By Leonard T. Skeggs, Frederic E. Dorer, Joseph R. Kahn, Kenneth E. Lentz (auth.), Irvine H. Page M.D., F. Merlin Bumpus Ph.D. (eds.)
The heritage of arterial high blood pressure is either lengthy and brief; lengthy, considering shiny (1827) first comparable hardness of the heart beat to hardness of the kidneys and hyper. trophy of the center; brief in that glossy learn begun within the past due twenties. so much of what we all know of those illnesses has been stumbled on some time past fifty years. the fashionable tale must have all started in 1897 whilst an extract of kidney was once proven to be pressor. yet little used to be performed with wisdom until eventually approximately 1929 while the connection of this kidney extract referred to as "renin" to high blood pressure used to be pos· tulated. The pressor results have been, despite the fact that, in contrast to so much of these visible with sub· stances comparable to epinephrine or vasopressin. Plasma was once required for motion of renin and the energetic substance looked to be protein. In 1939, it was once proven that renin was once no longer in itself a pressor substance yet fairly a proteolytic enzyme which produced a strong pressor substance performing on a substrate synthesized by means of the liver. Later it was once famous that the 1st definable step after the formation of this peptide was once cleaving of the decapeptide which had very little demonstrable task, with lack of amino acids to shape the octapeptide referred to as "angiotensin". inside a decade synthesis was once completed which made the substance to be had for world·wide study.
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Extra resources for Angiotensin
II were not. They interpreted their results to mean that there was a variable activity of converting enzyme in smooth muscle and that only a small part (1-5%) of the activity of Ang. I was due to its own intrinsic activity. The discordant results of YAMAMOTO et al. (1971) were due to an inexplicable loss of activity of the sample of pentapeptide inhibitor which they used (TURKER, personal communication). OPARIL et al. (1971) have confirmed that most of the activity of Ang. I on strips of rabbit aorta is abolished by a peptide inhibitor of conversion, indicating that intramural conversion account3 for that part of the activity which is abolished.
I and Ang. II (Fig. , 1971 (3)]. Furthermore, a convertingenzyme inhibitor specifically reduced the effects of Aug. I but not th'ose of Ang. II. 28 J. R. VANE: They concluded from these results that most of the contractor effects of Ang. I on the isolated vascular smooth muscle were produced after intramural conversion bAng. II. Calculation of the percentage conversion of Ang. I to Ang. II within the wall of the vascular strip (Fig. 5) showed higher activity for pulmonary arteries (30 to 43 %) than for any other artery tested.
I after intravenous injection, especially when the amount converted by blood in one circulation time (15-30 sec, SPECTOR, 1956) was calculated to be about 10%. LEE et al. [1971 (1)] have also calculated the half-life of physiological concentrations of Ang. 3 min. OPARIL et al. (1970) confirmed the relative unimportance of blood-converting enzyme in dogs, using both tritiated Ang. I and radioimmunoassay. They found that Ang. I had a half-life of 3 min and in 15 sec only 8 % had been converted. They, too, found angiotensinase activity but their measurements, like those of NG and VANE, did not reveal whether Ang.
Angiotensin by Leonard T. Skeggs, Frederic E. Dorer, Joseph R. Kahn, Kenneth E. Lentz (auth.), Irvine H. Page M.D., F. Merlin Bumpus Ph.D. (eds.)