Disease relevance of Angiotensin

• Angiotensin-converting enzyme 2 is the functional receptor for SARS-CoV; DC-SIGN and CD209L (L-SIGN) can enhance viral entry [1].
• Linkage of the angiotensin gene to essential hypertension [2].
• Treatment of chronic congestive heart failure with captopril, an oral inhibitor of angiotensin-converting enzyme [3].
• We investigated whether captopril, an angiotensin-converting-enzyme inhibitor, would reduce proteinuria in patients with advanced diabetic nephropathy [4].
• Association between a deletion polymorphism of the angiotensin-converting-enzyme gene and left ventricular hypertrophy [5].

Psychiatry related information on Angiotensin

• Lower rates were seen in the use of angiotensin-converting enzyme inhibitors at discharge (59.3% [49.2%-69.2%]); reperfusion, using thrombolytic therapy or coronary angioplasty (67.2% [59.8%-75.1%]); prescription of beta-blockers at discharge (49.5% [35.8%-61.5%]); and for smoking cessation advice (41.9% [32.8%-51.3%]) [6].
• The results suggest that Angiotensin II participates in the physiological control of the human esophageal motor activity [7].
• We have previously shown that atrial natriuretic polypeptide is present in the brain with the highest concentration in the hypothalamus and septum and that intracerebroventricular injection of atrial natriuretic polypeptide inhibits water drinking induced by centrally injected angiotensin II or 24-hour water deprivation in rats [8].
• These investigations indicate a pathway for thrombosis risk reduction via the plasma kallikrein/kinin and renin angiotensin systems [9].
• Alcohol consumption is controlled by angiotensin II [10].

High impact information on Angiotensin

• Aldosterone secretion by glomerulosa cells is stimulated by angiotensin II (ANG II), extracellular K(+), corticotrophin, and several paracrine factors [11].
• Angiotensin II also plays an important role in the regulation of body fluids, being a potent inducer of thirst and, in general, antagonizes the actions of ANP [12].
• The AV3V region is well provided with angiotensinergic nerve endings and angiotensin AT1 receptors, the receptor type responsible for acute responses to ANG II, and it responds vigorously to the dipsogenic action of ANG II [13].
• Angiotensin peptides generated from brain precursors may also be involved in functions that have little immediate effect on body fluid homeostasis and blood pressure control, such as cell differentiation, regeneration and remodeling, or learning and memory [13].
• Agonists, such as angiotensin II, contract mesangial cells through a signal transduction pathway that releases intracellular stores of Ca2+, which subsequently activate nonselective cation channels and Cl- channels to depolarize the plasma membrane [14].

Chemical compound and disease context of Angiotensin

• METHODS: We compared the hemodynamic, renal, and endocrine effects of captopril alone (25 mg), captopril plus icatibant (100 microg per kilogram of body weight), the angiotensin II subtype 1-receptor antagonist losartan (75 mg), and placebo in 20 subjects with normal blood pressure and 7 subjects with hypertension [15].
• Bradykinin and inhibition of angiotensin-converting enzyme in hypertension [16].
• Pheochromocytoma crisis induced by saralasin. Relation of angiotensin analogue to catecholamine release [17].
• However, there is evidence that the initial phase in the development of myocardial hypertrophy involves the formation of cardiac para- and/or autocrine factors like endothelin-1, norepinephrine or angiotensin II (refs. 7,8), the receptors of which are coupled to G-proteins of the Gq/11-, G12/13- and Gi/o-families [18].
• A patient with hypokalemic alkalosis, normotensive hyperreninism, hyperaldosteronism, increased levels of urinary and plasma prostaglandin E, and vascular hyporesponsivity to angiotensin II was thought to have Bartter's syndrome [19].

Biological context of Angiotensin

• These observations suggest that a functional element, perhaps involving angiotensin-mediated renal vasoconstriction, frequently has a role in the reduction in glomerular filtration rate that occurs in essential hypertension [20].
• In six patients with essential hypertension the threshold inhibitor dose was reduced to 10 microgram per kilogram; 30 kilogram per kilogram had an enhanced (P less than 0.01) effect on mean blood pressure (-11 +/- 2 mm Hg), renal blood flow (137 +/- 20 ml per 100 g per minute), and angiotensin II concentration (-29 +/- 12 pg per milliliter) [21].
• Saralasin, an angiotensin antagonist, was used to study the role of renin-angiotensin in the vasodilator-beta-blocker drug interaction in hypertensive subjects [22].
• COS-7 cells transfected with the cDNA expressed specific and high-affinity binding sites for angiotensin II, angiotensin II antagonist and a non-peptide specific antagonist for type-1 receptor [23].
• Atrial natriuretic peptides, produced in the mammalian cardiac atrium, are released into the general circulation and may be actively involved in the control of blood pressure and in fluid homeostasis as antagonists of the peripheral angiotensin system [24].

Anatomical context of Angiotensin

• Angiotensin peptides generated inside the blood-brain barrier may act as conventional neurotransmitters or, in view of the many instances of anatomic separation between sites of production and receptors, they may act as paracrine agents at a distance from their point of release [13].
• Inhibition of angiotensin-converting enzyme for diagnosis of renal-artery stenosis [25].
• To determine its utility as an aid in diagnosis of renovascular hypertension, we administered nonapeptide converting-enzyme inhibitor (CEI) (which inhibits conversion of angiotensin I to angiotensin II) (0.25 mg per kilogram) to 14 unselected hypertensive patients undergoing bilateral renal-vein catheterization [25].
• Angiotensin-converting enzyme in substantia nigra of schizophrenics [26].
• Prolonged subcultivation was accompanied by chromosomal abnormalities and eventual "crisis". Transformed cells did not exhibit endothelial-specific organelles (Weibel-Palade bodies) or factor VIII antigen, but angiotensin-converting enzyme occasionally was detectable in SVHEC cultures [27].

Associations of Angiotensin with other chemical compounds

• Two angiotensin-converting-enzyme inhibitors, captopril and enalapril, indistinguishable according to clinical assessments of efficacy and safety, had different effects on quality of life [28].
• We assessed vascular and hormonal responses to inhibition of peptidyldipeptide hydrolase, which converts angiotensin I to angiotensin II (converting enzyme) and degrades bradykinin (kininase II), in subjects given 10 meq of sodium to activate both systems [21].
• We therefore evaluated the long-term effects of the addition of the angiotensin-receptor blocker valsartan to standard therapy for heart failure [29].
• The sensitivity of blood vessels to the vasoconstrictor effects of the hormone angiotensin II appears to be modulated by the activity of the renin-angiotensin system [30].
• In contrast, the hypertrophic response was identical in wild-type and melusin-null mice after chronic administration of angiotensin II or phenylephrine at doses that do not increase blood pressure--that is, in the absence of cardiac biomechanical stress [31].

Gene context of Angiotensin

• AT1 receptors seem to mediate the major cardiovascular effects of angiotensin II [32].
• Also, angiotensin II induced expression of KLF5, which in turn activated platelet-derived growth factor-A (PDGF-A) and transforming growth factor-beta (TGF-beta) expression [33].
• Krüppel-like zinc-finger transcription factor KLF5/BTEB2 is a target for angiotensin II signaling and an essential regulator of cardiovascular remodeling [33].
• Moreover, stimulation of the angiotensin II type 1A receptor activated JNK3 and triggered the colocalization of beta-arrestin 2 and active JNK3 to intracellular vesicles [34].
• Using Agtr1a(-/-) mice, which lack AT(1A) receptors for angiotensin II, we have identified a novel function of the RAS to modulate the immune system [35].

Analytical, diagnostic and therapeutic context of Angiotensin

• Using shrinking split-drop micropuncture combined with simultaneous capillary perfusion in anaesthetized rats we report that 20 nanomolar alpha-rANP (the main component of ANP in rat plasma) added to the peritubular fluid had no direct effect on proximal fluid uptake whereas picomolar angiotensin II had a marked stimulatory action as reported [36].
• Circulating angiotensin II and adrenal receptors after nephrectomy [37].
• Immunocytochemical tests show that they contain both immunoreactive renin and angiotensin; direct radioimmunoassays show that they are positive for renin, angiotensin I, and angiotensin II; enzymatic assays show that they contain angiotensinogen and converting enzyme as well [38].
• Dose-related reductions in blood pressure, plasma renin activity, and plasma angiotensin II in parallel with increased plasma drug concentrations were observed after oral administration of A-72517 to conscious, salt-depleted dogs [39].
• Thus, the angiotensin-converting enzyme may participate in modulating the proliferative response of the vascular wall after arterial injury, and inhibition of this enzyme may have therapeutic applications to prevent the proliferative lesions that occur after coronary angioplasty and vascular surgery [40].

References