Hypertensin: The Substance Causing Renal Hypertension

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

doi:10.1038/144980a0

Cited by 38 publications

(11 citation statements)

References 2 publications

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“…Scientists, led by Irvine Page in Indianapolis and Eduardo Braun-Menéndez in Buenos Aires, identified renin as an enzyme and called the product of renin catalysis hypertensin (Braun-Menéndez) or angiotonin (Page) (Kohlstaedt et al, 1938;Muñoz et al, 1939;Braun-Menéndez et al, 1940;Page and Helmer, 1940). In 1958, both groups agreed to the name angiotensin (Braun-Menéndez and Page, 1958).…”

Section: A Discoverymentioning

confidence: 99%

A Modern Understanding of the Traditional and Nontraditional Biological Functions of Angiotensin-Converting Enzyme

et al. 2012

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Section: A Discoverymentioning

confidence: 99%

A Modern Understanding of the Traditional and Nontraditional Biological Functions of Angiotensin-Converting Enzyme

et al. 2012

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“…10 The fast pressor responses are produced by relatively high concentrations of Ang II, which induce a rapid contraction of the smooth muscle when administered as a bolus. 11 The response reaches the maximal pressor response in seconds and returns to normal levels in 2 to 3 minutes. The intracellular signaling involved in mediating such a rapid angiotensin-induced vasoconstriction has been investigated extensively.…”

Section: Can Normal Concentrations Of Angiotensin In Plasma Induce Anmentioning

confidence: 99%

Role of Angiotensin and Oxidative Stress in Essential Hypertension

1999

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Abstract-In this review, we examine the possibility that small increments in angiotensin II are responsible for an increase in blood pressure and maintenance of hypertension through the stimulation of oxidative stress. A low dose of angiotensin II (2 to 10 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 , which does not elicit an immediate pressor response), when given for 7 to 30 days by continuous intravenous infusion, can increase mean arterial pressure by 30 to 40 mm Hg. This slow pressor response to angiotensin is accompanied by the stimulation of oxidative stress, as measured by a significant increase in levels of 8-iso-prostaglandin F 2␣ (F 2 -isoprostane). Superoxide radicals and nitric oxide can combine chemically to form peroxynitrite, which can then oxidize arachidonic acid to form F 2 -isoprostanes. F 2 -isoprostanes exert potent vasoconstrictor and antinatriuretic effects. Furthermore, angiotensin II can stimulate endothelin production, which also has been shown to stimulate oxidative stress. In this way, a reduction in the concentration of nitric oxide (which is quenched by superoxide) along with the formation of F 2 -isoprostanes and endothelin could potentiate the vasoconstrictor effects of angiotensin II. We hypothesize that these mechanisms, which underlie the development of the slow pressor response to angiotensin II, also participate in the production of hypertension when circulating angiotensin II levels appear normal, as occurs in many cases of essential and renovascular hypertension.

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“…The possibility that renin was an enzyme was raised by Kohlstaedt et al 7 and by Munoz et al 8 in the late 1930s. Extensive studies consequently confirmed that renin itself did not have a direct pressor action, but that it acted upon a plasma substrate (now called angiotensinogen) to form ultimately the vasoactive material subsequently identified as the peptide angiotensin II (Figure 1).…”

Section: Renin As An Enzymementioning

confidence: 99%