Intestinal Vasoconstriction following Diuretic-Induced Volume Depletion: Role of Angiotensin and Vasopressin

1974 ◽  
Vol 52 (4) ◽  
pp. 829-839 ◽  
Author(s):  
J. Robert McNeill
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Adrenal Glands ◽  
Ethacrynic Acid ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Sympathoadrenal System ◽  
Volume Depletion ◽  
Angiotensin System ◽  
Vasoconstrictor Response

Intravenous administration of furosemide, ethacrynic acid, or chlorothiazide induced intestinal vasoconstriction in pentobarbital-anesthetized cats. The vasoconstrictor response following furosemide was prevented by nephrectomy or by replacement of urinary losses, indicating the response was dependent upon the volume-depletion produced by the drug. The intestinal vasoconstriction following furosemide was not reduced in animals subjected to acute intestinal denervation, adrenalectomy, and hypophysectomy. Similarly the response was not reduced in animals subjected to intestinal denervation and adrenalectomy, and administered SQ20881, an inhibitor of angiotensin-converting enzyme. However, administration of SQ20881 to hypophysectomized animals completely abolished the vasoconstriction even when the intestinal innervation and adrenal glands remained intact. The results suggest that the renin–angiotensin system and the vasopressin system play major roles in the mechanism of the intestinal vasoconstriction following diuretic-induced volume depletion and that the sympathoadrenal system plays little role in this response.

scholarly journals The ANG-(1–7)/ACE2/mas axis in the regulation of nephron function

2010 ◽  
Vol 298 (6) ◽  
pp. F1297-F1305 ◽  
Author(s):  
Carlos M. Ferrario ◽  
Jasmina Varagic
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Renin Angiotensin System ◽  
Therapeutic Interventions ◽  
Experimental Hypertension ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
A Site

The study of experimental hypertension and the development of drugs with selective inhibitory effects on the enzymes and receptors constituting the components of the circulating and tissue renin-angiotensin systems have led to newer concepts of how this system participates in both physiology and pathology. Over the last decade, a renewed emphasis on understanding the role of angiotensin-(1–7) and angiotensin-converting enzyme 2 in the regulation of blood pressure and renal function has shed new light on the complexity of the mechanisms by which these components of the renin angiotensin system act in the heart and in the kidneys to exert a negative regulatory influence on angiotensin converting enzyme and angiotensin II. The vasodepressor axis composed of angiotensin-(1–7)/angiotensin-converting enzyme 2/mas receptor emerges as a site for therapeutic interventions within the renin-angiotensin system. This review summarizes the evolving knowledge of the counterregulatory arm of the renin-angiotensin system in the control of nephron function and renal disease.

Role of bradykinin in angiotensin-converting enzyme knockout mice

2003 ◽  
Vol 284 (6) ◽  
pp. H1969-H1977 ◽  
Author(s):  
Hong D. Xiao ◽  
Sebastien Fuchs ◽  
Justin M. Cole ◽  
Kevin M. Disher ◽  
Roy L. Sutliff ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Knockout Mice ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Low Blood Pressure ◽  
Urine Concentrating Ability

Angiotensin-converting enzyme (ACE) plays a central role in the renin-angiotensin system. Whereas ACE is responsible for the production of angiotensin II, it is also important in the elimination of bradykinin. Constitutively, the biological function of bradykinin is mediated through the bradykinin B2 receptor. ACE knockout mice have a complicated phenotype including very low blood pressure. To investigate the role of bradykinin in the expression of the ACE knockout phenotype, we bred B2 receptor knockout mice with ACE knockout mice, thus generating a line of mice deficient in both the B2 receptor and ACE. Surprisingly, these mice did not differ from ACE knockout mice in blood pressure, urine concentrating ability, renal pathology, and hematocrit. Thus abnormalities of bradykinin accumulation do not play an important role in the ACE knockout phenotype. Rather, this phenotype appears due to the defective production of angiotensin II.

Renin Angiotensin System, Gut-Lung Cross Talk and Microbiota. Lessons from SARS-CoV Infections

2021 ◽  
Author(s):  
Andreia Matos ◽  
Alda Pereira da Silva ◽  
Joana Ferreira ◽  
Ana Carolina Santos ◽  
Maria Clara Bicho ◽  
...  
Keyword(s):  
Amino Acids ◽  
Cardiovascular Diseases ◽  
Severe Acute Respiratory Syndrome ◽  
Angiotensin Converting Enzyme ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Multiple Functions ◽  
Key Pathways

The two antagonistic systems of angiotensin converting enzyme (ACE)-1 and ACE-2 are in the “eye of the hurricane” of severe acute respiratory syndrome coronavirus (SARS-CoV-2). The receptor of the SARS-CoV-2 is the same as ACE-2, which causes its under-expression after binding it, followed by the internalization of the complex virus-ACE-2. ACE-2 have multiple functions with specially relevance in cardiovascular diseases. Furthermore, the non-enzymatic role of ACE-2 gives rise to a Hartnup disease, a phenocopy involving microbiota. With this chapter, we intent to explore the key pathways involved in SARS-CoV-2 infection, from the host perspective, considering our hypothesis related to transporter of neutral amino acids, which includes tryptophan precursor of serotonin and kynurenine.

scholarly journals Angiotensin-Converting Enzyme 2 (ACE2) Is a Key Modulator of the Renin Angiotensin System in Health and Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Chris Tikellis ◽  
M. C. Thomas
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Renin Angiotensin System ◽  
Main Role ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Organ Protection ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Health And Disease

Angiotensin-converting enzyme 2 (ACE2) shares some homology with angiotensin-converting enzyme (ACE) but is not inhibited by ACE inhibitors. The main role of ACE2 is the degradation of Ang II resulting in the formation of angiotensin 1–7 (Ang 1–7) which opposes the actions of Ang II. Increased Ang II levels are thought to upregulate ACE2 activity, and in ACE2 deficient mice Ang II levels are approximately double that of wild-type mice, whilst Ang 1–7 levels are almost undetectable. Thus, ACE2 plays a crucial role in the RAS because it opposes the actions of Ang II. Consequently, it has a beneficial role in many diseases such as hypertension, diabetes, and cardiovascular disease where its expression is decreased. Not surprisingly, current therapeutic strategies for ACE2 involve augmenting its expression using ACE2 adenoviruses, recombinant ACE2 or compounds in these diseases thereby affording some organ protection.

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