The blood‐pressure raising secretion of the ischaemic kidney

Fasciolo, J. C.; Houssay, B. A.; Taquini, Alberto C.

doi:10.1113/jphysiol.1938.sp003680

Cited by 83 publications

(20 citation statements)

References 2 publications

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“…Later on, in1934, Goldblatt et al, found that hypertension in animal models induced by renal ischemia caused a release of vasoconstrictor substance (Goldblatt, Lynch, Hanzal, & Summerville, 1934). After that, two independent groups were the first to report the end product of this cascade in 1939 and they named it as "Hypertensin" (Fasciolo, Houssay, & Taquini, 1938) and "Angiotonin" (Page, 1939), separately. Soon after, the two groups agreed on a common nomenclature of the vasopressor end product of renin activity as (angiotensin) (BraunMenendez & Page, 1958).…”

Section: Introduction Renin Angiotensin System (Ras)mentioning

confidence: 99%

Enhanced Angiotensin II-Induced Cardiac and Aortic Remodeling in ACE2 Knockout Mice

Alghamri

Weir

Anstadt

et al. 2012

J Cardiovasc Pharmacol Ther

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Mahmoud Alghamri. M.S., Department of Pharmacology and Toxicology, Wright State University, 2012. Enhanced Angiotensin II-Induced Cardiac and Aortic Remodeling in ACE2 Knockout Mice.Activation of the renin angiotensin system (RAS) is a well-known driving force, governing the aggravation and progression of CVD and associated target organ damage.Angiotensin (Ang) converting enzyme 2 (ACE2), a new member within the RAS family, was first cloned from the ventricle of patient with heart failure. ACE2 was shown to be upregulated under pathological conditions. We hypothesize that loss of ACE2 negatively affects cardiac function and exacerbates hypertrophic cardiomyopathy and aortic remodeling in response to Ang II. Eight weeks old ACE2 knock out (KO) and wild type (WT) mice were infused with Ang II s.c. (1000 ng/kg/min for 4 weeks) using osmotic pumps. Blood pressure (radiotelemetry), cardiac function (echocardiography) and cardiac/aortic structural damage (histology) were examined. At baseline before Ang II, ACE2 KO displayed a normal phenotype for cardiac function and blood pressure. After 4 weeks of Ang II infusion, the mean arterial pressure (MAP) was increased (~40% in WT and ~33% in ACE2 KO) with no differences between groups. However, ACE2 KO responded differently to the increased MAP. Cardiac function analysis revealed severe myocardial dysfunction shown by the lowered EF% (31% vs. 13%) as well as FS% (30% vs 6%) in ACE2 KO vs WT, respectively. In addition, the cardiac dysfunction was associated with hypertrophic cardiomyopathy shown by the increased left ventricular wall thickness as well as heart weight/ body weight ratio. Moreover, collagen staining in the myocardium and aorta revealed higher collagen percentage in ACE2 KO which indicates iv cardiovascular remodeling. Furthermore, results showed enhanced oxidative stress in the myocardium and aorta of Ang II infused ACE2 KO compared to Ang II WT. In conclusion, ACE2 attenuates myocardial maladaptive hypertrophy and cardiovascular remodeling in response to long term Ang II stimulation.v

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Section: Introduction Renin Angiotensin System (Ras)mentioning

confidence: 99%

Enhanced Angiotensin II-Induced Cardiac and Aortic Remodeling in ACE2 Knockout Mice

Alghamri

Weir

Anstadt

et al. 2012

J Cardiovasc Pharmacol Ther

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“…27 It became necessary to establish the nature of this compound and to characterize, purify, and isolate it to identify its chemical structure.…”

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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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“…The main cell type noted in the protective renomedullary transplants had the microscopic characteristics of the lipid-containing interstitial cells. These cells occurred INTRODUCTION An antihypertensive function of the normal kidney was proposed in relation to the Goldblatt experiment (1)(2)(3)(4)(5).…”

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Renomedullary Antihypertensive Function in Accelerated (Malignant) Hypertension

Muirhead¹,

Brooks²,

Pitcock³

et al. 1972

J. Clin. Invest.

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A B S T R A C T The antihypertensive function of the renal medulla was tested on accelerated (malignant) hypertension of the rabbit. A procedure for the development of accelerated hypertension of the rabbit of lethal proportions within 3 wk was established. This procedure consisted of the application of a rigid clip with a fixed and unyielding gap to the left renal artery and removal of the right kidney. Three additional manipulations, other than simple nephrectomy, were performed on the right kidney after application of the rigid clip to the left renal artery. These were: (a) a sham operation, (b) removal of the kidney and separation of the renal cortex and its autotransplantation in a fragmented state, and (c) removal of the kidney and separation of the renal medulla and its autotransplantation in a fragmented state. After the shamoperated kidney and autotransplanted renal medulla, the standardized accelerated hypertension did not develop, whereas after autotransplanted renal cortex it did. After a period of protection against accelerated hypertension, removal of either the sham-operated kidney or the renomedullary transplants was followed by a prompt rise in arterial pressure and death of the animal.

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The blood‐pressure raising secretion of the ischaemic kidney

Cited by 83 publications

References 2 publications

Enhanced Angiotensin II-Induced Cardiac and Aortic Remodeling in ACE2 Knockout Mice

Enhanced Angiotensin II-Induced Cardiac and Aortic Remodeling in ACE2 Knockout Mice

History About the Discovery of the Renin-Angiotensin System

Renomedullary Antihypertensive Function in Accelerated (Malignant) Hypertension

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