(Hypertension. 2000;35:693.)
© 2000 American Heart Association, Inc.
Editorial |
From Hypertension, Alton Ochsner Medical Foundation, New Orleans, La.
Correspondence to Edward D. Frohlich, MD, Editor-in-Chief, Hypertension, Alton Ochsner Medical Foundation, 1516 Jefferson Hwy, BH 514, New Orleans, LA 70121.
| Introduction |
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Recently, one report appeared in one of the most prestigious weekly medical journals indicating that angiotensin-converting enzyme inhibition therapy of patients with chronic renal failure will reduce "adrenergic hyperactivity."2 The concept apparently was deemed so novel that an accompanying editorial commentary was included in that issue of the journal.3 No references included in either communication referred to the well-known and well-established phenomenon of angiotensin II augmentation of adrenergic activity in medullary centers or in ganglionic function.4 5 Only a few weeks after this publication, yet another paper was published in a "sister journal" of the American Heart Association indicating increased sympathetic nerve activity in patients with renovascular hypertension.6 Again, no evidence was provided in the references to prior knowledge that increased angiotensin II augments adrenergic outflow from brain or in the paravertebral ganglia. By no means is this experience restricted to the foregoing cited work; it is rampant throughout the literature. And, not infrequently, it is aided and abetted by published statements in these papers stating that "this is the first report" a remark that frequently raises deep concern by one of my co-editors. This, of course, is based on the entire body of extant scientific research preceding any scientific communication. Clearly, any report of new knowledge is founded on a background of well-conceived and carefully documented scientific study.
This practice of a less than thorough review of the literature at best shows inadequate awareness of existing scientific knowledge by authors publishing in major scientific journals and at the worst does not serve science well. It belittles past contributions of other scientists and colleagues, demeans prior authoritative and respected peer-reviewed journal and published scientific knowledge, and it diminishes the authoritative status of the authors, reviewers, and editors of those journals that have published this work. Furthermore, it also obscures the context in which a truly new observation must be interpreted. If we are to expect others to respect and follow tried and tested scientific method and, if we expect that our journals should publish that which is new and exciting in a rapid fashion, let us begin with ourselves. Let us respect and honor our past colleagues and their work. On the other hand, this editorial statement is not a plea for an exhaustive recantation of the extant literature but a careful search for primary references of general value and interest that acknowledges the major contributions of our predecessors. And let us also remember what is literally meant by "research"it means, "look back!"
| Footnotes |
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| References |
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2.
Ligtenberg G, Blankestijn PJ, Oey PL, Klein IHH,
Kijkhorst-Oei L-T, Boomsma F, Wieneke GH, Van Huffelen AC, Koomans HA.
Reduction of sympathetic hyperactivity by enalapril in patients with
chronic renal failure. N Engl J Med. 1999;340:13211328.
3.
Devereux RB, Roman MJ. Sympathetic overactivity in
hypertensive patients with chronic renal disease. N Engl
J Med. 1999;340:13581359.
4. Scroop GC, Lowe RD. Efferent pathways of the cardiovascular response to vertebral artery infusions of angiotensin in man. Clin Sci. 1969;37:605619.[Medline] [Order article via Infotrieve]
5.
McCubbin JW, Page IH. Neurogenic component of chronic
renal hypertension. Science. 1963;139:210215.
6.
Johansson M, Elam M, Rundqvist B, Eisenhofer G,
Herlitz H, Lambert G, Friberg P. Increased sympathetic nerve activity
in renovascular hypertension. Circulation. 1999;99:25372542.
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E. D. Frohlich Professor John Douglas Swales Hypertension, May 1, 2001; 37(5): 1198 - 1198. [Full Text] |
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