Suggested Revision of Nomenclature--Angiotensin

Braun-Menendez, E; Page, Irvine H.

doi:10.1126/science.127.3292.242-a

Cited by 107 publications

(23 citation statements)

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“…The failure of a renin preparation to induce steroidogenesis in vitro even in the presence of beef serum, despite its clear activity in vivo (3), suggests that renin acts on steroid .production only via its ability to release angiotensin (6). The amount of beef serum used in incubation was presumably insufficient to supply significant amounts of angiotensin II.…”

Section: Discussionmentioning

confidence: 99%

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The Effect of Acth, Renin, Angiotensin Ii, and Various Precursors on Biosynthesis of Aldosterone by Adrenal Slices

Kaplan¹,

Barter²

1962

J. Clin. Invest.

169

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Angiotensin II has been shown to increase the excretion (1) and secretion (2) of aldosterone by normal human subjects, and the secretion of aldosterone by hypophysectomized, nephrectomized dogs (3)(4)(5). In the latter preparation (3), renin, which leads to the liberation of angiotensin in the circulation (6), has been shown to stimulate aldosterone secretion. The present studies were done to determine whether angiotensin and renin can act directly on the adrenal cortex. The slices were minced with scissors and weighed. Specimens weighing about 500 mg were placed in 5 ml of Krebs-Ringer bicarbonate medium containing glucose in a concentration of 200 mg per 100 ml. At least 4 vessels were incubated and analyzed separately for each portion of each experiment. Thus, there were at least 4 control vessels and at least 4 with each precursor or stimulating agent studied in each experiment. The tissues were kept chilled until incubation, which was started between 3 and 5 hours after the death of the cattle. Tissues were preincubated for 1 hour at 37°C under 5 per cent CO2-95 per cent 02 on the Dubnoff metabolic shaker. The preincubation medium was removed, and 5 ml of fresh medium was used to transfer the slices to vessels to which the appropriate precursor had been added with or without ACTH, renin, or angiotensin II. Incubation was for 2 hours.The control values for synthesis of aldosterone by the adrenals in vitro showed wide variations from experiment to experiment. The higher the control value, the less was the effect of any given stimulus. Thus, when production of aldosterone by the control beef slices was greater than 2 gsg per g of tissue per hour, experimental procedures produced little or no increase of synthesis. Therefore, only preparations with control values below 2 ,lg per g per hour are included. Factors which may have affected the control level of aldosterone production were water and salt deprivation. Control values were above 4 ,ug per g per hour only during the winter months when the ground was frozen and the cattle had no access to water for at least 24 to 48 hours before slaughter and limited access to water and salt for a longer period. A stimulatory effect of water deprivation on synthesis of aldosterone in vivo (7) and of salt depletion on synthesis in vitro (8) has been observed. Other factors may have led to this seasonal variation, a problem noted by others studying corticosteroid synthesis in vitro (9).The capacity of the tissue to respond to any given stimulus was found to decrease with the passage of time, so this was kept relatively constant in all experiments.Rat adrenal sections. The technique of Saffran and Schally (10) was closely followed. A quarter of one adrenal gland from each of eight 150-to 200-g SpragueDawley male rats was included in each of four vessels 715

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Section: Discussionmentioning

confidence: 99%

“…In the latter preparation (3), renin, which leads to the liberation of angiotensin in the circulation (6), has been shown to stimulate aldosterone secretion. The present studies were done to determine whether angiotensin and renin can act directly on the adrenal cortex.…”

mentioning

confidence: 99%

The Effect of Acth, Renin, Angiotensin Ii, and Various Precursors on Biosynthesis of Aldosterone by Adrenal Slices

Kaplan¹,

Barter²

1962

J. Clin. Invest.

169

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“…Initially, renin was discovered in kidney extracts by Tigersted and Bergman in 1898, and its role later was explained by Harry Goldblatt, in 1934 (8). It was not until 1939 that hypertensin was discovered by Braun-Menendez, and later in 1958, it was renamed angiotensin by BraunMenendez and Page (19,20). Subsequent experiments, including those done by Sir Arthur Guyton, elucidated the physiologic implications of the RAAS and highlighted the importance of the kidney in blood pressure control (97)(98)(99)(100)(101)(102)(103)(104)151).…”

Section: B Role Of the Raas In Oxidative Stress And Hypertensionmentioning

confidence: 99%

Redox Control of Renal Function and Hypertension

Nistala

Whaley‐Connell

Sowers

2008

Antioxidants & Redox Signaling

136

123

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“…Also at this meeting, Dr Braun Menéndez (for the Argentine team) and Dr Page (for the American group) arrived at a single nomenclature for the components of the enzymatic system. 49 Even though there was already a marketed name of Hypertensin, Braun Menéndez agreed to name the active final compound angiotensin, taking half of each original name. Similarly, the renin substrate was named angiotensinogen, and the enzymes that metabolize the peptide were termed angiotensinases.…”

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confidence: 99%

History About the Discovery of the Renin-Angiotensin System

2001

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Abstract-The history of the discovery of the renin-angiotensin system began in 1898 with the studies made by Tigerstedt and Bergman, who reported the pressor effect of renal extracts; they named the renal substance renin based on its origin. In 1934, Harry Goldblatt induced experimental hypertension in dogs by clamping a renal artery. About 1936, simultaneously in the Medical School of the University of Buenos Aires, Argentina, and in the Eli-Lilly Laboratories in Indianapolis, 2 independent groups of researchers, using the Goldblatt technique to produce experimental hypertension, demonstrated renal secretion of a pressor agent similar to renin. In the following years, both teams described the presence of a new compound in the renal vein blood of ischemic kidneys. This agent was extracted from blood with 70% acetone and had a short pressor effect. The final conclusion was that renin acted enzymatically on a plasma protein to produce the new substance. He related hypertrophy to an increased resistance to blood flow in the small vessels due to the altered condition of the blood. In 1868, George Johnson, 2 reporting studies on nephritis, suggested that hyaline-fibroid alterations in the renal vessels were due to an impure condition of the blood, which was also responsible for left ventricular hypertrophy. F.A. Mahomed, 3 using a primitive sphygmograph for the first time, described high blood pressure in 1872. He also linked left ventricular hypertrophy to hypertension due to nephritis and reported the presence of high blood pressure in patients without renal disease. 4,5 Finally, Riva-Rocci, 6 in 1896, described the first indirect sphygmomanometer to measure arterial pressure in humans, and in 1905, Korotkoff 7 defined the sounds that are named after him.The relationship between pathological alterations in the kidney and the development of systemic arterial hypertension had been postulated for many years. In this sense, Franz Volhard 8 suggested the existence of a circulating vasopressor substance. He classified the hypertensive patients: those with slight vascular damage as reds, and those with important vascular lesions-mostly in the kidney, pale skin, and cerebral damage (malignant hypertension)-as white.On the other hand, by the end of the nineteenth century, Tigerstedt, a Finnish professor of physiology working at the Karolinska Institute, and his assistant Bergman 9 analyzed the effect of renal extracts on arterial pressure. They discovered the presence of a pressor compound in the renal tissue of the rabbit, and based on its origin, they named it renin. The pressor activity could be extracted with glycerin, did not dialyze, and was stable at 56°C and was destroyed by boiling. Moreover, they showed that the renal vein blood increased blood pressure when injected into nephrectomized animals. They also detected the potentiation and protraction of the pressor response to renin in the nephrectomized recipient. They explained that the association between renal disease and cardiac hypertrophy was due to the kidney ...

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Suggested Revision of Nomenclature--Angiotensin

Cited by 107 publications

References 5 publications

The Effect of Acth, Renin, Angiotensin Ii, and Various Precursors on Biosynthesis of Aldosterone by Adrenal Slices

The Effect of Acth, Renin, Angiotensin Ii, and Various Precursors on Biosynthesis of Aldosterone by Adrenal Slices

Redox Control of Renal Function and Hypertension

History About the Discovery of the Renin-Angiotensin System

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