Why the study?
Does sodium accumulation determine the magnitude of blood pressure rise in experimental renal hypertension in dogs?
Does sodium accumulation determine the magnitude of blood pressure rise in experimental renal hypertension in dogs?
In a canine model of renal hypertension, sodium accumulation is not required for hypertension to develop but exacerbates the magnitude of the blood pressure increase.
Challenges necessity of sodium accumulation for hypertension onset in this model; leaves open its role in modulating severity in patients.
After unilateral nephrectomy and application of a Goldblatt clamp to the remaining renal artery, there was sodium retention of approximately 123 mEq in 15 days. At this time, blood pressure increased from 95 to 142 mm Hg without demonstrable changes in plasma volume or cardiac output. When the accumulation of sodium was prevented and a negative balance induced by a low sodium diet and a single dose of a diuretic agent postoperatively, the blood pressure increased from 102 to 139 mm Hg, but it increased further, to 155 mm Hg, after a normal sodium diet had been restored and there had been a gain of 189 mEq of sodium above control. The accumulation of sodium after application of the Goldblatt clamp does not appear to be necessary for the emergence of hypertension, but it does appear to play some part in determining the magnitude of the rise in pressure.
No takes yet. Share an insight, caveat, or question.
James Conway (1968) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: