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Prostanoids and blood pressure: which way is up?
Helene Francois, Thomas M. Coffman
Helene Francois, Thomas M. Coffman
Published September 15, 2004
Citation Information: J Clin Invest. 2004;114(6):757-759. https://doi.org/10.1172/JCI22929.
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Commentary

Prostanoids and blood pressure: which way is up?

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Abstract

Members of the family of prostanoids, made up of prostaglandins and thromboxanes, are generated via COX-mediated metabolism of arachidonic acid. These lipid mediators exhibit wide-ranging biological actions that include regulating both vasomotor tone and renal sodium excretion. As COX inhibition is often associated with sodium retention leading to edema and hypertension, prostanoids appear to have a role in preventing the development of high blood pressure. On the other hand, prostaglandin E2 (PGE2) and PGI2 have also been implicated as determinants of renin secretion. A new study suggests that PGI2 plays a critical role in stimulating renin release and promoting hypertension following renal artery stenosis.

Authors

Helene Francois, Thomas M. Coffman

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Figure 1

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The juxtaglomerular apparatus. Integration of the regulated secretion of...
The juxtaglomerular apparatus. Integration of the regulated secretion of renin is carried out at the JGA. There are three major pathways regulating the secretion of renin by granular cells at the JGA: the baroreceptor, the macula densa mechanism, and direct stimulation by the sympathetic nervous system. The renal baroreceptor monitors renal perfusion pressure and signals an increase in renin when renal perfusion pressure falls. In the macula densa mechanism, macula densa cells sense the decrease in chloride ions in the filtrate in the distal tubule, thereby stimulating release of renin. Increased activity of renal sympathetic nerves directly stimulates renin release via activation of β adrenergic receptors. Sympathetic innervation also modulates both the baroreceptor and macula densa mechanisms.

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