Urinary kallikrein activity, renal hemodynamics, and electrolyte handling during chronic beta blockade with propranolol in hypertension.

Propranolol has been reported to diminish renal perfusion and impair sodium excretion, but the relationship of these phenomena has not been well characterized during chronic propranolol administration in hypertensive man, nor has the potential involvement of the renal kallikreinkinin system been explored. Fifteen essential hypertensive white men were treated with both placebo and oral propranolol for 1 month each, with dosage titrated for blood pressure control. Propranolol normalized mean arterial pressure (from 112.6 ± 1.9 to 94.0 ± 2.8 mm Hg, p 0.1), even in the face of a diminished glomerular filtration rate, and was sustained by an increase in the fractional excretion of sodium (from 0.75 ± 0.09 to 0.96 ± 0.06%, p < 0.05). This is perhaps related to diminished mineralocorticoid activity as reflected by decreased plasma aldosterone concentration (from 68.4 ± 9.6 to 61.4 ± 16.1 pgAnl, p < 0.02), increased urinary sodium/potassium ratio (from 2.41 ± 0.33 to 3.12 ± 0.30, p < 0.01), and correlation between fractional sodium excretion increment with urinary sodium/potassium ratio increment (r = 0.82, p < 0.01). Preservation of sodium homeostasis was also indicated by constancy in body weight, plasma volume, and blood volume. Kallikrein changes did not correlate with changes in renal sodium handling. (Hypertension 4742–749, 1982