The substance causing renal hypertension

Braun-Menendez, E; Fasciolo, J. C.; Leloir, Luis F.; Muñoz, J. M.

doi:10.1113/jphysiol.1940.sp003850

Cited by 348 publications

(98 citation statements)

References 6 publications

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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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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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“…Renin was a central subject of intense investigation because of its role in blood pressure regulation before the discovery of angiotensinogen. Early studies by two groups, led respectively by Page and Braun-Menendez, independently demonstrated that renin was not the direct cause of experimental hypertension, but rather it acted on a substance in plasma to yield a heat-stable peptide possessing both pressor and vasoconstrictor functions [1], [2].…”

Section: Introductionmentioning

confidence: 99%

The angiotensin II type 1 receptor and receptor-associated proteins

et al. 2001

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The mechanisms of regulation, activation and signal transduction of the angiotensin II (Ang II) type 1 (AT1) receptor have been studied extensively in the decade after its cloning. The AT1 receptor is a major component of the renin-angiotensin system (RAS). It mediates the classical biological actions of Ang II. Among the structures required for regulation and activation of the receptor, its carboxyl-terminal region plays crucial roles in receptor internalization, desensitization and phosphorylation. The mechanisms involved in heterotrimeric G-protein coupling to the receptor, activation of the downstream signaling pathway by G proteins and the Ang II signal transduction pathways leading to specific cellular responses are discussed. In addition, recent work on the identification and characterization of novel proteins associated with carboxyl-terminus of the AT1 receptor is presented. These novel proteins will advance our understanding of how the receptor is internalized and recycled as they provide molecular mechanisms for the activation and regulation of G-protein-coupled receptors.

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“…We had no evidence at that time as to the nature of the decrease, and it was merely suggested that angiotonin was an intermediate rather than an end product in these closely associated reactions. This has proved to be true, and the catalyst causing the further breakdown was shown by Fasciolo, Leloir, and Mufioz (20,4) to be an enzyme denominated hypertensinase by them. In line with the nomenclature employed by us (22, 23) this becomes "angiotonase.…”

mentioning

confidence: 97%

A Kinetic Analysis of the Renin-Angiotonin Pressor System and the Standardization of the Enzymes Renin and Angiotonase

Plentl¹,

Page²

1943

Journal of Experimental Medicine

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Sufficient is now known of the renal vasopressor system and its relationship to the mechanism of hypertension to justify a more exacting analysis of it. Shortly after the discovery of angiotonin it was noted that when renin and plasma were allowed to interact, angiotonin at first increased and then slowly began to decrease (3). We had no evidence at that time as to the nature of the decrease, and it was merely suggested that angiotonin was an intermediate rather than an end product in these closely associated reactions. This has proved to be true, and the catalyst causing the further breakdown was shown by Fasciolo, Leloir, and Mufioz (20,4) to be an enzyme denominated hypertensinase by them. In line with the nomenclature employed by us (22, 23) this becomes "angiotonase."Good evidence had suggested that the reaction between renin and reninsubstrate is enzymatic, but proof that this is so came from a recent kinetic analysis of the problem demonstrating the reaction to be of the first order (1). Since both physiological and chemical investigation of renin depends on the ability to assay it quantitatively, we have sought such a method.The methods of bioassay of renin have recently been summarized by Goldblatt, Katz, Lewis, and Richardson (11) in a paper in which they described a method of assaying renin which does not differ appreciably from some previously reported. They overlooked an important contribution by Leloir et al. (5) in which there is proposed a renin unit based upon the amount of pressor substance (anagiotonin) formed. The method of Goldblatt, Katz, Lewis, and Richardson and previous methods referred to by them, are based upon the determination of the rise in arterial pressure elicited by intravenous injection of given amounts of renin solution. Since renin itself is not a pressor substance, it should not be tested for its pressor but for its enzymatic action; that is, in terms of renin-substrate decomposed or angiotonin formed. Similar arguments apply to destruction of angiotonin by angiotonase. A satisfactory method for the assay of angiotonase has been described by Page and Helmer (21).Since kidney extracts usually contain both renin and angiotonase the assay of renin becomes difficult because angiotonase interferes with the determination

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The substance causing renal hypertension

Cited by 348 publications

References 6 publications

Redox Control of Renal Function and Hypertension

Redox Control of Renal Function and Hypertension

The angiotensin II type 1 receptor and receptor-associated proteins

A Kinetic Analysis of the Renin-Angiotonin Pressor System and the Standardization of the Enzymes Renin and Angiotonase

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