Chemical formula: C₅₀H₇₁N₁₃O₁₂ Molecular mass: 1,046.179 g/mol PubChem compound: 172198
Angiotensin II raises blood pressure by vasoconstriction; increased aldosterone release via direct action of angiotensin II on the vessel wall is mediated by binding to the G-protein-coupled angiotensin II receptor type 1 on vascular smooth muscle cells which stimulates Ca2+/calmodulindependent phosphorylation of myosin and causes smooth muscle contraction.
Angiotensin II is titrated to effect for each individual patient. In the ATHOS-3 trial, the median time to increase blood pressure was approximately 5 minutes. The effect on blood pressure is sustained for at least the first three hours of continuous intravenous infusion. Due to the short half-life of angiotensin II (less than one minute), an abrupt withdrawal of angiotensin may lead to rebound hypotension. Therefore, once underlying shock is sufficiently improved, a slow down-titration is recommended by gradual decrements of up to 15 ng/kg per minute, as needed, based on blood pressure.
Angiotensin II is titrated to effect for each individual patient. Plasma levels of angiotensin II were evaluated at baseline and hour 3 of infusion in the phase 3 pivotal study.
No specific studies have been conducted to investigate the distribution of angiotensin II.
No specific studies have been conducted to investigate the metabolism and excretion of angiotensin II. The plasma half-life of angiotensin II administered intravenously is less than one minute. It is metabolised by end terminal cleavage (at both the amino and carboxy termini) in a variety of tissues including erythrocytes, plasma and many of the major organs (ie, intestine, kidney, liver and lung).
No trials have been conducted to investigate the pharmacokinetics of angiotensin II in renally impaired patients since the kidneys are not a major organ for angiotensin II metabolism or excretion.
No trials have been conducted to investigate the pharmacokinetics of angiotensin II in patients with hepatic impairment since the liver is not a major organ for angiotensin II metabolism or excretion.
In a cardiovascular safety pharmacology study in normotensive dogs, angiotensin II elicited increased heart rate, systemic vascular resistance, left ventricular systolic pressure and left ventricular diastolic pressure, and PR interval prolongation.
In a 48-hour continuous intravenous administration of angiotensin II in neonatal lambs, the nominal dose rates of 4, 12 and 40 ng/kg/min were well tolerated. No treatment related adverse effects were observed.
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