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Potassium Depletion Exacerbates Essential Hypertension

G. Gopal Krishna, MD; and Shiv C. Kapoor, PhD
[+] Article and Author Information

Portions of this work were presented at the American Society of Nephrology Meetings (1989) in Washington, D.C. and were published in abstract form.

Grant Support: In part by a New Investigator Award (Dr. Krishna) from the U.S. Public Health Service (R23HL37372) and grants RR003934 and RR00040 and from the General Clinical Research Centers, Division of Research Resources, National Institutes of Health.

Requests for Reprints: G. Gopal Krishna, MD, Renal Electrolyte Section, University of Pennsylvania, 700 Clinical Research Building, 422 Curie Boulevard, Philadelphia, PA 19104-6144.

Current Author Addresses: Drs. Krishna and Kapoor: Renal Electrolyte Section, University of Pennsylvania, 700 Clinical Research Building, 422 Curie Boulevard, Philadelphia, PA 19104-6144.


©1991 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1991;115(2):77-83. doi:10.7326/0003-4819-115-2-77
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Objective: To determine the effect of potassium depletion on blood pressure in patients with essential hypertension.

Design: Double-blind, randomized, crossover study, with each patient serving as his or her own control.

Setting: Clinical research center at a university hospital.

Patients: Twelve patients with hypertension.

Interventions: Patients were placed on 10-day isocaloric diets providing a daily potassium intake of either 16 mmol or 96 mmol. The intake of sodium (120 mmol/d) and other minerals was kept constant. On day 11 each patient received a 2-litre isotonic saline infusion over 4 hours.

Measurements: Blood pressure; urinary excretion rates for sodium, potassium, calcium, and phosphorous; glomerular filtration rate; renal plasma flow; and plasma levels of vasoactive hormones.

Main Results: With low potassium intake, systolic blood pressure increased (P = 0.01) by 7 mm Hg (95% Cl, 3 mm Hg to 11 mm Hg) and diastolic pressure increased (P = 0.04) by 6 mm Hg (Cl, 1 mm Hg to 11 mm Hg), whereas plasma potassium concentration decreased (P < 0.001) by 0.8 mmol/L (Cl, 0.4 to 1.0 mmol/L). In response to a 2-litre isotonic saline infusion, the mean arterial pressure increased similarly on both diets but reached higher levels on low potassium intake (115 ± 2 mm Hg compared with 109 ± 2 mm Hg, P = 0.03). Potassium depletion was associated with a decrease in sodium excretion (83 ± 6 mmol/d compared with 110 ± 5 mmol/d, P < 0.001). Plasma renin activity and plasma aldosterone concentrations also decreased in patients during low potassium intake, but concentrations of arginine vasopressin and atrial natriuretic peptide, glomerular filtration rate, and renal plasma flow were unchanged. Further, low potassium intake increased urinary excretion of calcium and phosphorus and of plasma immunoreactive parathyroid hormone levels.

Conclusion: Dietary potassium restriction increases blood pressure in patients with essential hypertension. Both sodium retention and calcium depletion may contribute to the increase in blood pressure during potassium depletion.

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