Classic Papers Revisited  |   February 2017
Snakes and Hypertension
Author Notes
  • From the Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medicine Emeritus, Baltimore, Maryland.
  • Submitted for publication September 13, 2016. Accepted for publication September 14, 2016.
    Submitted for publication September 13, 2016. Accepted for publication September 14, 2016.×
  • Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are available in both the HTML and PDF versions of this article. Links to the digital files are provided in the HTML text of this article on the Journal’s Web site (www.anesthesiology.org).
    Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are available in both the HTML and PDF versions of this article. Links to the digital files are provided in the HTML text of this article on the Journal’s Web site (www.anesthesiology.org).×
  • Address for correspondence to Edward D. Miller, Jr., M.D., Dean/CEO, Johns Hopkins Medicine Emeritus, John Hopkins University, Professor of Anesthesiology and Critical Care Medicine, 132 SE Rio Casarano, Port St. Lucie, Florida 34984. emiller@jhmi.edu. Information on purchasing reprints may be found at www.anesthesiology.org or on the masthead page at the beginning of this issue. Anesthesiology’s articles are made freely accessible to all readers, for personal use only, 6 months from the cover date of the issue.
Article Information
Classic Papers Revisited / Cardiovascular Anesthesia
Classic Papers Revisited   |   February 2017
Snakes and Hypertension
Anesthesiology 2 2017, Vol.126, 321-324. doi:10.1097/ALN.0000000000001441
Anesthesiology 2 2017, Vol.126, 321-324. doi:10.1097/ALN.0000000000001441
Abstract

Inhibition of Angiotensin Conversion in Experimental Renovascular Hypertension. By Miller ED Jr, Samuels A, Haber E, and Barger AC. Science 1972; 177:1108–9. Reprinted with permission from AAAS.

Constriction of the renal artery and controlled reduction of renal perfusion pressure is followed by a prompt increase in systemic renin activity and a concomitant rise in blood pressure in trained, unanesthetized dogs. The elevated blood pressure induced by the renal artery stenosis can be prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro, which blocks conversion of angiotensin I to angiotensin II. Further, the nonapeptide can restore systemic pressure to normal in the early phase of renovascular hypertension. These results offer strong evidence that the renin– angiotensin system is responsible for the initiation of hypertension in the unilaterally nephrectomized dog with renal artery constriction.