The Hemodynamic Effects of Potassium Deficiency in the Dog

GALVEZ, OSCAR G.
BAY, WILLIAM H.
ROBERTS, BERTRAM W.
FERRIS, THOMAS F.

Department of Medicine, Ohio State University College of Medicine, Columbus, Ohio.

Address for reprints: Thomas F. Ferris, M.D., Department of Medicine, Ohio State University School of Medicine, 410 West 10th Avenue, Columbus, Ohio 43210.

Supported in part by Research Grants HL 13653 and HL 5957 from the National Institutes of Health, and a grant from the Central Ohio Heart Chapter of the American Heart Association.

Circulation Research 40(5):p I11-I16, May 1977.

SUMMARY

Potassium deficiency for 3 weeks in dogs caused 374 ± 38 mEq of sodium retention with increase in body weight, plasma volume, and inulin space. Cardiac output increased from 3.7 ± 0.6 to 5 ± 0.6 liters/min (P <0.02) and systemic vascular resistance decreased from 3,050 ± 590 to 2,000 ± 286 dynes/cm per sec²(P <0.05). Plasma renin activity (PRA) increased from 0.4 ± 0.1 to 17.2 ± 0.9 ng/ml per hour (P <0.01) without change in plasma aldosterone. Angiotensin sensitivity decreased from a rise of 37 ± 4 mm Hg in mean arterial pressure (MAP) to 10 ng/kg per min before potassium depletion to a rise of 10 ± 2 mm Hg after hypokalemia. Urinary prostaglandin E (PGE) excretion increased from control values of 1,224 to 1,556 ng/day to 9,352 ± 3,670 after 21 days of hypokalemia (P< 0.01). Indomethacin, 150 mg a day for 3 days, decreased urinary PGE to control values as PRA decreased from 17.2 ± 5.9 to 1.1 ± .3 ng/ml per hour and angiotensin sensitivity was partially restored.

These findings indicate that hypokalemia increased urinary PGE with extracellular fluid volume expansion, decreased sensitivity to angiotensin and increase in PRA.