(Hypertension. 2001;37:e11.)
© 2001 American Heart Association, Inc.
Letters to the Editor |
Emeritus Professor, University of Montréal
| Introduction |
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The 2000 Nobel Prize in Medicine goes in part to Dr Arvid Carlsson for his recognition of the role of dopamine not only in the brain but also in the periphery.1 This was further extended by his collaborator Dr Snider who recognized dopamine as a stress-released catecholamine2 and subsequently summarized it in relation to hypertension.3 This reminds us that in 1935, Dr Irvine H. Page, who is not well known for his contributions to the field of neuroscience, was the first to observe4 a very particular form of paroxysmal hypertension with sympathetic discharge in the absence of pheochromocytoma. He wisely observed that in contrast to the pheochromocytoma-related paleness, those patients had a "blush over the face, neck and trunk as well as nausea during the paroxysm." He concluded that this resulted from irritation of sympathetic and parasympathetic centers in the diencephalon. The subsequent discovery of norepinephrine as a dominant sympathetic marker in the 1950s raised hope but failed to demonstrate a relationship to the above episodes.
Primarily, this was due to the fact that norepinephrine was not found elevated and would cause paleness rather than flushing due to norepinephrine-induced vasoconstriction. Facing this enigma,5 Dr. Page, reminded of Carlssons work, argued strongly in favor of dopamine. In his words, this "orphan catecholamine," in its action, best fit his original clinical description4 of flushing and nausea (he later added polyuria).6
Further studies of these paroxysms, probably more common
than in pheochromocytoma and summarized under the
"pseudopheochromocytoma"
heading,7 have shown
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