Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q9UID3 (FFR)
 233 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin resistance and impairment of the renal depressor system have been thought to be involved in the development of essential hypertension. However, the relationship between insulin resistance and this system is still unclear. To clarify this relationship, we investigated the role of the renal depressor system in a rat model of insulin-resistant hypertension. Sprague-Dawley rats were fed a standard diet (control) or a fructose-rich diet (FFR), and their blood pressures were measured every week. Urinary dopamine (uDA), urinary kallikrein (uKAL) activity and urinary nitric oxide (uNOx) levels were also measured each week, and the renal mRNA expression levels of endothelial nitric oxide synthase (eNOS), aromatic-L-amino-acid decarboxylase (AADC), and kallikrein (KAL) activity were compared at the end of the study. The blood pressure of FFR was elevated significantly from 2 weeks after the start of fructose loading. The uDA level was lower in FFR than in control rats throughout the study period (p<0.01), and the expression level of AADC mRNA was enhanced in FFR (p<0.05). There was a tendency of negative correlation between uDA level and systolic blood pressure (SBP) (r=-0.49, p=0.056). uNOx level was lower in FFR throughout the study period (p<0.05), and the eNOS mRNA expression level in the kidney was lower in FFR than in control rats (p<0.05). There was a negative correlation between uNOx level and SBP (r=-0.68, p <0.01). On the other hand, there was no significant difference in the kallikrein-kinin system between FFR and control rats. In conclusion, impairment in functions of the renal dopamine and NO systems occur in FFR, and this impairment may be caused by insulin resistance and may contribute to the development of hypertension.
 ...
PMID:The role of renal natriuretic and depressor systems in insulin-resistant hypertensive rats. 1530 87

The present study examines the effect of chronic administration of dealcoholized red wine Malbec (DRW) on vascular remodeling and NAD(P)H oxidase and endothelial nitric oxide synthase activity (eNOS) in an experimental model of metabolic syndrome induced by fructose administration. Thirty-day old male Wistar rats were fed a normal rat diet (control) or the same diet plus 10% fructose in drinking water (FFR). During the last 4 weeks of a 10-week period of the corresponding diet, a subgroup of control and FFR (n=8 each) received DRW in their drinking water. Systolic blood pressure (SBP), a homeostasis model assessment of insulin resistance (HOMA-IR), aortic NAD(P)H oxidase and eNOS activity in the heart and vascular tissue were evaluated. Vascular remodeling was evaluated in the left carotid artery (CA) and interlobar, arcuate and interlobular renal arteries (RA) through lumen to media (L/M) ratio determination. At the end of the study FFR increased the SBP (p < 0.001), HOMA-IR (p < 0.001), and aortic NAD(P)H oxidase activity (p < 0,05) but reduced cardiac and vascular eNOS activity (p < 0.01), L/M ratio in CA (p < 0.001) and RA (p < 0.01) compared with the C group. DRW reduced SBP (p < 0.05), aortic NAD(P)H oxidase (p < 0.05), and recovered eNOS activity (p < 0.001) and L/M in CA (p < 0.001) and RA (p < 0.001) compared with FFR. This study provides new data about the beneficial effect of DRW on oxidative stress and vascular remodeling in the experimental model of metabolic syndrome. Data suggest the participation of mechanisms involving oxidative stress in FFR alterations and the usefulness of natural antioxidant substances present in red wine in the reversion of these changes.
 ...
PMID:Dealcoholized red wine reverse vascular remodeling in an experimental model of metabolic syndrome: role of NAD(P)H oxidase and eNOS activity. 2177 63