ANGIOTENSINII,HUMAN

1046.18

1045.534546

2017-001-1

M089EFU921

DTXSID4036778|DTXSID30196288

C173802

C09|C - Cardiovascular system

406.34000

2.34

orange Powder

1.4±0.1 g/cm3

809.08°C (rough estimate)

1.664

soluble in water (25 mg/ml), and 5% Acetic Acid (1 mg/ml).

−20°C

353.79 Ų [M+2H]2+ [CCS Type: DT, Method: stepped-field]|436.24 Ų [M+3H]3+ [CCS Type: DT, Method: stepped-field]|314.38 Ų [M+H]+ [CCS Type: DT, Method: stepped-field]

NONH for all modes of transport

3

BW2165000

Overdose with angiotensin II would be expected to result in hypertension, necessitating close monitoring and supportive care. Effects are also expected to be brief as the half-life of angiotensin II is less than one minute. In the ATHOS-3 clinical study there was a higher incidence of arterial and venous thrombotic and thromboembolic events in patients who received angiotensin II compared to placebo treated patients. The major imbalance was in deep venous thromboses - which prompts the potential need to use concurrent venous thromboembolism (VTE) prohphylaxis. Adverse effects of noticeable potential (>= 10%) include thromboembolic events (ie. like deep vein thrombosis) including arterial and venous thrombotic events, thrombocytopenia, tachycardia, and fungal infection. Effects whose potential are < 10% include delirium, acidosis, hyperglycemia, peripheral ischemia. Concomitant use of angiotensin converting enzymes (ACE) inhibitors may increase the response of angiotensin II. Concomitant use of angiotensin II blockers (ARBs) may decrease the response to angiotensin II. There are no formal data regarding the safe use of angiotensin II in pregnant women. However, septic or other distributive shock is a medical emergency that can be fatal if left untreated. Delaying treatment in pregnant women with hypotension associated with septic or otherdistributive shock is likely to increase the risk of maternal and fetal morbidity and mortality. There is no formal data regarding whether or not angiotensin II may become present in human milk and there is no data available on the effects of angiotensin II on the breastfed child or the effects on milk production. The safety and efficacy of angiotensin II in pediatric patients has not yet been established. There is no difference in the safety or efficacy between patients less than 65 years old and those 65 years or older when treated with angiotensin II. There is no difference in pharmacokinetics between male and female patients. The pharmacokinetics of angiotensin II are not expected to be influenced by renal impairment or hepatic impairment.

Angiotensin II is a vasoconstrictor indicated for increasing blood pressure in adults with septic or other distributive shock.|FDA Label|Giapreza is indicated for the treatment of refractory hypotension in adults with septic or other distributive shock who remain hypotensive despite adequate volume restitution and application of catecholamines and other available vasopressor therapies.

Angiotensin II is a naturally occurring peptide hormone of the renin-angiotensin-aldosterone-system (RAAS) that has the capacity to cause vasoconstriction and an increase in blood pressure in the human body. In the RAAS, juxtaglomerular cells of the renal afferent arteriole synthesize the proteolytic enzyme renin. Although stored in an inactive form called pro-renin, decreases in arterial blood pressure or extracellular fluid volume depletion can cause various enzymatic reactions to release active renin into the systemic circulation and surrounding tissues. Such renin release allows for the production of the alpha-2-globulin angiotensinogen predominantly in the liver and to some extent, the kidneys and other organs. Angiotensin I, itself a decapeptide with weak biological activity, is produced from angiotensinogen and then quickly converted to angiotensin II by angiotensin converting enzymes (ACE). Consequently, angiotensin II demonstrates its strong vasopressor activity when it is rapidly degraded by aminopeptidases A and M into further entities like angiotensin III and angiotensin IV, respectively. Such species like angiotensin III can then bind and interact with specific G protein coupled receptors like angiotensin receptor 1, or AT-1 where strong vasoconstricson can occur. Furthermore, in the ATHOS-3 clinical trial, for the 114 (70%) patient subjects in the angiotensin II arm who reached the target mean arterial pressure (MAP) at Hour 3, the median time to reach the target MAP endpoint was approximately 5 minutes. The angiotensin II was titrated to effect for each individual patient..

Drugs used to cause constriction of the blood vessels. (See all compounds classified as Vasoconstrictor Agents.)

Following the intravenous infusion of angiotensin II in adult patients with septic or other distributive shock, the serum levels of angiotensin II observed were similar at baseline and hour 3 after the intravenous infusion. After 3 hours of treatment, the serum level of angiotensin I (the angiotensin II precursos peptide) is however, reduced by about 40%.|The official prescribing information notes that no specific studies have been conducted that examine the elimination of angiotensin II.|The official prescribing information for angiotensin II notes that no specific studies have yet been conducted that examine the distribution of angiotensin II.|The official prescribing information notes that the clearnace of angiotensin II is not dependent on hepatic function or renal function.

It is metabolized by aminopeptidase A and angiotensin converting enzyme 2 to angiotensin-(2-8) [angiotensin III] and angiotensin-(1-7), respectively in plasma, erythrocytes and many of the major organs (i.e. intestine, kidney, liver and lung). Angiotensin II type 1 receptor (AT1) mediated activity of angiotensin III is approximately 40% of angiotensin II; however, aldosterone synthesis activity is similar to angiotensin II. Angiotensin-(1-7) exerts the opposite effects of angiotensin II on AT1 receptors and causes vasodilation. Nevertheless, the official prescribing information also notes that no formal studies have been conducted that examine the metabolism of angiotensin II.

The plasma half-life of intravenously administered angiotensin II is less than one minute.

As part of the renin-angiotensin-aldosterone-system (RAAS), angiotensin II raises blood pressure by vasoconstriction, increased aldosterone release by the adrenal zona glomerulosa, sodium and water reabsorption in the proximal tubular cells, and vasopressin secretion The direct action of angiotensin II on surrounding vessel walls is facilitated by binding to the G-protein-coupled angiotensin II receptor type 1 (AT-1) on vascular smooth muscle cells, which stimulates Ca2+/calmodulin-dependent phosphorylation of myosin and causes smooth muscle contraction that results in vasoconstriction. The RAAS is ultimately regulated by a negative feedback effect of angiotensin II on renin production by the juxtaglomerular cells of the renal afferent arteriole. Unresuscitated septic shock associated with marked hypovolemia, extracellular fluid volume depletion, decreased cardiac output, low arterial blood pressure and decreased systemic vascular resistance causes an increase in renin secretion by the juxtaglomerular cells, resulting in elevated angiotensin II plasma levels and an increased secretion of aldosterone from the adrenal cortex. Angiotensin II binding to AT-1 receptors causes dose-dependent vasoconstriction of both afferent and efferent glomerular arterioles. The most pronounced effect of angiotensin II results on efferent arterioles, resulting in reduced renal blood flow and increased glomerular filtration pressure.

5 L Isoleucine Angiotensin II

Human drugs -> Giapreza -> EMA Drug Category|Agents acting on the renin-angiotensin system -> Human pharmacotherapeutic group|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients