TY - JOUR
T1 - Prostaglandins in the sodium excretory response to altered renal arterial pressure in dogs
AU - Carmines, P. K.
AU - Bell, P. D.
AU - Roman, R. J.
PY - 1985
Y1 - 1985
N2 - Acute variations in renal arterial pressure are associated with corresponding alterations in absolute and fractional sodium excretion, even under conditions of highly efficient autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR). Since prostaglandins recently have been implicated in the regulation of sodium excretion, we investigated the hypothesis that the renal prostaglandin system participates in 'pressure natriuresis'. Anesthetized sodium-replete dogs were subjected to partial carotid artery constriction to elevate systemic arterial pressure. Under these control conditions, sodium excretion was 103 ± 18 μeq/min (n = 17) and urinary prostaglandin E2 excretion averaged 4.6 ± 1.5 ng/min (n = 8). Decreases in renal arterial pressure within the autoregulatory range reduced sodium excretion (2.1%/mmHg) and prostaglandin E2 excretion (1.7%/mmHg), whereas GFR and RBF were not affected. There was a significant correlation between the changes in sodium and prostaglandin E2 excretion rates (r = 0.932, P < 0.01). In 9 dogs treated with indomethacin, sodium excretion was reduced by 70% while GFR and autoregulatory capability were unaffected. There was a marked attenuation of the effect of changes in arterial pressure on sodium excretion, with this parameter exhibiting changes averaging 0.6%/mmHg (P < 0.001). These observations suggest that the renal prostaglandin system may exert an important influence on the pressure-natriuresis mechanism.
AB - Acute variations in renal arterial pressure are associated with corresponding alterations in absolute and fractional sodium excretion, even under conditions of highly efficient autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR). Since prostaglandins recently have been implicated in the regulation of sodium excretion, we investigated the hypothesis that the renal prostaglandin system participates in 'pressure natriuresis'. Anesthetized sodium-replete dogs were subjected to partial carotid artery constriction to elevate systemic arterial pressure. Under these control conditions, sodium excretion was 103 ± 18 μeq/min (n = 17) and urinary prostaglandin E2 excretion averaged 4.6 ± 1.5 ng/min (n = 8). Decreases in renal arterial pressure within the autoregulatory range reduced sodium excretion (2.1%/mmHg) and prostaglandin E2 excretion (1.7%/mmHg), whereas GFR and RBF were not affected. There was a significant correlation between the changes in sodium and prostaglandin E2 excretion rates (r = 0.932, P < 0.01). In 9 dogs treated with indomethacin, sodium excretion was reduced by 70% while GFR and autoregulatory capability were unaffected. There was a marked attenuation of the effect of changes in arterial pressure on sodium excretion, with this parameter exhibiting changes averaging 0.6%/mmHg (P < 0.001). These observations suggest that the renal prostaglandin system may exert an important influence on the pressure-natriuresis mechanism.
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U2 - 10.1152/ajprenal.1985.248.1.f8
DO - 10.1152/ajprenal.1985.248.1.f8
M3 - Article
AN - SCOPUS:0021962858
VL - 17
SP - F8-F14
JO - American Journal of Physiology - Renal Physiology
JF - American Journal of Physiology - Renal Physiology
SN - 0363-6127
IS - 1
ER -