Renal interstitial hydrostatic pressure and urinary sodium excretion in rats with angiotensin-converting enzyme inhibitor-induced papillary atrophy.
The importance of angiotensin type-1 (AT1) receptor stimulation during renal development has recently been established in both pharmacological and knockout models. We have previously reported irreversible and progressive papillary atrophy and a reduced baseline renal interstitial hydrostatic pressure (RIHP) after neonatal angiotensin-converting enzyme (ACE) inhibition. The aim of the present study was to investigate the consequences of these abnormalities on urinary sodium excretion during acute extracellular sodium loading. 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 was assessed in relation to mean arterial pressure (MAP) and RIHP responses in adult anaesthetised rats during moderate (1.5 and 3 % body weight) and severe (9 % body weight) saline-induced volume expansion. Control rats responded to the moderate volume expansion by increasing MAP by 16 +/- 6 % and RIHP by 40 +/- 23 %, respectively. In neonatally enalapril-treated rats, however, MAP and RIHP remained unchanged and were associated with a smaller increase in sodium excretion (44 +/- 11 % of the total amount infused versus 71 +/- 16 % for controls, P < 0.05). In contrast, severe volume expansion resulted in marked pressure rises in both the enalapril-treated group (36 +/- 12 and 112 +/- 48 % of baseline for MAP and RIHP, respectively) and the control group (34 +/- 21 and 130 +/- 34 % of baseline for MAP and RIHP, respectively). Moreover, the increases in MAP and RIHP were associated with complete excretion of the severe sodium challenge within 60 min in both treatment groups. We conclude that a RIHP response appears to be a prerequisite for adequate urinary sodium excretion in this model of papillary atrophy. Hence, an intact renal medulla is not mandatory in the renal handling of sodium during extracellular loading.
Nilsson
A B
AB
Department of Physiology, Institute of Physiology & Pharmacology, Goteborg University, Sweden.
Guron
G S
GS
Adams
M A
MA
Friberg
P
P
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001284:Atrophy / Q000473:pathology; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D006439:Hemodynamics; D006874:Hydrostatic Pressure; D007668:Kidney / Q000473:pathology / Q000503:physiopathology*; D007679:Kidney Medulla / Q000187:drug effects* / Q000473:pathology*; D009318:Natriuresis / Q000187:drug effects; D010952:Plasma Substitutes / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012965:Sodium Chloride / Q000494:pharmacology; D013997:Time Factors
D000806:Angiotensin-Converting Enzyme Inhibitors; D010952:Plasma Substitutes; D012965:Sodium Chloride