Modulation of sympathetic vasoconstriction by potassium

A high-sodium diet accelerates the rise in blood pressure in stroke-prone spontaneously hypertensive rats (SHRSP). The blood pressure-increasing effect of sodium loading is associated with the following abnormalities in noradrenaline metabolism: (a) noradrenaline release from sympathetic nerve endings is facilitated (especially after stimulation, such as exposure to cold); (b) noradrenaline inactivation is reduced mainly as a consequence of diminished neuronal uptake of noradrenaline; and (c) the sensitivity of vascular smooth muscle to noradrenaline is enhanced. These changes in noradrenaline metabolism are partially reversed when the concentration of potassium in a high-sodium diet is increased from 100 to 250 mmol K+/kg diet. That is, the neuronal uptake of noradrenaline is improved, the sensitivity of vascular smooth muscle to noradrenaline is attenuated, and the release of noradrenaline into the plasma is reduced. The reversal of abnormalities in noradrenaline metabolism is accompanied by a substantial blood pressure reduction following potassium repletion in SHRSP. Hence, the addition of potassium to the diet may be regarded as an antihypertensive measure which affects noradrenaline metabolism in such a way that sympathetic vasoconstriction is attenuated.