Renal interstitial hydrostatic pressure and urinary sodium excretion in rats with angiotensin-converting enzyme inhibitor-induced papillary atrophy

The importance of angiotensin type-1 (AT(1)) receptor-stimulation during re nal development has recently been established in both pharmacological and k nockout models. We have previously reported irreversible and progressive pa pillary atrophy and a reduced baseline renal interstitial hydrostatic press ure (RIHP) after neonatal angiotensin-converting enzyme (ACE) inhibition. T he aim of the present study was to investigate the consequences of these ab normalities on urinary sodium excretion during acute extracellular sodium l oading. Rats were treated neonatally with enalapril (10 mg kg(-1) day(-1)) or saline control from days 3 to 23 after birth. Urinary sodium excretion w as assessed in relation to mean arterial pressure (MAP) and RIHP responses in adult anaesthetised rats during moderate (1.5 and 3 % body weight) and s evere (9 % body weight) saline-induced volume expansion. Control rats respo nded to the moderate volume expansion by increasing MAP by 16 +/- 6 % and R IHP by 40 +/- 23 %, respectively. In neonatally enalapril-treated rats, how ever, MAP and RIHP remained unchanged and were associated with a smaller in crease in sodium excretion (44 +/- 11 % of the total amount infused versus 71 +/- 16 % for controls, P < 0.05). In contrast, severe volume expansion r esulted in marked pressure rises in both the enalapril-treated group (36 +/ - 12 and 112 +/- 48 % of baseline For MAP and RIHP, respectively) and the c ontrol group (34 +/- 21 and 130 +/- 34 % of baseline for MAP and RIHP, resp ectively). Moreover, the increases in MAP and RIHP were associated with com plete excretion of the severe sodium challenge within 60 min in both treatm ent groups. We conclude that a RIHP response appears to be a prerequisite f or adequate urinary sodium excretion in this model of papillary atrophy. He nce, an intact renal medulla is not mandatory in the renal handling of sodi um during extracellular loading.