The effect of alpha-lipoic acid on mitochondrial superoxide and glucocorticoid-induced hypertension.

Aims: To examine the effect of alpha-lipoic acid, an antioxidant with mitochondrial superoxide inhibitory properties, on adrenocorticotrophic hormone- (ACTH-HT) and dexamethasone-induced hypertensions (DEX-HT) in rats and if any antihypertensive effect is mediated via mitochondrial superoxide inhibition.

Methods: In a prevention study, rats received ground food or alpha-lipoic-acid-laced food (10 mg/rat/day) for 15 nights. Saline, adrenocorticotrophic hormone (ACTH, 0.

How do glucocorticoids cause hypertension: role of nitric oxide deficiency, oxidative stress, and eicosanoids.

The exact mechanism by which glucocorticoid induces hypertension is unclear. Several mechanisms have been proposed, although there is evidence against the role of sodium and water retention as well as sympathetic nerve activation. This review highlights the role of nitric oxide-redox imbalance and their interactions with arachidonic acid metabolism in glucocorticoid-induced hypertension in humans and experimental animal models.

Effects of sepiapterin supplementation and NOS inhibition on glucocorticoid-induced hypertension.

Background: Glucocorticoid-induced hypertension is associated with imbalance between nitric oxide (NO) and superoxide. One of the pathways that causes this imbalance is endothelial NO synthase (eNOS) uncoupling. In the present study, adrenocorticotrophic hormone (ACTH)- and dexamethasone-treated rats were further treated with sepiapterin, a precursor of tetrahydrobiopterin, or N-nitro-L-arginine (NOLA), an inhibitor of NOS, to investigate the role of eNOS uncoupling in glucocorticoid-induced hypertension.

Blood pressure measurement in pregnancy: the effect of arm circumference and sphygmomanometer cuff size.

This study aimed to assess the difference in blood pressure readings between the standard and large cuff and to determine if such a difference applies over a range of arm circumferences (ACs) in pregnancy. We measured blood pressure on 219 antenatal women. Six blood pressure readings were taken, three with a standard 'adult' and three with a 'large' cuff, in random order.

Hemodynamics of dexamethasone-induced hypertension in the rat.

Although dexamethasone (DEX) is known to cause hypertension in humans and in animals, the hemodynamic characteristics of DEX-induced hypertension (DEX-HT) in the rat remain unclear. This study evaluated central and regional hemodynamics, and the role of total peripheral resistance (TPR) using a vasodilator minoxidil. Rats were divided into four groups, namely saline (n=20), DEX (n=21), minoxidil+saline (n=10) and minoxidil+DEX (n=10).

The role of 20-hydroxyeicosatetraenoic acid in adrenocorticotrophic hormone and dexamethasone-induced hypertension.

Objective: 20-hydroxyeicosatetraenoic acid (20-HETE) is a potent constrictor in small arteries and also has natriuretic properties. Urinary 20-HETE excretion is increased in adrenocorticotrophic hormone (ACTH)-induced hypertensive rats. In the present study, we investigated the effect of a specific enzyme inhibitor of 20-HETE production, N-hydroxy-N'-(4-butyl-2-methylphenyl) formamidine (HET0016), on glucocorticoid-induced hypertension in rats, a sodium-independent model.

Reactive oxygen species and glucocorticoid-induced hypertension.

1. There is increasing evidence for a role of oxidative stress and nitric oxide deficiency in experimental glucocorticoid-induced hypertension, as evidenced by increased biomarkers of oxidative stress; the effectiveness of antioxidants or reduced NADPH oxidase antagonists in lowering blood pressure; and secondary upregulation of endogenous antioxidant enzymes in response to oxidative stress. 2.

Role of xanthine oxidase in dexamethasone-induced hypertension in rats.

1. Glucocorticoid-induced hypertension (GC-HT) in the rat is associated with nitric oxide-redox imbalance. 2.