Renal function after myocardial infarction and cardiac arrest in rats: role of ANP-induced albuminuria?
Renal function was measured by clearance technique before and after acute myocardial infarction (MI) induced by left coronary artery ligation in male Sprague-Dawley rats. The animals were anaesthetized with halothane-nitrous oxide, paralysed with pancuronium and artificially ventilated. All parameters were stable throughout the experiment in sham-operated time control animals (n = 8). After MI, rats developed left ventricular dysfunction with increased left ventricular end-diastolic pressure and decreased mean arterial pressure. MI produced antidiuresis and antinatriuresis without changes in glomerular filtration rate (GFR), lithium clearance or renal albumin excretion (n = 8). The antidiuretic and antinatriuretic responses to MI were similar in rats with chronic bilateral renal denervation (n = 5). Three additional rats with chronic bilateral renal denervation had cardiac arrest and were resuscitated with cardiac massage, i.v. lidocaine and intracardiac adrenaline administration. These animals showed a transient increase in urine flow rate, sodium and albumin excretion with maximum 30-60 min after resuscitation, while GFR and lithium clearance were normal. Since cardiac ischaemia and sympathetic stimulation are strong stimuli for the release of atrial natriuretic peptide (ANP), we examined if ANP (0.25, 0.50, and 1.00 microg kg(-1) min(-1), n = 8 per dose) affects urinary albumin excretion. ANP increased dose-dependently the urine/plasma concentration ratio of albumin relative to inulin, which suggests that ANP increases the glomerular permeability for albumin. We conclude that MI causes stimulation of renal tubular sodium and water reabsorption by a mechanism which is independent of intact renal innervation. MI does not produce any change in renal albumin excretion in rats, but transient albuminuria may be observed in rats following cardiac arrest and/or manoeuvres used in cardiac resuscitation. Since ANP produces albuminuria, we speculate that ANP may be an important mediator of albuminuria in states with elevated plasma concentrations of ANP.
Nielsen
S H
SH
Department of Clinical Biochemistry, Sundby Hospital, Copenhagen, Denmark.
Magid
E
E
Spannow
J
J
Christensen
S
S
Lam
H R
HR
Petersen
J S
JS
D000419:Albuminuria / Q000503:physiopathology*; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology; D003714:Denervation; D005919:Glomerular Filtration Rate / Q000502:physiology; D006323:Heart Arrest / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D007668:Kidney / Q000294:innervation / Q000503:physiopathology*; D008094:Lithium / Q000652:urine; D008297:Male; D009203:Myocardial Infarction / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000652:urine
D009320:Atrial Natriuretic Factor; D008094:Lithium; D012964:Sodium