General Information:

Id: 1,989 (click here to show other Interactions for entry)
Diseases: Cardiovascular disease
Diabetes mellitus, type II - [OMIM]
Insulin resistance
Myocardial infarction - [OMIM]
Nephropathy, diabetic
Neuropathy, diabetic
Retinopathy, diabetic
Stroke, ischemic - [OMIM]
Mammalia
review
Reference: Lardizabal JA and Deedwania PC(2010) The role of renin-angiotensin agents in altering the natural history of type 2 diabetes mellitus Curr Cardiol Rep 12: 464-471 [PMID: 20809236]

Interaction Information:

Comment The glycometabolic effects of ACEIs are purported to be modulated by their actions on bradykinin, NO, and angiotensin II (AT II).
Formal Description
Interaction-ID: 15664

drug/chemical compound

ACE inhibitor

affects_activity of

gene/protein

Angiotensin II

Comment AT II, a powerful vasoconstrictor and growth factor, can interfere with the normal insulin signaling pathway through serine phosphorylation of specific insulin receptors in the muscle cell, contributing to the insulin resistance observed in essential hypertension.
Formal Description
Interaction-ID: 15670

gene/protein

Angiotensin II

decreases_activity of

process

insulin receptor signaling pathway

Comment AT II, a powerful vasoconstrictor and growth factor, can interfere with the normal insulin signaling pathway through serine phosphorylation of specific insulin receptors in the muscle cell, contributing to the insulin resistance observed in essential hypertension.
Formal Description
Interaction-ID: 15671

gene/protein

Angiotensin II

increases_activity of

disease

Insulin resistance

Comment AT II is a strong mediator of oxidative stress via the NADPH pathway.
Formal Description
Interaction-ID: 15672

gene/protein

Angiotensin II

increases_activity of

process

response to oxidative stress

Comment ACE catalyzes the conversion of angiotensin I to AT II, increasing the levels of circulating AT II. Being biochemically identical to the kininase II enzyme, ACE also promotes the degradation of bradykinin, leading to reductions in both bradykinin and NO levels. Treatment with ACEI agents, by blocking the actions of ACE, causes reduction in the levels of AT II, as well as increase in the levels of bradykinin and NO, which results not only in vasodilatation but also enhanced insulin insensitivity and improved cellular glucose uptake.
Formal Description
Interaction-ID: 15673

gene/protein

ACE

increases_quantity of

gene/protein

Angiotensin II

Drugbank entries Show/Hide entries for ACE
Comment ACE catalyzes the conversion of angiotensin I to AT II, increasing the levels of circulating AT II. Being biochemically identical to the kininase II enzyme, ACE also promotes the degradation of bradykinin, leading to reductions in both bradykinin and NO levels. Treatment with ACEI agents, by blocking the actions of ACE, causes reduction in the levels of AT II, as well as increase in the levels of bradykinin and NO, which results not only in vasodilatation but also enhanced insulin insensitivity and improved cellular glucose uptake.
Formal Description
Interaction-ID: 15677

drug/chemical compound

ACE inhibitor

decreases_quantity of

gene/protein

Angiotensin II

Comment ARBs, conversely, are able to attenuate the negative effects of AT II on cellular insulin signaling by specifically inhibiting the AT II type 1 receptors. The ARB-related improvement in insulin-stimulated glucose uptake has been documented not only in muscle and hepatic cells, but in adipose tissue as well.
Formal Description
Interaction-ID: 15680

drug/chemical compound

Angiotensin II type 1 receptor blocker

decreases_activity of

gene/protein

Angiotensin II