What is the difference between angiotensin 1 and angiotensin 2

Both Ang II receptors are involved in hypoxia-induced neovascularization. A large set of experimental evidence suggests that activation of the AT 1 receptor results in proangiogenic effects, whereas AT 2 receptors mediate apoptosis and thus antiangiogenic effects. Furthermore, bradykinin through its B 1 or B 2 receptors is a potent activator of experimental hypoxia-induced neovascularization.

Thus, pharmacologic blockade of the AT 1 receptor and resulting overactivation of AT 2 receptors could impair or delay neovascularization in ischemic tissues in patients receiving chronic treatment with angiotensin receptor blockers.

In contrast, increased tissue bradykinin resulting from inhibition of converting enzyme could help to restore functional vascularization in ischemic tissues. These basic concepts deserve a second reading and reevaluation to discuss differences in vascular protection in large clinical trials with different classes of drugs acting on the renin-angiotensin system. Control of plasma sodium and potassium concentrations, and the regulation of blood volume and pressure, are all hormonal mechanisms that are impaired by low angiotensin levels.

Absence of angiotensin can be associated with retention of potassium, loss of sodium, decreased fluid retention increased urine output and low blood pressure. About Contact Events News. Search Search. You and Your Hormones. Students Teachers Patients Browse. Human body. Home Hormones Angiotensin. Angiotensin Angiotensin is a protein hormone that causes blood vessels to become narrower.

It helps to maintain blood pressure and fluid balance in the body. Alternative names for angiotensin The different forms of angiotensin are denoted by Roman numerals, angiotensin I—IV. The clinical relevance of these differing pharmacologic properties of ACE inhibitors and AT1 blockers have not yet been established. However, in patients with essential hypertension compared with normal volunteers, the M value, a measure of glucose clearance and insulin sensitivity, is reduced. Both the ACE inhibitor delapril and the AT1 blocker candesartan have shown a beneficial effect on insulin sensitivity, and candesartan appears to restore the M value to normal.

While ACE inhibitors have been shown to have strongly beneficial actions in the kidneys, comparable data are not yet available for AT1 blockers.