Effects of atrial natriuretic peptide chronic treatment on arterial blood pressure and renal nitric oxide system in spontaneously hypertensive rats.

MARÍA ÁNGELES COSTA; DANIELA RODRÍGUEZ IERACE; ROSANA ELESGARAY; MARÍA FLORENCIA VISINTINI JAIME; CAROLINA CANIFFI; ANA MARIA BALASZCZUK; MYRIAM MAC LAUGHLIN; CRISTINA ARRANZ

Berlín, Alemania

Congreso; Eighteenth European Meeting of Hypertension. 22nd Scientific Meeting of the International Society of Hypertension.; 2008

Objective: The aim was to study the effects of chronic atrial natriuretic peptide (ANP) treatment on systolic blood pressure(SBP) and renal nitric oxide(NO)system in spontaneously hypertensive rats (SHR). in spontaneously hypertensive rats (SHR). The aim was to study the effects of chronic atrial natriuretic peptide (ANP) treatment on systolic blood pressure(SBP) and renal nitric oxide(NO)system in spontaneously hypertensive rats (SHR). Methods: 8-weeks (8W) and 12-weeks (12W) 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 7 days. SBP was recorded and nitrites and nitrates excretion (NOx, end products of NO) were determined during the experimental time. At the end of this period, the animals were sacrificed by decapitation and NO synthase (NOS) activity (using [14C] L-arginine as substrate) were determined in renal medulla and cortex. or ANP (100 ng/hour.rat), during 7 days. SBP was recorded and nitrites and nitrates excretion (NOx, end products of NO) were determined during the experimental time. At the end of this period, the animals were sacrificed by decapitation and NO synthase (NOS) activity (using [14C] L-arginine as substrate) were determined in renal medulla and cortex. 8-weeks (8W) and 12-weeks (12W) 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 7 days. SBP was recorded and nitrites and nitrates excretion (NOx, end products of NO) were determined during the experimental time. At the end of this period, the animals were sacrificed by decapitation and NO synthase (NOS) activity (using [14C] L-arginine as substrate) were determined in renal medulla and cortex. Results: Chronic infusion of ANP diminished SBP (8W: WKY= -8±2 vs SHR= -15±6 mmHg; 12W: WKY= -13±3 vs SHR= -25±10 mmHg, ns) and increased NOx (8W: WKY= 35±8 % vs SHR= 18±4 %*; 12W: WKY= 41±10 % vs SHR= 23±4 %, *p<0.01) in both ages in SHR and WKY. 35±8 % vs SHR= 18±4 %*; 12W: WKY= 41±10 % vs SHR= 23±4 %, *p<0.01) in both ages in SHR and WKY. Chronic infusion of ANP diminished SBP (8W: WKY= -8±2 vs SHR= -15±6 mmHg; 12W: WKY= -13±3 vs SHR= -25±10 mmHg, ns) and increased NOx (8W: WKY= 35±8 % vs SHR= 18±4 %*; 12W: WKY= 41±10 % vs SHR= 23±4 %, *p<0.01) in both ages in SHR and WKY. Renal cortex Renal cortex Renal cortex Renal medulla Renal medulla Renal medulla Saline ANP % Increase Saline ANP % Increase WKY 8W 189±9 322±19* 70±10 281±12 423±15* 50±6 SHR 8W 362±18# 496±34*# 37±5# 490±18# 588±±20*# 20±3# WKY 12W 289±15 400±17* 38±4 388±18 506±26* 30±3 SHR 12W 468±19# 595±23*# 27±3# 594±25# 742±29*# 25±2# * p<0.01 vs saline same group; # p< 0.01 vs WKY same treatment. ANP increased renal NOS activity in both groups but the enzyme stimulation was more marked in WKY than SHR. Conclusions: These results would suggest that up-regulation of renal NO-system is a compensatory mechanism for the elevation of systolic blood pressure during the development of hypertension in SHR. The increased activity of NO-system induced by ANP was associated to a decrease in arterial blood pressure. The impaired response of renal NO system in hypertensive animals compared with normotensive ones, would be one of the mechanisms involved in the development and/or the maintenance of the high blood pressure in this model of hypertension. the development of hypertension in SHR. The increased activity of NO-system induced by ANP was associated to a decrease in arterial blood pressure. The impaired response of renal NO system in hypertensive animals compared with normotensive ones, would be one of the mechanisms involved in the development and/or the maintenance of the high blood pressure in this model of hypertension. These results would suggest that up-regulation of renal NO-system is a compensatory mechanism for the elevation of systolic blood pressure during the development of hypertension in SHR. The increased activity of NO-system induced by ANP was associated to a decrease in arterial blood pressure. The impaired response of renal NO system in hypertensive animals compared with normotensive ones, would be one of the mechanisms involved in the development and/or the maintenance of the high blood pressure in this model of hypertension.