WordNet

an agent that retards or restrains the action of angiotensin II
the 9th letter of the Roman alphabet (同)i
any of several vasoconstrictor substances (trade name Hypertensin) that cause narrowing of blood vessels (同)angiotonin, Hypertensin

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/04/15 12:42:37」(JST)

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Angiotensin is a peptide hormone that causes vasoconstriction and a subsequent increase in blood pressure. It is part of the renin-angiotensin system, which is a major target for drugs that lower blood pressure. Angiotensin also stimulates the release of aldosterone, another hormone, from the adrenal cortex. Aldosterone promotes sodium retention in the distal nephron, in the kidney, which also drives blood pressure up.

Angiotensin is an oligopeptide and is a hormone and a powerful dipsogen. It is derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver. It plays an important role in the renin-angiotensin system. Angiotensin was independently isolated in Indianapolis and Argentina in the late 1930s (as 'angiotonin' and 'hypertensin', respectively) and subsequently characterised and synthesized by groups at the Cleveland Clinic and Ciba laboratories in Basel, Switzerland.^[3]

Precursor, and types of angiotensin

Angiotensinogen

Angiotensinogen is an α-2-globulin produced constitutively and released into the circulation mainly by the liver. It is a member of the serpin family, although it is not known to inhibit other enzymes, unlike most serpins. Plasma angiotensinogen levels are increased by plasma corticosteroid, estrogen, thyroid hormone, and angiotensin II levels.

Angiotensinogen is also known as renin substrate. Human angiotensinogen is 453 amino acids long, but other species have angiotensinogen of varying sizes. The first 12 amino acids are the most important for activity.

Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu-Val-Ile-...

Angiotensin I

Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu | Val-Ile-...

Renin–angiotensin–aldosterone system

Angiotensin I (CAS# 11128-99-7) is formed by the action of renin on angiotensinogen. Renin cleaves the peptide bond between the leucine (Leu) and valine (Val) residues on angiotensinogen, creating the ten-amino acid peptide (des-Asp) angiotensin I. Renin is produced in the kidneys in response to renal sympathetic activity, decreased intrarenal blood pressure (<90mmHg systolic blood pressure^[4] ) at the juxtaglomerular cells, or decreased delivery of Na+ and Cl- to the macula densa.^[5] If a reduced NaCl concentration^[6] in the distal tubule is sensed by the macula densa, renin release by juxtaglomerular cells is increased. This sensing mechanism for macula densa-mediated renin secretion appears to have a specific dependency on chloride ions rather than sodium ions. Studies using isolated preparations of thick ascending limb with glomerulus attached in low NaCl perfusate were unable to inhibit renin secretion when various sodium salts were added but could inhibit renin secretion with the addition of chloride salts.^[7] This, and similar findings obtained in vivo,^[8] has led some to believe that perhaps "the initiating signal for MD control of renin secretion is a change in the rate of NaCl uptake predominantly via a luminal Na,K,2Cl co-transporter whose physiological activity is determined by a change in luminal Cl concentration."^[9]

Angiotensin I appears to have no biological activity and exists solely as a precursor to angiotensin II.

Angiotensin II

Asp-Arg-Val-Tyr-Ile-His-Pro-Phe | His-Leu

Angiotensin I is converted to angiotensin II (AII) through removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE), primarily through ACE within the lung (but also present in endothelial cells and kidney epithelial cells). ACE found in other tissues of the body has no physiological role (ACE has a high density in the lung, but activation here promotes no vasoconstriction, angiotensin II is below physiological levels of action).^{[citation needed]} Angiotensin II acts as an endocrine, autocrine/paracrine, and intracrine hormone.

ACE is a target for inactivation by ACE inhibitor drugs, which decrease the rate of Angiotensin II production. Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates an IP3-dependent mechanism leading to a rise in intracellular calcium levels and ultimately causing contraction). In addition, angiotensin II acts at the [[Na/H⁺ exchanger]] in the proximal tubules of the kidney to stimulate Na reabsorption and H⁺ excretion which is coupled to bicarbonate reabsorption. This ultimately results in an increase in blood volume, pressure, and pH.^[10] Hence, ACE inhibitors are major anti-hypertensive drugs.

Other cleavage products of ACE, seven or 9 amino acids long, are also known; they have differential affinity for angiotensin receptors, although their exact role is still unclear. The action of AII itself is targeted by angiotensin II receptor antagonists, which directly block angiotensin II AT₁ receptors.

Angiotensin II is degraded to angiotensin III by angiotensinases located in red blood cells and the vascular beds of most tissues. It has a half-life in circulation of around 30 seconds, whereas, in tissue, it may be as long as 15–30 minutes.

Angiotensin III

Asp | Arg-Val-Tyr-Ile-His-Pro-Phe

Angiotensin III has 40% of the pressor activity of angiotensin II, but 100% of the aldosterone-producing activity. Increases mean arterial pressure.

Angiotensin IV

Arg | Val-Tyr-Ile-His-Pro-Phe

Angiotensin IV is a hexapeptide that, like angiotensin III, has some lesser activity.

Effects

See also Renin-angiotensin system#Effects

Angiotensins II, III and IV have a number of effects throughout the body:

Adipic

Angiotensins "modulate fat mass expansion through upregulation of adipose tissue lipogenesis ... and downregulation of lipolysis " ^[11]

Cardiovascular

They are potent direct vasoconstrictors, constricting arteries and veins and increasing blood pressure. This effect is achieved through activation of the GPCR AT1, which signals through a Gq protein to activate Phospholipase C, and subsequently increase intracellular calcium.^[12]

Angiotensin II has prothrombotic potential through adhesion and aggregation of platelets and stimulation of PAI-1 and PAI-2.^[13]^[14]

When cardiac cell growth is stimulated, a local (autocrine-paracrine) renin-angiotensin system is activated in the cardiac myocyte, which stimulates cardiac cell growth through protein kinase C. The same system can be activated in smooth muscle cells in conditions of hypertension, atherosclerosis, or endothelial damage. Angiotensin II is the most important Gq stimulator of the heart during hypertrophy, compared to endothelin-1 and α1 adrenoreceptors.^{[citation needed]}

Neural

Angiotensin II increases thirst sensation (dipsogen) through the subfornical organ of the brain, decreases the response of the baroreceptor reflex, and increases the desire for salt. It increases secretion of ADH in the posterior pituitary and secretion of ACTH in the anterior pituitary. It also potentiates the release of norepinephrine by direct action on postganglionic sympathetic fibers.

Adrenal

Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain sodium and lose potassium. Elevated plasma angiotensin II levels are responsible for the elevated aldosterone levels present during the luteal phase of the menstrual cycle.

Renal

Angiotensin II has a direct effect on the proximal tubules to increase Na⁺ reabsorption. It has a complex and variable effect on glomerular filtration and renal blood flow depending on the setting. Increases in systemic blood pressure will maintain renal perfusion pressure; however, constriction of the afferent and efferent glomerular arterioles will tend to restrict renal blood flow. The effect on the efferent arteriolar resistance is, however, markedly greater, in part due to its smaller basal diameter; this tends to increase glomerular capillary hydrostatic pressure and maintain glomerular filtration rate. A number of other mechanisms can affect renal blood flow and GFR. High concentrations of Angiotensin II can constrict the glomerular mesangium, reducing the area for glomerular filtration. Angiotensin II is a sensitizer to tubuloglomerular feedback, preventing an excessive rise in GFR. Angiotensin II causes the local release of prostaglandins, which, in turn, antagonize renal vasoconstriction. The net effect of these competing mechanisms on glomerular filtration will vary with the physiological and pharmacological environment.

Direct Renal effects of angiotensin II (not including aldosterone release)
Target	Action	Mechanism^[15]
renal artery & afferent arterioles	vasoconstriction (weaker)	VDCCs → Ca²⁺ influx
efferent arteriole	vasoconstriction (stronger)	(probably) activate Angiotensin receptor 1 → Activation of G_q → ↑PLC activity → ↑IP₃ and DAG → activation of IP₃ receptor in SR → ↑intracellular Ca²⁺
mesangial cells	contraction → ↓filtration area	activation of G_q → ↑PLC activity → ↑IP₃ and DAG → activation of IP₃ receptor in SR → ↑intracellular Ca²⁺ VDCCs → Ca²⁺ influx
proximal tubule	increased Na⁺ reabsorption	adjustment of Starling forces in peritubular capillaries to favour increased reabsorption efferent and afferent arteriole contraction → decreased hydrostatic pressure in peritubular capillaries efferent arteriole contraction → increased filtration fraction → increased colloid osmotic pressure in peritubular capillaries increased sodium–hydrogen antiporter activity
tubuloglomerular feedback	increased sensitivity	increase in afferent arteriole responsiveness to signals from macula densa
medullary blood flow	reduction

References

^ "Human PubMed Reference:".
^ "Mouse PubMed Reference:".
^ Basso N, Terragno NA (Dec 2001). "History about the discovery of the renin-angiotensin system". Hypertension. 38 (6): 1246–9. doi:10.1161/hy1201.101214. PMID 11751697.
^ "JAMA Article Jan 2012".
^ Williams GH, Dluhy RG (2008). "Chapter 336: Disorders of the Adrenal Cortex". In Loscalzo J, Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL. Harrison's principles of internal medicine. McGraw-Hill Medical. ISBN 0-07-146633-9.
^ Skott O., and Briggs J.P.: Direct demonstration of macula densa-mediated renin secretion. Science 1987; 237: pp. 1618-1620
^ Kirchner K.A., Kotchen T.A., Galla J.H., and Luke R.G.: Importance of chloride for acute inhibition of renin by sodium chloride. Am J Physiol 1978; 235: pp. F444-450
^ Kim S.M., Mizel D., Huang Y.G., Briggs J.P., and Schnermann J.: Adenosine as a mediator of macula densa-dependent inhibition of renin secretion. Am J Physiol Renal Physiol 2006; 290: pp. F1016-1023
^ "Function of the Juxtaglomerular Apparatus: Control of Glomerular Hemodynamics and Renin Secretion" Jürgen B. Schnermann and Hayo Castrop, in Seldin and Giebisch's The Kidney, Chapter 23, 757-801
^ Le, Tao (2012). First Aid for the Basic Sciences. Organ Systems. McGraw-Hill. p. 625.
^ Yvan-Charvet L, Quignard-Boulangé A (Jan 2011). "Role of adipose tissue renin-angiotensin system in metabolic and inflammatory diseases associated with obesity". Kidney International. 79 (2): 162–8. doi:10.1038/ki.2010.391. PMID 20944545.
^ Kanaide, Hideo; Ichiki, Toshihiro; Nishimura, Junji; Hirano, Katsuya (2003-11-28). "Cellular Mechanism of Vasoconstriction Induced by Angiotensin II It Remains To Be Determined". Circulation Research. 93 (11): 1015–1017. doi:10.1161/01.RES.0000105920.33926.60. ISSN 0009-7330. PMID 14645130.
^ Skurk T, Lee YM, Hauner H (May 2001). "Angiotensin II and its metabolites stimulate PAI-1 protein release from human adipocytes in primary culture". Hypertension. 37 (5): 1336–40. doi:10.1161/01.HYP.37.5.1336. PMID 11358950.
^ Gesualdo L, Ranieri E, Monno R, Rossiello MR, Colucci M, Semeraro N, Grandaliano G, Schena FP, Ursi M, Cerullo G (Aug 1999). "Angiotensin IV stimulates plasminogen activator inhibitor-1 expression in proximal tubular epithelial cells". Kidney International. 56 (2): 461–70. doi:10.1046/j.1523-1755.1999.00578.x. PMID 10432384.
^ Boulpaep EL, Boron WF (2005). Medical Physiology: a Cellular and Molecular Approach. St. Louis, Mo: Elsevier Saunders. p. 771. ISBN 1-4160-2328-3.

External links

The MEROPS online database for peptidases and their inhibitors: I04.953
Angiotensins at the US National Library of Medicine Medical Subject Headings (MeSH)
Human AGT genome location and AGT gene details page in the UCSC Genome Browser.

UpToDate Contents

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1. Chapter 2B：レニン－アンギオテンシン系 chapter 2b renin angiotensin system
2. 高血圧治療におけるレニン・アンギオテンシン系阻害 renin angiotensin system inhibition in the treatment of hypertension
3. 心不全におけるアンギオテンシン変換酵素阻害剤およびアンギオテンシン受容体拮抗剤：
作用機序 angiotensin converting enzyme inhibitors and receptor blockers in heart failure mechanisms of action
4. 心臓におけるアンギオテンシンⅡの作用 actions of angiotensin ii on the heart
5. ACE 阻害薬誘発性血管浮腫 ace inhibitor induced angioedema

English Journal

Bioavailability of angiotensin I-converting enzyme (ACE) inhibitory peptides derived from Virgibacillus halodenitrificans SK1-3-7 proteinases hydrolyzed tilapia muscle proteins.

Toopcham T1, Mes JJ2, Wichers HJ2, Roytrakul S3, Yongsawatdigul J4.
Food chemistry.Food Chem.2017 Apr 1;220:190-197. doi: 10.1016/j.foodchem.2016.09.183. Epub 2016 Sep 29.
The angiotensin I-converting enzyme (ACE) inhibitory activity of protein hydrolysates from tilapia muscle fractions, namely mince (M), washed mince (WM), and sarcoplasmic protein (SP), were investigated. Each fraction was hydrolyzed by Virgibacillus halodenitrificans SK1-3-7 proteinases for up to 24
PMID 27855889

Fish skin gelatin hydrolysates produced by visceral peptidase and bovine trypsin: Bioactivity and stability.

Ketnawa S1, Benjakul S2, Martínez-Alvarez O3, Rawdkuen S4.
Food chemistry.Food Chem.2017 Jan 15;215:383-90. doi: 10.1016/j.foodchem.2016.07.145. Epub 2016 Jul 28.
The peptidase from the viscera of farmed giant catfish was used for producing gelatin hydrolysates (HG) and compared with those produced from commercial bovine trypsin (HB). The degree of hydrolysis (DH) observed suggests that proteolytic cleavage rapidly occurred within the first 120min of incubati
PMID 27542490

Japanese Journal

Suppressive Effects of Glucose-Dependent Insulinotropic Polypeptide on Cardiac Hypertrophy and Fibrosis in Angiotensin Ⅱ-Infused Mouse Models

Circulation journal : official journal of the Japanese Circulation Society 80(9), 1988-1997, 2016-09
NAID 40020916012

Transtubular Potassium Concentration Gradient as a Surrogate Measure of Arterial Underfilling in Acute Decompensated Heart Failure

Circulation journal : official journal of the Japanese Circulation Society 80(9), 1965-1970, 2016-09
NAID 40020916002

Related Pictures

★リンクテーブル★

リンク元	「アンギオテンシン1」「アンギオテンシンI」
拡張検索	「angiotensin II receptor blocker」「angiotensin II type 1 receptor」「angiotensin II type 2 receptor」「angiotensin I-converting enzyme」「1-sarcosine-8-isoleucine angiotensin II」
関連記事	「I」「Id」「angiotensin」

「アンギオテンシン1」

AGT
Available structures
PDB	Ortholog search: PDBe RCSB
List of PDB id codes
	4FYS, 1N9U, 1N9V, 2JP8, 2WXW, 2X0B, 3CK0, 3WOO, 3WOR, 4AA1, 4APH, 5E2Q
Identifiers
Aliases	AGT, ANHU, SERPINA8, angiotensinogen
External IDs	MGI: 87963 HomoloGene: 14 GeneCards: AGT
Gene ontology
Molecular function	• type 1 angiotensin receptor binding; • hormone activity; • superoxide-generating NADPH oxidase activator activity; • growth factor activity; • type 2 angiotensin receptor binding; • protein binding; • sodium channel regulator activity; • serine-type endopeptidase inhibitor activity; • angiotensin receptor binding; • receptor agonist activity;
Cellular component	• cytoplasm; • extracellular region; • extracellular exosome; • blood microparticle; • extracellular space; • cytosol;
Biological process	• uterine smooth muscle contraction; • renal system process; • regulation of extracellular matrix assembly; • vasoconstriction; • positive regulation of cholesterol esterification; • positive regulation of catalytic activity; • positive regulation of cardiac muscle hypertrophy; • phospholipase C-activating G-protein coupled receptor signaling pathway; • cell surface receptor signaling pathway; • cellular response to mechanical stimulus; • blood vessel remodeling; • positive regulation of reactive oxygen species metabolic process; • stress-activated MAPK cascade; • artery smooth muscle contraction; • positive regulation of extrinsic apoptotic signaling pathway; • regulation of systemic arterial blood pressure by renin-angiotensin; • positive regulation of activation of JAK2 kinase activity; • regulation of apoptotic process; • positive regulation of cellular protein metabolic process; • regulation of blood vessel size; • negative regulation of neurotrophin TRK receptor signaling pathway; • positive regulation of branching involved in ureteric bud morphogenesis; • regulation of long-term neuronal synaptic plasticity; • positive regulation of renal sodium excretion; • kidney development; • positive regulation of fibroblast proliferation; • cellular sodium ion homeostasis; • ERK1 and ERK2 cascade; • activation of phospholipase C activity; • angiotensin maturation; • positive regulation of extracellular matrix constituent secretion; • positive regulation of transcription, DNA-templated; • positive regulation of blood pressure; • negative regulation of cell growth; • positive regulation of peptidyl-tyrosine phosphorylation; • G-protein coupled receptor signaling pathway; • regulation of norepinephrine secretion; • positive regulation of inflammatory response; • catenin import into nucleus; • female pregnancy; • positive regulation of protein tyrosine kinase activity; • negative regulation of tissue remodeling; • regulation of heart rate; • regulation of blood pressure; • positive regulation of macrophage derived foam cell differentiation; • regulation of vasoconstriction; • positive regulation of NF-kappaB transcription factor activity; • positive regulation of NAD(P)H oxidase activity; • nitric oxide mediated signal transduction; • G-protein coupled receptor signaling pathway coupled to cGMP nucleotide second messenger; • smooth muscle cell proliferation; • positive regulation of epidermal growth factor receptor signaling pathway; • regulation of blood volume by renin-angiotensin; • regulation of cardiac conduction; • regulation of calcium ion transport; • regulation of transmission of nerve impulse; • regulation of blood vessel diameter by renin-angiotensin; • cell growth involved in cardiac muscle cell development; • regulation of renal sodium excretion; • positive regulation of cytokine production; • positive regulation of membrane hyperpolarization; • response to muscle activity involved in regulation of muscle adaptation; • negative regulation of sodium ion transmembrane transporter activity; • positive regulation of nitric oxide biosynthetic process; • cytokine secretion; • angiotensin-mediated drinking behavior; • cell-cell signaling; • renin-angiotensin regulation of aldosterone production; • aging; • vasodilation; • positive regulation of endothelial cell migration; • low-density lipoprotein particle remodeling; • regulation of cell proliferation; • regulation of cell growth; • positive regulation of cell proliferation; • fibroblast proliferation; • negative regulation of angiogenesis; • positive regulation of gap junction assembly; • positive regulation of phosphatidylinositol 3-kinase signaling; • positive regulation of superoxide anion generation; • positive regulation of L-arginine import into cell; • positive regulation of L-lysine import into cell; • positive regulation of glucose import in response to insulin stimulus; • positive regulation of cardiac muscle cell apoptotic process; • angiotensin-activated signaling pathway; • positive regulation of vascular smooth muscle cell proliferation; • positive regulation of cytosolic calcium ion concentration; • negative regulation of gene expression; • regulation of renal output by angiotensin; • negative regulation of endopeptidase activity; • positive regulation of vascular associated smooth muscle cell migration; • regulation of molecular function;
	Sources:Amigo / QuickGO
RNA expression pattern
	More reference expression data
Orthologs
	183
	11606
	ENSG00000135744
	ENSMUSG00000031980
	P01019
	P11859
	NM_000029
	NM_007428
	NP_000020
	n/a
	Wikidata
View/Edit Human	View/Edit Mouse

　　[★]

英: angiotensin I
関: アンジオテンシンI、アンギオテンシンI、アンジオテンシン1

「アンギオテンシンI」

　　[★]

英: angiotensin I
同: アンジオテンシン
関: [[]]

「angiotensin II receptor blocker」

　　[★]

アンジオテンシンII受容体遮断薬、アンジオテンシンII受容体拮抗薬、アンギオテンシンII受容体遮断薬、アンギオテンシンII受容体拮抗薬

「angiotensin II type 1 receptor」

　　[★]

1型アンジオテンシンII受容体、1型アンギオテンシンII受容体

関: angiotensin type 1 receptor、AT1 receptor、type 1 angiotensin receptor

「angiotensin II type 2 receptor」

　　[★]

2型アンジオテンシンII受容体、2型アンギオテンシンII受容体

関: angiotensin type 2 receptor、AT2 receptor、type 2 angiotensin receptor

「angiotensin I-converting enzyme」

　　[★]

アンジオテンシンI変換酵素、アンギオテンシンI変換酵素

関: angiotensin-converting enzyme、peptidyl-dipeptidase A

「1-sarcosine-8-isoleucine angiotensin II」

　　[★]

1-サルコシン-8-イソロイシンアンジオテンシンII

「I」

　　[★]

「Id」

　　[★]

イディオタイプ idiotype idiotypic
inhibitor of DNA binding

「angiotensin」

　　[★] アンジオテンシン

[1] "Human PubMed Reference:".

[2] "Mouse PubMed Reference:".

[pmid11751697-3] Basso N, Terragno NA (Dec 2001). "History about the discovery of the renin-angiotensin system". Hypertension. 38 (6): 1246–9. doi:10.1161/hy1201.101214. PMID 11751697.

[4] "JAMA Article Jan 2012".

[isbn0-07-146633-9-5] Williams GH, Dluhy RG (2008). "Chapter 336: Disorders of the Adrenal Cortex". In Loscalzo J, Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL. Harrison's principles of internal medicine. McGraw-Hill Medical. ISBN 0-07-146633-9.

[6] Skott O., and Briggs J.P.: Direct demonstration of macula densa-mediated renin secretion. Science 1987; 237: pp. 1618-1620

[7] Kirchner K.A., Kotchen T.A., Galla J.H., and Luke R.G.: Importance of chloride for acute inhibition of renin by sodium chloride. Am J Physiol 1978; 235: pp. F444-450

[8] Kim S.M., Mizel D., Huang Y.G., Briggs J.P., and Schnermann J.: Adenosine as a mediator of macula densa-dependent inhibition of renin secretion. Am J Physiol Renal Physiol 2006; 290: pp. F1016-1023

[9] "Function of the Juxtaglomerular Apparatus: Control of Glomerular Hemodynamics and Renin Secretion" Jürgen B. Schnermann and Hayo Castrop, in Seldin and Giebisch's The Kidney, Chapter 23, 757-801

[10] Le, Tao (2012). First Aid for the Basic Sciences. Organ Systems. McGraw-Hill. p. 625.

[adipose_review-11] Yvan-Charvet L, Quignard-Boulangé A (Jan 2011). "Role of adipose tissue renin-angiotensin system in metabolic and inflammatory diseases associated with obesity". Kidney International. 79 (2): 162–8. doi:10.1038/ki.2010.391. PMID 20944545.

[12] Kanaide, Hideo; Ichiki, Toshihiro; Nishimura, Junji; Hirano, Katsuya (2003-11-28). "Cellular Mechanism of Vasoconstriction Induced by Angiotensin II It Remains To Be Determined". Circulation Research. 93 (11): 1015–1017. doi:10.1161/01.RES.0000105920.33926.60. ISSN 0009-7330. PMID 14645130.

[skurk-13] Skurk T, Lee YM, Hauner H (May 2001). "Angiotensin II and its metabolites stimulate PAI-1 protein release from human adipocytes in primary culture". Hypertension. 37 (5): 1336–40. doi:10.1161/01.HYP.37.5.1336. PMID 11358950.

[Gesualdo-14] Gesualdo L, Ranieri E, Monno R, Rossiello MR, Colucci M, Semeraro N, Grandaliano G, Schena FP, Ursi M, Cerullo G (Aug 1999). "Angiotensin IV stimulates plasminogen activator inhibitor-1 expression in proximal tubular epithelial cells". Kidney International. 56 (2): 461–70. doi:10.1046/j.1523-1755.1999.00578.x. PMID 10432384.

[isbn1-4160-2328-3-15] Boulpaep EL, Boron WF (2005). Medical Physiology: a Cellular and Molecular Approach. St. Louis, Mo: Elsevier Saunders. p. 771. ISBN 1-4160-2328-3.

v t e Autacoids

Kinins	Kininogen (HMWK, LMWK) Bradykinin Kallidin Tachykinins Urotensin-II

Others	Angiotensin Eicosanoid Histamine Platelet-activating factor Serotonin

匿名

検索

案内

angiotensin I