomized rats infused continuously with a physiological dose of corticosterone (1 mg/day) were 5 times less sensitive to the antinatriuretic and 25 times less sensitive to the kaliuretic actions of aldosterone when administered acutely than were control adrenalectomized rats. 3. The long term effects of infusions of physiological doses of aldosterone and corticosterone were assessed in adrenalectomized rats maintained in metabolic cages. Aldosterone lowered plasma renin activity and reduced fluid (0.3% NaCl) intake; these effects were diminished when aldosterone and corticosterone were infused simultaneously. Plasma renin activity and fluid intake were correlated in long term infusion experiments. Both hormones had hypokalaemic effects but these were not additive. Corticosterone, but not aldosterone, increased systolic blood pressure and plasma sodium levels. 4. We conclude that glucocorticoid effects on water and electrolyte metabolism are different from those of mineralocorticoids, that glucocorticoids may antagonize mineralocorticoid effects and that interactions between mineralocorticoids and glucocorticoids may be important in long term blood pressure regulation.


1982 ◽  
Vol 63 (s8) ◽  
pp. 195s-197s ◽  
Author(s):  
T. Kono ◽  
F. Oseko ◽  
F. Ikeda ◽  
H. Imura ◽  
M. C. Khosla ◽  
...  

1. When the angiotensin II-(4-8)-pentapeptide was infused intravenously at rates of 0.31-5.55 nmol min−1 kg−1 for 10–120 min into five normal men or two patients with Bartter's syndrome, no significant change was observed in blood pressure, plasma renin activity and plasma aldosterone, and the lowest dose did not inhibit the captopril-induced increase in plasma renin activity in the normal men. 2. An intravenous infusion of the pentapeptide at 9–0 nmol min−1 kg−1 for 15 min significantly raised blood pressure in the five normal men but not in patients with Bartter's syndrome. Blood pressure returned to the pre-treatment level 60 min after the cessation of the infusion in the normal men. 3. At the same dose level none of the seven subjects examined showed any significant change in plasma renin activity and plasma aldosterone. 4. Angiotensin II-(5-8)-tetrapeptide was infused intravenously into one of the normal men at a rate of 41.5 nmol min−1 kg−1 for 15 min, but it caused no significant change in blood pressure, plasma renin activity and plasma aldosterone. 5. These results suggest that the pentapeptide and probably the tetrapeptide do not possess renin-suppressing and steroidogenic actions in man but that the former peptide does elicit a modest pressor action with a prolonged duration.


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