Differential sympathetic and angiotensinergic responses in rats submitted to low- or high-salt diet.
The present study was designed to evaluate, in Wistar rats, the effect of high- or low-salt diet on the hemodynamic parameters and on the renal and lumbar sympathetic nerve activity. The renal gene expression of the renin angiotensin system components was also evaluated, aiming to find some correlation between salt intake, sodium homeostasis and blood pressure increase. Male Wistar rats received low (0.06% Na, TD 92141-Harlan Teklad), a normal (0.5% Na, TD 92140), or a high-salt diet (3.12% Na, TD 92142) from weaning to adulthood. Hemodynamic parameters such as cardiac output and total peripheral resistance, and the renal and lumbar sympathetic nerve activity were determined (n=45). Plasma renin activity, plasma and renal content of angiotensin (ANG) I and II, and the renal mRNA expression of angiotensinogen, renin, AT1 and AT2 receptors were also measured (n=24). Compared to normal- and low-salt diet-, high-salt-treated rats were hypertensive and developed an increase (P<0.05) in total peripheral resistance and lumbar sympathetic nerve activity. A decrease in renal renin and angiotensinogen-mRNAs and in plasma ANG II and plasma renin activity was also found in salt overloaded animals. The renal sympathetic nerve activity was higher (P<0.05) in low- compared to high-salt-treated rats, and was associated with an increase (P<0.05) in renal ANG I and II and with a decrease (P<0.05) in AT2 renal mRNA. Plasma ANG I and II and plasma renin activity were higher in low- than in normal-salt rats. Our results show that increased blood pressure is associated with increases in lumbar sympathetic nerve activity and total peripheral resistance in high-salt-treated rats. However, in low-salt-treated rats an increase in the renal sympathetic nerve was correlated with an increase in the renal content of ANG I and II and with a decrease in AT2 renal mRNA. These changes are probably in favor of the antinatriuretic response and the sodium homeostasis in the low-salt group.
Carillo
B A
BA
Department of Physiology, Federal University of São Paulo, School of Medicine, São Paulo, SP, Brazil.
Beutel
A
A
Mirandola
D A
DA
Vidonho
A F
AF
Furukawa
L N S
LN
Casarini
D
D
Campos
R R
RR
Dolnikoff
M S
MS
Heimann
J C
JC
Bergamaschi
C T
CT
D000803:Angiotensin I / Q000097:blood / Q000235:genetics / Q000378:metabolism; D000804:Angiotensin II / Q000097:blood / Q000235:genetics / Q000378:metabolism; D000808:Angiotensinogen / Q000097:blood / Q000235:genetics* / Q000378:metabolism; D000809:Angiotensins / Q000097:blood / Q000235:genetics* / Q000378:metabolism; D000818:Animals; D005786:Gene Expression Regulation / Q000187:drug effects; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology; D007668:Kidney / Q000187:drug effects / Q000294:innervation / Q000378:metabolism; D008297:Male; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012083:Renin / Q000097:blood / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017673:Sodium Chloride, Dietary / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000502:physiology
D000809:Angiotensins; D012333:RNA, Messenger; D017673:Sodium Chloride, Dietary; D000808:Angiotensinogen; D000804:Angiotensin II; D000803:Angiotensin I; D012083:Renin