General Information:

Id: 2,183
Diseases: Diabetes mellitus, type II - [OMIM]
Insulin resistance
Rattus norvegicus
male
12-wk-old spontaneously hypertensive rats (SHR/NHsd, haplotype RT1k)
article
Reference: Potenza MA et al.(2005) Insulin resistance in spontaneously hypertensive rats is associated with endothelial dysfunction characterized by imbalance between NO and ET-1 production Am. J. Physiol. Heart Circ. Physiol. 289: H813-H822 [PMID: 15792994]

Interaction Information:

Comment Twelve-week-old male spontaneously hypertensive rats (SHR) were hypertensive and insulin resistant compared with control Wistar-Kyoto (WKY) rats.
Formal Description
Interaction-ID: 18280

phenotype

hypertension

cooccurs with

disease

Insulin resistance

in SHR rats
Comment In WKY rats, insulin stimulated dose-dependent relaxation of mesenteric arteries precontracted with norepinephrine (NE) ex vivo. This depended on intact endothelium and was blocked by genistein, wortmannin, or N(omega)-nitro-l-arginine methyl ester (inhibitors of tyrosine kinase, PI3-kinase, and NO synthases, respectively).
Formal Description
Interaction-ID: 18281

complex/PPI

Insulin

increases_activity of

via tyrosine kinase, PI3-kinase, and NO synthases
Comment In WKY rats, insulin stimulated dose-dependent relaxation of mesenteric arteries precontracted with norepinephrine (NE) ex vivo. This depended on intact endothelium and was blocked by genistein, wortmannin, or N(omega)-nitro-l-arginine methyl ester (inhibitors of insulin receptor tyrosine kinase, PI3-kinase, and NO synthases, respectively).
Formal Description
Interaction-ID: 18282

complex/PPI

Insulin receptor

affects_activity of

if induced by insulin
Comment In WKY rats, insulin stimulated dose-dependent relaxation of mesenteric arteries precontracted with norepinephrine (NE) ex vivo. This depended on intact endothelium and was blocked by genistein, wortmannin, or N(omega)-nitro-l-arginine methyl ester (inhibitors of insulin receptor tyrosine kinase, PI3-kinase, and NO synthases, respectively).
Formal Description
Interaction-ID: 18283

complex/PPI

Phosphatidylinositol 3-kinase

affects_activity of

if induced by insulin
Comment In WKY rats, insulin stimulated dose-dependent relaxation of mesenteric arteries precontracted with norepinephrine (NE) ex vivo. This depended on intact endothelium and was blocked by genistein, wortmannin, or N(omega)-nitro-l-arginine methyl ester (inhibitors of insulin receptor tyrosine kinase, PI3-kinase, and NO synthases, respectively).
Formal Description
Interaction-ID: 18284

gene/protein

NOS

affects_activity of

if induced by insulin
Drugbank entries Show/Hide entries for NOS
Comment Vasodilation in response to insulin (but not ACh) was impaired by 20% in SHR.
Formal Description
Interaction-ID: 18285

phenotype

hypertension

decreases_activity of

if induced by insulin
Comment Vasodilation in response to insulin (but not ACh) was impaired by 20% in SHR.
Formal Description
Interaction-ID: 18286

phenotype

hypertension

NOT decreases_activity of

if induced by acetylcholine
Comment Preincubation of arteries with insulin significantly reduced the contractile effect of norepinephrine (NE) by 20% in WKY but not SHR rats.
Formal Description
Interaction-ID: 18287

drug/chemical compound

Noradrenaline

increases_activity of

Comment Preincubation of arteries with insulin significantly reduced the contractile effect of norepinephrine (NE) by 20% in WKY but not SHR rats.
Formal Description
Interaction-ID: 18288

complex/PPI

Insulin

decreases_activity of

drug/chemical compound

Noradrenaline

Comment Preincubation of arteries with insulin significantly reduced the contractile effect of norepinephrine (NE) by 20% in WKY but not SHR rats.
Formal Description
Interaction-ID: 18289

complex/PPI

Insulin

NOT decreases_activity of

drug/chemical compound

Noradrenaline

in SHR rats
Comment Insulin-stimulated endothelin-1 (ET-1) secretion is mediated by MAPK signaling.
Formal Description
Interaction-ID: 18290

complex/PPI

Insulin

increases_quantity of

gene/protein

Endothelin-1

via MAPK signaling