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The ability to excrete sodium under acute increase in renal perfusion pressure has not been observed in young, prehypertensive SHR. Some reports indicate the abnormality in urinary kallikrein (Ka) excretion in SHR, but it has not been studied how the renal Ka contributes to the development of hypertension. Studies were performed on male, young SHR and WKY at 4 to 5 weeks of age. Under intraperitoneal anesthesia with sodium ethylmalonylthiourea, isotonic saline containing polyfructosan was infused at 0.4ml/100g Body Wt/h. Each urine sample was collected during the 4 different phases; the control period (phase I), the period when the renal perfusion pressure was acutely increased and stabilized following left carotid occlusion and vagotomy (phase II), after the renal perfusion pressure was decreased to the level of the control period by adjusting the screw clamp which was placed around the aorta above the renal arteries (phase III), and lastly, after the release of the screw clamp (phase IV). Urinary Ka was measured fluorometrically. The results are summarized as follows:

The effect of an acute increase in renal perfusion pressure on urinary sodium, water and kallikrein excretion in young SHR