The hemodynamic effects of potassium deficiency in the dog.

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 less than 0.02) and systemic vascular resistance decreased from 3,050 +/- 590 to 2,000 +/- 286 dynes/cm per sec2 (P less than 0.05). Plasma renin activity (PRA) increased from 0.4 +/- 0.1 to 17.2 +/- 0.9 ng/ml per hour (P less than 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 less than 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.

Studies of the mechanism of contralateral polyuria after renal artery stenosis.

Acute renal artery stenosis in hydropenic dogs caused a contralateral increase in urine volume and free water clearance without change in glomerular filtration, renal blood flow, or osmolar clearance. The increase in urine volume was not dependent on the development of hypertension since it occurred in animals pretreated with trimethaphan but was dependent upon angiotensin since it was presented with angiotensin blockade with Saralasin. The effect was not caused by angiotensin inhibiting antidiuretic hormone release since the polyuria occurred in hypophysectomized animals receiving a constant infusion of 10 muU/kg per min of aqueous Pitressin. Since the rise in urine volume was associated with an increase in renal vein prostaglandin E concentration and was prevented by pretreatment with indomethacin (5 mg/kg) the results suggest that the rise in plasma angiotensin after renal artery stenosis causes an increase in contralateral prostaglandin E synthesis with resultant antagonism to antidiuretic hormone at the collecting tubule.