Direct relationship between urinary prostaglandin E and sodium excretion in essential hypertensive patients

Papanicolaou, N.; Lefkos, N.; Safar, Michel E.; Pâris, M.; Bariéty, J; Milliez, M.

doi:10.1007/bf01953093

Cited by 15 publications

(2 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For PGE2, both natriuretic [15] as well as antinatriuretic [17,26] actions have been proposed, while sometimes no clear relationship could be found [19]. For PGE2, both natriuretic [15] as well as antinatriuretic [17,26] actions have been proposed, while sometimes no clear relationship could be found [19].…”

Section: Renal Prostaglandins and Kidney Functionmentioning

confidence: 99%

Prostaglandin-Ausscheidung im Urin bei Neugeborenen: Beziehung zu Nierenfunktion und Blutdruck

et al. 1980

View full text Add to dashboard Cite

Section: Renal Prostaglandins and Kidney Functionmentioning

confidence: 99%

Prostaglandin-Ausscheidung im Urin bei Neugeborenen: Beziehung zu Nierenfunktion und Blutdruck

et al. 1980

View full text Add to dashboard Cite

“…Moreover, some patients showed an increase in PGE2 with a decrease in blood pressure even on salt loading. Papanicolaou et al (1976) suggested that PGE2 has a saluretic action because they observed a close relation between urinary sodium and PGE2 excretion, especially with rates of sodium excretion above 200 mEq/day. Kawasaki et al (1978) and Nielsen et al (1979) showed that in humans, so¬ dium excretion is equal to sodium intake on day 5 of a fixed salt intake.…”

Section: Discussionmentioning

confidence: 96%

Involvement of endogenous prostaglandins in salt-induced hypertension

Ogihara

Gotoh

Tabuchi

et al. 1985

Acta Endocrinologica

View full text Add to dashboard Cite

Insufficient production of prostaglandins, which are possible antihypertensive agents, may be a pathogenetic factor in hypertensive patients on salt loading. We compared the levels of plasma PGE2, plasma renin activity (PRA) and urinary 6-Keto-PGF1\g=a\(6-O-PGF1\g=a\), a major stable metabolite of PGI2, on day 5 of salt deprivation and also on day 5 of subsequent salt loading in 17 patients with essential hypertension. Salt loading decreased plasma PGE2, and slightly increased urinary 6-O-PGF1\g=a\. On salt loading, a positive correlation was found between the levels of plasma PGE2 and urinary sodium excretion. On salt deprivation, PRA was significantly correlated with plasma PGE2. The per cent change in mean blood pressure on changing from salt restriction to salt loading was inversely correlated with the per cent change in PGE2, and positively correlated with the per cent change in 6-O-PGF1\g=a\excretion. These findings suggest that on salt restriction, PGE2 is involved in the renin-angiotension system and that on salt loading, PGE2 is produced to compensate for the excessive sodium. The finding that PGE2 production was attenuated progressively as the mean blood pressure increased on salt loading in patients with essential hypertension suggests that insufficient compensatory PGE2

show abstract

Vaskul�re, thrombozyt�re und renale Prostaglandine

1979

View full text Add to dashboard Cite

Prostaglandins (PG) are highly unsaturated, cyclic fatty acids with 20 carbon atoms which are biosynthesized from dihomo-gamma-linolenic, arachidonic and eicosapentaenoic acids. These fatty acids are either ingested or are biosynthesized from linoleic and linolenic acids, respectively. The PG-precursor fatty acids are liberated from membrane phospholipids by phospholipase A and are converted to prostaglandins by the multienzyme complex PG-synthetase. The activity of the PG-system is influenced by extracellular hormonal, neural and mechanical stimuli and by intracellular factors such as ion-concentration and activity of the enzymes adenyl- and guanylcyclase. Prostaglandins are tissue hormones or autacoids which act on their receptors near their site of synthesis and degradation. The prostaglandin family constitutes a group of more than 10 natural occurring compounds showing a variety of biological actions. In arteries and veins the different PG:s have vasodilating as well as vasoconstricting effects. In addition, they are involved in the regulation of vascular smooth muscle proliferation. Within the kidney PG:s have vascular and tubular actions. They antagonize the effect of ADH, mediate renin secretion and are involved in the control of electrolyte balance. In the regulation of platelet aggregation and platelet adhesion PG:s have opposite functions: Prostacyclin which is synthesized in the vascular wall antagonizes the aggregating action of Thromboxane A2 which is formed in the platelets. A defect or an imbalance in the production of PG:s in the vascular wall, in platelets or in the kidney is assumed to play a pathogenetic role in a variety of cardiovascular and renal diseases such as in hypertension, atherosclerosis, persistent ductus arteriosus and Bartter's syndrome.

show abstract

Direct relationship between urinary prostaglandin E and sodium excretion in essential hypertensive patients

Cited by 15 publications

References 13 publications

Prostaglandin-Ausscheidung im Urin bei Neugeborenen: Beziehung zu Nierenfunktion und Blutdruck

Prostaglandin-Ausscheidung im Urin bei Neugeborenen: Beziehung zu Nierenfunktion und Blutdruck

Involvement of endogenous prostaglandins in salt-induced hypertension

Vaskul�re, thrombozyt�re und renale Prostaglandine

Contact Info

Product

Resources

About