1. Blood pressure, blood volume and renal blood flow were determined in 101 men; forty-three were normal subjects and fifty-eight were untreated permanent essential hypertensive patients with normal renal function and equilibrated sodium balance. 2. A significant negative pressure—volume relationship was observed overall. The relationship could be expressed as a hyperbola whose slope expressed the reduction in blood volume per unit rise in pressure: the higher the blood pressure, the lower the slope. Thus essential hypertensive subjects have a smaller decrement in blood volume per unit rise in pressure than normal subjects. 3. The relation between change in blood volume and change in pressure was confirmed in each individual by defining for each a ratio Δ V /ΔP, statistically identical with the hyperbolic slope d V /dP. The Δ V /ΔP ratio was found to be well correlated with the renal blood flow and the creatinine clearance. No correlation existed between the total blood volume and these two renal parameters. 4. It is concluded that the present study demonstrates a blood volume regulation disturbance in essential hypertension and provides evidence from human studies that a renal defect accompanies high blood pressure.
1. Renal venous prostaglandin concentrations (PGA, PGE and PGF) were determined, together with renal plasma flow, urinary output and blood pressure changes, before and after infusion of sodium chloride solution (saline) in four normotensive and three hypertensive subjects. 2. No changes in blood pressure and in glomerular filtration rate were observed. 3. Saline infusion induced a significant increase in renal venous PGA and PGE, and also in total and non-cortical renal plasma flow and urinary output. There was an insignificant increase in renal venous PGF. 4. These findings show that prostaglandin release after saline infusion is associated with changes in renal blood flow and suggest that the natriuretic and diuretic effect of saline could be the result of prostaglandin release.
1. Acute renal failure was induced in conscious rats by subcutaneous injection of glycerol. 2. Expansion of the extracellular space by infusion of 150 mmol/l sodium chloride (saline) partly protected the animals against acute renal failure. 3. This protective effect of saline infusion disappeared when the animals were treated with indomethacin. This effect could be reversed by the addition of prostaglandin (PGE 2 ) to the saline infusion. 4. We suggest that prostaglandins may be involved in mediating the protection afforded by saline infusion against acute renal failure due to glycerol.