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Nicolas Papanicolaou, MD
Theodore Mountokalakis Paris

Arch Intern Med. 1976;136(6):733.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

In their article on renal and renovascular hypertension, Hunt et al¹ postulated that prostaglandins (PGs) might be involved in the pathogenesis of hypertension that is a result of kidney disease. In a study on functional changes accompanying renal artery stenosis in man, we had indirect evidence indicative of a role of PGs in the physiopathologic alterations occurring in renovascular hypertension. Eleven patients with unilateral stenosis of the main renal artery were studied. All patients had undergone surgery subsequent to the study, and their conditions had proved to be "cured" or notably improved by surgical treatment.² The main results are shown in the Table.

In all cases, a striking decrease of extraction of p-aminohippurate and a decrease of reabsorbed sodium were found. Extraction of p-aminohippurate is considered as an index of the fraction of total renal plasma flow to the medulla. Although medullary flow . . . [Full Text PDF of this Article]

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