PERSONAL DE APOYO
ELESGARAY Rosana
congresos y reuniones científicas
Título:
Influence of atrial natriuretic peptide treatment on cardiovascular and renal nitric oxide system in spontaneously hypertensive rats.
Autor/es:
MARÍA ÁNGELES COSTA; DANIELA RODRÍGUEZ IERACE; ROSANA ELESGARAY; MARÍA FLORENCIA VISINTINI JAIME; CAROLINA CANIFFI; ANA MARIA BALASZCZUK; CRISTINA ARRANZ
Lugar:
Buenos Aires, Argentina.
Reunión:
Congreso; World Congress of Cardiology 2008; 2008
Resumen:
Introduction:
We have previously demonstrated that nitric oxide (NO) system mediates
atrial natriuretic peptide (ANP) hypotensive, natriuretic and diuretic
effects in normotensive rats. We also showed that ANP would stimulate NO
synthase (NOS) activity interacting with natriuretic peptides receptors
NPR-A/B, increasing cGMP, and/or NPR-C, coupled via G protein, which
activates Ca2+-calmodulin dependent NOS. Objective:
The aim of the present study was to investigate the effects of chronic
ANP infusion on systolic blood pressure (SBP) and cardiovascular and
renal NO system in spontaneously hypertensive rats (SHR). Methods:
16-weeks old SHR and normotensive Wistar-Kyoto rats (WKY) were infused
subcutaneously (osmotic pumps) with saline (NaCl 0.9%) or ANP (100
ng/hour.rat), during seven days. SBP was recorded and nitrites and
nitrates excretion (NOx, metabolic end products of NO) were determined
during the experimental time. At the end of this period, the animals
were sacrificed by decapitation and NOS activity (using [14C] L-arginine
as substrate) were determined in aorta artery (A), right atria (RA),
left ventricle (LV) and renal medulla (M) and cortex (C). Results:
Chronic infusion of ANP diminished SBP (WKY= -13±3 vs SHR= -25 ± 10
mmHg, ns) and increased NOx (WKY = 41 ± 10 % vs SHR = 23 ± 4 %,
p<0.01) in both groups. ANP increased NOS activity in all studied
tissues in both groups but the enzyme stimulation was more marked in WKY
than SHR. (A: WKY= 51 ± 4 % vs SHR = 40 ± 3 % *; RA: WKY = 46 ± 4 % vs
SHR = 38 ± 3 %*; LV: WKY = 41 ± 3 % vs SHR = 30 ± 4 % *; C: WKY = 38 ± 4
% vs SHR = 27 ± 3 % *; M: WKY = =30 ± 3 % vs SHR = 25 ± 2 % *; *
p<0.01)
Table: NOS activity (pmol/g tissue.min) induced by saline or ANP in WKY and SHR animals
WKY + Saline
WKY + ANP
SHR + Saline
SHR + ANP
Aorta artery
205 ± 12
313 ± 15 *
339 ± 16 #
474 ± 18 *
Right atria
198 ± 11
289 ± 10 *
321 ± 15 #
444 ± 19 *
Left ventricle
212 ± 14
506 ± 26 *
327 ± 16 #
425 ± 20 *
Renal cortex
289 ± 15
400 ± 17 *
468 ± 19 #
595 ± 23 *
Renal medulla
388 ± 18
506 ± 26 *
594 ± 25 #
742 ± 29 * * p<0.01 vs saline infusion same group, # p<0.01 vs WKY + saline. Conclusions:
These results would suggest that up-regulation of cardiovascular and
renal NO-system is a compensatory mechanism for the elevation of
systolic blood pressure during the development of hypertension in SHR.
The chronic treatment with ANP increased the activity of this system
associated with a decrease in arterial blood pressure. The impaired
response to ANP of cardiovascular and renal NO system in hypertensive
animals, would be one of the mechanisms involved in the development
and/or the maintenance of the high blood pressure in this model of
genetic hypertension.