The intravenous injection of angiotensin II results in a sharp rise in systolic and diastolic pressures. The response is consistently reproducible when small doses of an-giotensin II are injected; however, larger amounts of the peptide produce tachyphylaxis (loss of response on repeated administration). The mechanism underlying tachy-phylaxis to angiotensin II is unknown, but it may involve receptor internalization and/or desensitization. Subcutaneous and intramuscular injections are much less potent and have a longer duration of action than do comparable doses given intravenously. Infusions that cause an immediate pressor response tend to result in tachyphylaxis over several hours. On a molar basis, angiotensin II is about 40 times as potent as norepinephrine. The pressor response to angiotensin II is caused by its direct receptor-mediated effect on vascular smooth muscle. The peptide stimulates the formation of the second messenger inositol 1,4,5-triphosphate, which results in a release of intracellular Ca++ and ultimately smooth muscle contraction.
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