Modulación eritropoyética por Renina-Angiotensina-Aldosterona

D´ANNA MARIA CECILIA; VEUTHEY TANIA V; GATTI CHRISTIAN; GIAMBELLUCA MIRIAM; ELIA ALEJANDRA; LOPEZ GUSTAVO; ROQUE MARTA ELENA

Tandil, Argentina

Congreso; X Congreso Argentino de Ciencias Morfológicas; 2006

Universidad Nacional del Centro - Facultad de Ciencias Veterinarias

In previous studies we showed that the pharmacological inhibition of theRenin-Angiotensin-Aldosterone (RAA) system affects the time range ofthe splenic restorative response to hemolysis and that the kidney assumes apost-hemolytic erythropoietic function. The objective was to assess whetherthe kidney presents a delayed response analog to the spleen when the RAAaxis is inactivated. Mice CF1 (43±3g) were grouped into: 1) G1 CONTROL(n=33): 300ml physiological solution (PS) intraperitoneal (ip) (10days); 2) G2+ENALAPRILATE (E) (n=33): Enalaprilate ip (10mg/kg/300mL) (10 days); 3) G1+PHZ; G2+E+PHZ: phenylhydrazine (PHZ) ip(60mg/kg/300mL) (Days:10,12); 4) G3(-E/-PHZ) (n=33): ip PS (20 days).Retroorbital blood was obtained until day 20 (every/2 days) (n=3). Anemiaevolution and recovery were assessed by means of Hb, HCT, and reticulocytes.The dissected kidney, fixed using Bouin solution and 10% formalin,was processed for H&E. Statistical significance was set at P<0.05. Micereceived free food and water. Cellular islands that characterize active erythropoiesiswere semi-quantified with a pre-established score (10xfields): a)0-2 islands/10fields:+; b) 3-7 islands/10 fields:++; c) 8-10 islands/10fields:+++; d) >10 islands/10fields:++++. In G2+E+PHZ, Hb (13.7g/dL±1.2), HCT (49.5%±0.7), and reticulocytes (33%±5) showed a delayedrecovery of anemia (day:20) with regard to G1+PHZ (Day:16): Hb: 14.2g/dL±1.3; HCT: 50.0%±0.8; reticulocytes31%±4 (P<0.05). Renal cellularityconfirmed the delayed erythropoietic recovery: 1) G2+E (Day0):+; 2)G2+E+PHZ (Day16):++; Day20:++++; 3) G1CONTROL (Day 0): +; 4)G1+PHZ (Day16):++++; Day20:+; 5) G3(-E/-PHZ): (Day 0,16,20):+. Thekidney behaves in the same way as the spleen with regard to erythron recoverywhen the erythropoiesis is modulated by inactivation of the RAAaxis. We may conclude that inducers of cellular adhesion to the medullarstroma and/or stromal inhibitor production would affect the migration andnestling of erythropoietic precursors in these tissues.