Rosiglitazone restores nitric oxide synthase‐dependent reactivity of cerebral arterioles in rats exposed to prenatal alcohol

2021 ◽  
Author(s):  
Partha S. Saha ◽  
Kirsten R. Kim Sawtelle ◽  
Brittany N. Bamberg ◽  
Denise M. Arrick ◽  
Michael J. Watt ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cerebral Arterioles ◽  
Prenatal Alcohol ◽  
Oxide Synthase

scholarly journals The Key Role of Caveolin-1 in Estrogen-Mediated Regulation of Endothelial Nitric Oxide Synthase Function in Cerebral Arterioles In vivo

2001 ◽  
Vol 21 (8) ◽  
pp. 907-913 ◽  
Author(s):  
Hao-Liang Xu ◽  
Elena Galea ◽  
Roberto A. Santizo ◽  
Verna L. Baughman ◽  
Dale A. Pelligrino
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Functional Activity ◽  
Endothelial Nitric Oxide Synthase ◽  
Down Regulation ◽  
Caveolin 1 ◽  
Cerebral Arterioles ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

The marked impairment in cerebrovascular endothelial nitric oxide synthase (eNOS) function that develops after ovariectomy may relate to the observation that the abundance of cerebral vascular eNOS and its endogenous inhibitor, caveolin-1, vary in opposite directions with chronic changes in estrogen status. The authors endeavored, therefore, to establish a link between these correlative findings by independently manipulating, in ovariectomized female rats, eNOS and caveolin-1 expression, while monitoring agonist (acetylcholine)-stimulated eNOS functional activity. In the current study, the authors showed that individually neither the up-regulation of eNOS (through simvastatin treatment), nor the down-regulation of caveolin-1 (through antisense oligonucleotide administration) is capable of restoring eNOS function in pial arterioles in vivo in these estrogen-depleted rats. Only when eNOS up-regulation and caveolin-1 down-regulation are combined is activity normalized. These results establish a mechanistic link between the estrogen-associated divergent changes in the abundance of caveolin-1 and eNOS protein and eNOS functional activity in cerebral arterioles.

Impaired nitric oxide synthase-dependent dilatation of cerebral arterioles in type II diabetic rats

Life Sciences ◽  
2003 ◽  
Vol 73 (26) ◽  
pp. 3415-3425 ◽  
Author(s):  
RoseAnn M Schwaninger ◽  
Hong Sun ◽  
William G Mayhan
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Diabetic Rats ◽  
Type Ii ◽  
Cerebral Arterioles ◽  
Oxide Synthase

scholarly journals Losartan improves impaired nitric oxide synthase-dependent dilatation of cerebral arterioles in type 1 diabetic rats

2008 ◽  
Vol 1209 ◽  
pp. 128-135 ◽  
Author(s):  
Denise M. Arrick ◽  
Glenda M. Sharpe ◽  
Hong Sun ◽  
William G. Mayhan
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Diabetic Rats ◽  
Cerebral Arterioles ◽  
Oxide Synthase

Impairment of nitric oxide synthase-dependent dilatation of cerebral arterioles during infusion of nicotine

2003 ◽  
Vol 284 (2) ◽  
pp. H528-H534 ◽  
Author(s):  
Qin Fang ◽  
Hong Sun ◽  
William G. Mayhan
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Nitric Oxide Synthase ◽  
Maintenance Dose ◽  
Oxygen Radicals ◽  
Cerebral Vessels ◽  
Before And After ◽  
Pial Arterioles ◽  
Cerebral Arterioles ◽  
Oxide Synthase

The effects of nicotine on nitric oxide synthase (NOS)-dependent reactivity of cerebral arterioles remain uncertain. Our first goal was to examine whether infusion of nicotine alters NOS-dependent reactivity of cerebral arterioles. Our second goal was to examine the mechanisms that may account for the effects of nicotine on cerebral arterioles. We measured the diameter of pial arterioles to NOS-dependent (ADP and acetylcholine) and NOS-independent (nitroglycerin) agonists before and after the infusion of nicotine (2 μg · kg−1· min−1iv for 30 min, followed by a maintenance dose of 0.35 μg · kg−1· min−1). ADP- and acetylcholine-induced vasodilatation was impaired after the infusion of nicotine. In contrast, nicotine did not alter vasodilatation to nitroglycerin. Next, we examined whether the impaired responses of pial arterioles during infusion of nicotine may be related to oxygen radicals. We found that application of superoxide dismutase or tetrahydrobiopterin during infusion of nicotine could prevent impaired NOS-dependent vasodilatation. Thus acute exposure of cerebral vessels to nicotine specifically impairs NOS-dependent dilatation via the production of oxygen radicals possibly related to an alteration in the utilization of tetrahydrobiopterin.

Effects of Chronic Nitric Oxide Synthase Inhibition on Cerebral Arterioles in Rats

Hypertension ◽  
1997 ◽  
Vol 30 (5) ◽  
pp. 1097-1104 ◽  
Author(s):  
Jean-Marc Chillon ◽  
Shams Ghoneim ◽  
Gary L. Baumbach
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cerebral Arterioles ◽  
Oxide Synthase

scholarly journals Tetrahydrobiopterin rescues impaired responses of cerebral resistance arterioles during type 1 diabetes

2016 ◽  
Vol 14 (1) ◽  
pp. 33-39 ◽  
Author(s):  
William G Mayhan ◽  
Denise M Arrick
Keyword(s):  
Nitric Oxide ◽  
Type 1 Diabetes ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Therapeutic Potential ◽  
Diabetic Rats ◽  
Cerebral Arterioles ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Our goal was to test the hypothesis that administration of tetrahydrobiopterin (BH4) would improve impaired endothelial nitric oxide synthase–dependent dilation of cerebral arterioles during type 1 diabetes. In addition, we examined the influence of BH4 on levels of superoxide in brain tissue. In vivo diameter of cerebral arterioles in nondiabetic and diabetic rats was measured in response to endothelial nitric oxide synthase–dependent agonists (acetylcholine and adenosine 5′-diphosphate) and an endothelial nitric oxide synthase–independent agonist (nitroglycerine) before and during application of BH4 (1.0 µM). We also measured levels of superoxide from cortex tissue in nondiabetic and diabetic rats under basal states and during BH4. Acetylcholine and adenosine 5′-diphosphate dilated cerebral arterioles in nondiabetic rats, but this vasodilation was significantly impaired in diabetic rats. In contrast, nitroglycerine produced similar vasodilation in nondiabetic and diabetic rats. Application of BH4 did not enhance vasodilation in nondiabetic rats but improved impaired cerebral vasodilation in diabetic rats. Basal superoxide levels were increased in cortex tissue from diabetic rats, and BH4 reduced these levels to that found in nondiabetic rats. Thus, BH4 is an important mediator of endothelial nitric oxide synthase–dependent responses of cerebral arterioles in diabetes and may have therapeutic potential for the treatment of cerebral vascular disease.

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