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Abstract
The mechanism of the diuretic braking phenomenon was studied in nine male hypertensive
patients by assessing the diurnal pattern of renal sodium (Na) excretion during furosemide
therapy, and the response to a test dose of furosemide (10 to 15 mg hr-1 i.v.) infused
alone and with chlorothiazide (500 mg bolus i.v.). Patients were studied after one
month of twice-daily administration of: placebo (P): chlorothiazide 500 mg (C); furosemide
40 mg (F); furosemide with spironolactone (100 mg b.i.d.) for the last 36 hours (F
+ S; N = 6). During F therapy, furosemide-induced natriuresis was followed by six
hour periods of decreased UNaV. Diuretic therapy with F or C for one month reduced
BP, but did not alter body weight, plasma volume (PV), glomerular filtration rate
or PAH clearance. After P, the test infusion of furosemide increased fractional Na
excretion (FENa) by +10.5 +/- 0.7%; this increment was reduced after therapy with
F (+8.9 +/- 0.7%; P less than 0.05), C (+8.5 +/- 1.0%; P less than 0.01), or F + S
(+8.9 +/- 0.9%; P less than 0.05). Renal furosemide excretion was greater (P less
than 0.05) after F and C treatments (133 +/- 10 micrograms.min-1 and 130 +/- 13 micrograms.min-1,
respectively) compared with P (94 +/- 9 micrograms.min-1). After P, a test dose of
chlorothiazide given during furosemide infusion increased FENa further (+7.5 +/- 1.2%);
this increment was greater after therapy with F (+10.1 +/- 1.4%; P less than 0.01)
and F + S (+11.3 +/- 0.8%; P less than 0.05) but not after C (+6.3 +/- 1.5%; P greater
than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)