The experimental observation that led to discovery of angiotensin. 1939 Buenos Aires, Argentina.

Fasciolo, J. C.

doi:10.1161/01.hyp.16.2.194

Cited by 15 publications

(20 citation statements)

References 7 publications

(3 reference statements)

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“…J.B. Señorans studied under Bernard's disciples and continued to promote his physiological interests (Houssay & Buzzo, 1937;Charreau, 2016), among them, the problem of hypertension (Fasciolo, Houssay & Taquini, 1938;Irving, 1965). This led eventually to the discovery of the renal factor involved in hypertension, named 'hypertensin' (Fasciolo et al, 1938;Braun-Menendez, 1939;Fasciolo, 1990). The influence of Bernard's ideas was also strong in the USA (Olmsted, 1935), leading to the parallel discovery of the same hypertensive factor in the Lilly Laboratory for Clinical Research in Indianapolis, there named 'angiotonin' (Page & Helmer, 1940).…”

Section: Introductionmentioning

confidence: 99%

The chloride anion as a signalling effector

Valdivieso

Santa‐Coloma

2019

Biological Reviews

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The specific role of the chloride anion (Cl−) as a signalling effector or second messenger has been increasingly recognized in recent years. It could represent a key factor in the regulation of cellular homeostasis. Changes in intracellular Cl− concentration affect diverse cellular functions such as gene and protein expression and activities, post‐translational modifications of proteins, cellular volume, cell cycle, cell proliferation and differentiation, membrane potential, reactive oxygen species levels, and intracellular/extracellular pH. Cl− also modulates functions in different organelles, including endosomes, phagosomes, lysosomes, endoplasmic reticulum, and mitochondria. A better knowledge of Cl− signalling could help in understanding the molecular and metabolic changes seen in pathologies with altered Cl− transport or under physiological conditions. Here we review relevant evidence supporting the role of Cl− as a signalling effector.

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Section: Introductionmentioning

confidence: 99%

The chloride anion as a signalling effector

Valdivieso

Santa‐Coloma

2019

Biological Reviews

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“…infusion of the converting enzyme inhibitor captopril; and (iii) i.c.v. infusion of the AngII antagonist Sar 1 ‐Ile 8 ‐AngII (sarile) inhibited H‐NaCl‐S intake of sodium‐depleted animals at doses up to 20‐fold lower than doses infused i.v., which did not alter this behaviour. Therefore, the authors concluded that AngII of brain origin is the peptide important for need‐induced sodium intake.…”

Section: Homeostatic Control Of Sodium Intakementioning

confidence: 99%

“…Contrary to the conclusion derived from injections of non‐ peptide antagonists is the decrease in arterial pressure induced by 5 min i.c.v. infusion of the peptide AngII receptor antagonist [Sar 1 ,Thr 8 ]‐AngII (sarthran) in sodium‐replete normotensive rats. 35 The peptide antagonist is perhaps necessary to be infused for several minutes due to endogenous peptidases; however, single injections of losartan or PD123319 antagonize the pressor effect of exogenous angiotensins for several hours.…”

Section: Angiotensin II and Arterial Pressure In Sodium Depletion‐indmentioning

confidence: 99%

“…Angiotensin, a hybrid of angiotonin and hypertensin, so named by agreement among its discoverers, describes precisely physiological and pathological roles for this peptide in the cardiovascular system. 1 Angiotensin (Ang)II, established as a physiologically important form of angiotensin, produces a variety of responses mediated by brain and peripheral AngII receptors, ranging from cellular to behavioural levels. Responses related to hydromineral balance and cardiovascular function include increases in arterial pressure, natriuresis (when injected into the brain), aldosterone secretion, sodium retention, vasopressin release, water intake and NaCl solution intake.…”

Section: Introductionmentioning

confidence: 99%

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Brain Versus Peripheral Angiotensin Ii Receptors In Hypovolaemia: Behavioural And Cardiovascular Implications

Luca

Sugawara

Menani

2000

Clin Exp Pharma Physio

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1. Angiotensin (Ang)II is involved in responses to hypovolaemia, such as sodium appetite and increase in blood pressure. Target areas subserving these responses for AngII include the cardiovascular system in the periphery and the circumventricular organs in the brain. 2. Conflicting data have been reported for the role of systemic versus brain AngII in the mediation of sodium appetite. 3. The role for systemic AngII and systemic AngII receptors in the control of blood pressure in hypovolaemia is well established. In contrast with systemic injections, i.c.v injections of AngII non-peptide AT1 and AT2 receptor antagonists, such as losartan and PD123319, do not reduce arterial pressure in sodium-depleted (furosemide injection plus removal of ambient sodium for 24 h) rats. Thus, brain AngII receptors are likely not important for cardiovascular responses to hypovolaemia induced by sodium depletion. 4. Intracerebroventricular injections of losartan or PD123319 increase arterial pressure when injected at relatively high doses. This hypertensive effect is unlikely to be an agonist effect on brain AngII receptors. Increases in arterial pressure produced by i.c.v. losartan are attenuated by lesions of the tissue surrounding the anterior third ventricle (AV3V). The hypertensive effect of i.c.v. AngII is abolished by lesions of the AV3V. 5. Hypertension induced by AngII receptor antagonists is consistent with hypotension induced by AngII acting in the brain. However, the full physiological significance of this hypotensive effect mediated by brain AngII receptors remains to be determined.

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“…The renin–angiotensin system (RAS) had its beginnings at the end of the 19th century (Tigerstedt & Bergman, 1898), and, over the following six decades, all of its components were identified and functionally characterised (see Fasciolo, 1990; Page & Bumpus, 1961). Renin, released from the kidney, cleaved a decapeptide from a plasma protein, renin substrate (angiotensinogen).…”

Section: Introductionmentioning

confidence: 99%

How ACE inhibitors transformed the renin–angiotensin system

Bakhle

2020

British J Pharmacology

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The renin-angiotensin system (RAS) now underlies the successful treatment of almost 50% of the patients in cardiovascular medicine, with serious possibilities of extension to diabetes, Alzheimer's disease and cancer. This clinical transformation started just over 50 years ago, with the unexpected identification of a bradykininpotentiating peptide from snake venom, as a potent inhibitor of ACE which led to the development of the first synthetic inhibitor, captopril, followed by the angiotensin receptor blockers. This article analyses the transformation of the RAS into its different stages, from academic experiments to clinical use and back to the laboratory, identifying the critical events involved, both clinical and scientific. The analysis also assesses the contributions of chance, coincidence, and conviction that were crucial in this transformation. Although questions remain, the transformation of the RAS over the past five decades provides a success story for medicine, for pharmacology, and, most significantly, for patients.

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The experimental observation that led to discovery of angiotensin. 1939 Buenos Aires, Argentina.

Cited by 15 publications

References 7 publications

The chloride anion as a signalling effector

The chloride anion as a signalling effector

Brain Versus Peripheral Angiotensin Ii Receptors In Hypovolaemia: Behavioural And Cardiovascular Implications

How ACE inhibitors transformed the renin–angiotensin system

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