Glomerular haemodynamics, the renal sympathetic nervous system and sepsis-induced acute kidney injury.
Pyrogen, when administered intravenously to normotensive and hypertensive men, produced initially vasoconstriction and subsequently marked renal vasodilatation, both resulting from direct effects on the renal vasculature. The absolute renal plasma flow, both during control observations and at the height of renal hyperemia, was greater in normotensives, but the percentage change was greater in hypertensive subjects. Extraction of p-aminohippurate diminished during renal hyperemia. Medullary renal plasma flow was higher in normotensive subjects both during control observations and at the height of renal hyperemia. Simultaneously with the development of renal hyperemia, sodium excretion increased without alterations in filtered load of sodium and was prompt in its development in normotensives and delayed in hypertensives. This is attributed to a transient, small, yet probably significant decrease in filtered load of sodium during vasoconstriction immediately following the administration of pyrogen. Simultaneously with the development of renal hyperemia, there was in both groups an increase in solute excretion and tubular reabsorption of solute-free water.