Local vascular effects of hypokalemia, alkalosis, hypercalcemia, and hypomagnesemia

Abstract

Blood flowing through the vascular beds of the dog forelimb, kidney, and heart was transiently rendered hypokalemic (1.9 meq/ liter), alkalotic (pH 7.54), hypercalcemic (6.4 to 13.5 meq/ liter), hypomagnesemic (1.2 meq/liter), and hypocalcemic (3.0 meq/liter), singly and in various combinations, while observing resistance to flow and heart contractility. This was accomplished by holding flow rate constant while measuring the effects of rapid intra-arterial infusion of various artificial solutions upon perfusion pressure and left ventricular contractile force. The new findings are a) in situ limb small vessels and kidney vessels respond to local hypokalemia with slight constriction; b) in situ limb small vessels and kidney vessels respond to combinations of local hypokalemia, hypercalcemia, alkalosis, and hypomagnesemia with much more marked constriction than occurs with any one of the abnormalities alone; c) intact heart responds to local hypercalcemia with increased contractile force, to alkalosis with increased coronary resistance, and to combinations of hypokalemia, hypercalcemia, alkalosis, and hypomagnesemia with increased contractile force and increased coronary resistance; and d) in situ limb small vessels and intact heart respond to local hypocalcemia with dilation and decreased contractile force, respectively.

The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects

“…No significant or consistent influences on glomerular filtration rate or renal plasma flow have been reported following administration of potassium salts in amounts of the same order of magnitude used in the present studies. On the other hand, potassium depletion has been reported to reduce GFR and RPF (25) and acute hypokalemia has been noted to increase renal resistance (26). However, much more drastic or prolonged potassium depletion than that applied in the present studies was required to produce these changes.…”

Effects of chronic potassium deficiency on plasma renin activity

“…The resulting decrease in sodium delivery to the macula densa might be expected to stimulate renin release (14). Finally, the increased renin release might be directly related to increased renal resistance during potassium depletion (15). However, this is unlikely to be the sole or major stimulus since during the first few days of depletion, renin is greatly elevated while renal blood flow is still almost unchanged (16).…”

“…Five female mongrel dogs, weighing [10][11][12][13][14][15][16][17][18][19][20][21][22][23] Plasma renin activities were determined by a modification (8) of the method of Boucher, Veyrat, de Champlain, and Genest (9). This method measures renin indirectly by assaying the quantity of angiotensin generated during a 3 hr plasma incubation under standardized conditions.…”

My forty-three years with in situ small and large blood vessels.

“…In Oklahoma, in 1963, 24 using a dilutional method, and in Michigan, in 1972, 25 using a miniature hemodialyzer interposed in the arterial supply, we showed that local hypokalemia produces vasoconstriction in peripheral vascular beds, just the opposite of the vasodilation we observed in the dog forelimb with local hyperkalemia in 1959. 21 In 1966, Overbeck reported that this potassium vasodilation in the dog forelimb appears to be reduced in dogs with onekidney, one wrapped hypertension, a form of low renin hypertension.…”