Disease relevance of ANGIOTENSIN II

• Angiotensin II (AII) is a critical factor in cardiac remodeling which involves hypertrophy, fibroblast proliferation, and extracellular matrix production [1].
• A similar objection can be made to the application of the term to the relations between renin or angiotensin-II concentrations and blood-pressure in some forms of hypertension [2].
• The role of raised plasma renin and angiotensin-II concentrations in the development of acute renal failure in man was examined in patients in shock from various causes and in patients in whom hypotension was used to promote haemostasis [3].
• Although patients who were hypotensive for periods of 1 h 45 min to 4 h to promote haemostasis during surgery had similarly raised plasma-renin activity and angiotensin-II concentrations in peripheral venous blood, they did not have acute renal failure [3].
• Ten of the thirteen patients in shock had raised angiotensin-II concentrations in peripheral blood and acute renal failure manifested by oliguria, increasing serum-creatinine, a urine osmolality of less than 400 mos-mol/kg and a urine/plasma osmolality ratio of less than 1-5 [3].

Psychiatry related information on ANGIOTENSIN II

• It inhibited the drinking caused by water deprivation, the drinking response to intracerebroventricular application of angiotensin-II, as well as the drinking evoked by systemic administration of isoprenaline [4].
• The possible physiological significance of independent and parallel peripheral and cerebral renin-angiotensin systems for the control of drinking behavior mediated by angiotensin-II is discussed [5].
• The evolving role of angiotensin-II receptor blockers in cardiovascular risk reduction. Case study [6].
• However, so far no study has firmly established that such immunosuppressive therapy is indeed superior to aggressive supportive therapy as it is available nowadays, i.e. high dose ACE-inhibitors and/or angiotensin-II receptor blockers, smoking cessation etc [7].
• As insignificant increase of spontaneous locomotor activity in rats lesioned to CA did not interfere with the cognitive effect of AII and AII(3-7) [8].

High impact information on ANGIOTENSIN II

• BACKGROUND: It is unknown whether either the angiotensin-II-receptor blocker irbesartan or the calcium-channel blocker amlodipine slows the progression of nephropathy in patients with type 2 diabetes independently of its capacity to lower the systemic blood pressure [9].
• Whereas many different enzymes are able to cleave angiotensinogen (renin substrate) to release angiotensin I (AI) or angiotensin II (AII), angiotensinogen is the only known precursor of AI and AII [10].
• In fact, the distribution of ANP and AII and their receptors in the CNS overlaps considerably [11].
• Here we show that the AT1 receptor can be activated by mechanical stress through an angiotensin-II-independent mechanism [12].
• Taken together, these results provide the first evidence that osteopontin is a potentially important mediator of AII regulation of cardiac fibroblast behavior in the cardiac remodeling process [1].

Chemical compound and disease context of ANGIOTENSIN II

• Three models of experimental hypertension, each having a different circulating AII and AL profile, were examined and compared with their controls: renovascular hypertension, where both AII and AL are increased; infrarenal aorta banding, where AII and AL are normal; and a chronic infusion of AL, where AII is suppressed or normal and AL is increased [13].
• The hypertension was renin-dependent since plasma renin activity increased 6-fold and the angiotensin II (AII) antagonist, saralasin, significantly reduced MAP and regional resistances [14].
• Vasoconstriction to hypoxia, angiotensin II (AII), and prostaglandin F2 alpha (PGF2 alpha) was enhanced or unchanged in LPS-treated rats despite NOS induction [15].
• Losartan, an angiotensin-II receptor antagonist, reduces hematocrits in kidney transplant recipients with posttransplant erythrocytosis [16].
• These results show that in conscious sheep rapid and major increases in plasma AVP, ACTH, and AII follow acute moderate hemorrhage [17].

Biological context of ANGIOTENSIN II

• To investigate the gene expression of major angiotensin-II-forming enzymes in left ventricles of normal (n = 9) and failing human hearts (n = 20), we established a competitive RNA-polymerase chain reaction (PCR) for mRNA quantification of angiotensin-I converting enzyme (ACE) and human heart chymase [18].
• ANP (10(-7), 10(-6) M) also suppressed AII-induced RNA and protein syntheses (by 30-40%) with the concomitant reduction of the cell size [19].
• The renal vasculature was also relatively unresponsive to an intravenous infusion of AII (5 ng X kg-1 X min-1) during late gestation (day 19); in particular, the fall in ERPF in response to AII (16 +/- 3%) was markedly less than that observed in the prepregnant condition (34 +/- 3%; P less than 0.05) [20].
• Six weeks later, CBDL rats showed higher plasma angiotensin-II and endothelin-1 (P <.01), 56% reduction in peripheral resistance and 73% reduction in pulmonary resistance (P <.01), 87% increase in cardiac index and 30% increase in heart weight (P <.01), and increased myocardial nitric oxide (NO) synthesis [21].
• In severe cases of TTS, however, angiotensin-II-induced vasoconstriction acts as an additional deleterious factor by further reducing the renal blood flow in donors [22].

Anatomical context of ANGIOTENSIN II

• Recent evidence suggests that vasoconstrictive substances, such as angiotensin II (AII), may function as a vascular smooth muscle growth promoting substance [19].
• Direct determination of mesangial cell prostaglandin-E2 production showed that dopamine did not change either basal synthesis or angiotensin-II-stimulated synthesis of prostaglandin [23].
• We show that ANF transcription is activated directly by the AII type 1 receptor and precedes the development of myocyte hypertrophy [24].
• Effects of angiotensin-II and potassium on phospholipid metabolism in the adrenal zona glomerulosa [25].
• Formation of Peak A was blocked by inclusion of non-radiolabeled AII into the incubation mixture, and could be formed by repulsing fresh macrophages with isolated Peaks B and B1, and to only a minor extent with Peak C [26].

Associations of ANGIOTENSIN II with other chemical compounds

• Bicarbonate transport increased in animals on a high-sodium intake and following AII administration, and the latter was inhibited by the AII (AT1) receptor antagonist DuP 753; acute renal denervation lowered bicarbonate transport [27].
• The role of cyclic AMP in the stimulation of corticotropin (ACTH) release by corticotropin-releasing factor (CRF), angiotensin II (AII), vasopressin (VP), and norepinephrine (NE) was examined in cultured rat anterior pituitary cells [28].
• Inhibition of AR in VSMC also prevented the activation of NF-kappa B by basic fibroblast growth factor (bFGF), angiotensin-II (Ang-II), and platelet-derived growth factor (PDGF-AB) [29].
• The compound was found to selectively inhibit activation of the ERK pathway by AII, but not the stimulation of p70 S6 kinase, phospholipase C, or tyrosine phosphorylation [30].
• Macrophages were cultured with [125I]-AII or [3H]-AII for various times, and the AII products in the culture supernatant fluid and solubilized cell lysate (macrophage-associated AII) were analyzed by chromatography on Sephadex G-25 [26].

Gene context of ANGIOTENSIN II

• Endothelin-1 and angiotensin-II stimulate delayed mitogenesis in cultured rat aortic smooth muscle cells: evidence for common signaling mechanisms [31].
• CYP11B2 mRNA levels were increased in cultured zona glomerulosa cells by physiological levels of angiotensin-II [32].
• Roles of intracellular and extracellular calcium in the kinetic profile of adrenocorticotropin secretion by perifused rat anterior pituitary cells. II. Arginine vasopressin, oxytocin, and angiotensin-II stimulation [33].
• We previously reported that the rat posterior pituitary contains a potent PRL-releasing factor (PRF) which is distinct from oxytocin (OT), TRH, and angiotensin II (AII) [34].
• To elucidate the possible involvement of angiotensin II (AII) in the pathogenesis of microvascular changes in severe hypertension, we investigated the effects of angiotensin II type 1 (AT1) receptor antagonist and angiotensin-converting enzyme inhibitor (ACEI) on the expression of adhesion molecules of leukocytes and brain microvessels [35].

Analytical, diagnostic and therapeutic context of ANGIOTENSIN II

• In this same region the circular dichroism difference spectra of DEPC-modified N alpha-acetyl-L-histidine and DEPC-modified angiotensin-II had two much weaker bands (delta [theta]233 nm = +1000 degree.cm2.dmol-1 and delta[theta]252nm = -600 degree.cm2.dmol-1 for N alpha-acetyl-L-histidine) [36].
• There are no data reported from clinical trials about possible interactions between angiotensin-II receptor antagonists and aspirin [37].
• Administration of this AII antagonist to the normal rabbits prevented them from showing pressor hyperresponsiveness following the cross-circulation of blood [38].
• RESEARCH DESIGN AND METHODS: In a case-control study, the ACE insertion/deletion (I/D) gene, the angiotensinogen (AGT) gene (M235T), and the angiotensin II (AII) type 1 receptor gene (AT1 A1166C) were examined in 110 Chinese type 2 diabetic patients [39].
• The effects of angiotensin II (AII), epinephrine, and changes in perfusion pressure on glomerular capillary and afferent arteriolar pressures were assessed using the in vitro blood perfused juxtamedullary nephron (JMN) preparation [40].

References