Endogenous angiotensin II modulates the effect of atrial natriuretic peptide on extracellular fluid partition.
Atrial natriuretic peptide (ANP) has been shown to promote a fluid shift from the intravascular toward the interstitial compartment and to interact with the renin-angiotensin system at the renal as well as the extrarenal level. In the present studies, the interaction between the renin-angiotensin system and the effects of ANP infusion (100 ng.kg-1 x min-1 for 45 min) on arterial pressure and hematocrit were assessed in bilaterally nephrectomized, anesthetized rats. In a first series of experiments, suppression of angiotensin II generation was achieved by chronic (10 days) treatment by the angiotensin-converting-enzyme inhibitor (ACEI) captopril in rats maintained on a low-sodium diet. ACEI pretreatment prevented the rise in hematocrit associated with ANP infusion (+2.1 +/- 0.1 vs. +5.8 +/- 0.2%, P < 0.05), without influencing the effect of ANP on arterial pressure. In ACEI-pretreated rats, acute administration of angiotensin II at a subpressor dose (2.5 ng.kg-1 x min-1) restored the ANP-induced increase in hematocrit. In a second series of experiments, acute blockade of the renin-angiotensin system was obtained by the ACEI enalaprilat or the nonpeptide angiotensin II receptor antagonist losartan (both 1 mg/kg i.v. bolus). In the presence of either enalaprilat or losartan, the ANP-induced increase in hematocrit was similarly prevented. These results indicate that the effect of ANP on vascular permeability is modulated by endogenous angiotensin II, possibly due to distinct influences of the two peptides at the level of pre- and postcapillary resistances.
Valentin
J P
JP
Department of Medicine, Centre Hospitalier Universitaire, Montpellier, France.
Nafrialdi
N
N
Ribstein
J
J
Mimran
A
A
D000804:Angiotensin II / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D001713:Biphenyl Compounds / Q000494:pharmacology; D001794:Blood Pressure / Q000502:physiology; D002216:Captopril / Q000494:pharmacology; D015773:Enalaprilat / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism*; D006400:Hematocrit; D007093:Imidazoles / Q000494:pharmacology; D019808:Losartan; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D011945:Receptors, Angiotensin / Q000187:drug effects / Q000502:physiology; D012084:Renin-Angiotensin System / Q000502:physiology; D013777:Tetrazoles / Q000494:pharmacology
D000806:Angiotensin-Converting Enzyme Inhibitors; D001713:Biphenyl Compounds; D007093:Imidazoles; D011945:Receptors, Angiotensin; D013777:Tetrazoles; D000804:Angiotensin II; D009320:Atrial Natriuretic Factor; D002216:Captopril; D015773:Enalaprilat; D019808:Losartan