The L-arginine-nitric oxide pathway in hypertension

Kelm, Malte

doi:10.1007/s11906-003-0015-z

Cited by 40 publications

(27 citation statements)

References 97 publications

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“…Evidence for a role for eNOS in affecting blood pressure is quite strong (Forte et al, 1997;Kelm, 2003). Disruption of eNOS gene in mice leads to hypertension (Forte et al, 1997).…”

Section: Rgz Reduces Map and Increases Renal Namentioning

confidence: 99%

Rosiglitazone Activates Renal Sodium- and Water-Reabsorptive Pathways and Lowers Blood Pressure in Normal Rats

Song

Knepper²,

Hu³

et al. 2003

J Pharmacol Exp Ther

125

122

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Synthetic agonists of the peroxisomal proliferator-activated receptor subtype ␥ (PPAR-␥) are highly beneficial in the treatment of type II diabetes. However, they are also associated with fluid retention and edema, potentially serious side effects of unknown origin. These studies were designed to test the hypothesis that rosiglitazone (RGZ, PPAR-␥ agonist) may activate sodium-and water-reabsorptive processes in the kidney, possibly in response to a drop in mean arterial blood pressure (MAP), as well as directly through PPAR-␥. Targeted proteomics of the major renal sodium and water transporters and channel proteins was used to identify potentially regulated sites of renal sodium and water reabsorption. RGZ (47 or 94 mg/kg diet) was fed to male, Sprague-Dawley rats (ϳ270g) for 3 days. MAP, measured by radiotelemetry, was decreased significantly in rats fed either level of RGZ, relative to control rats. Delta MAP from baseline was Ϫ3.2 Ϯ 1.2 mm Hg in rats fed high-dose RGZ versus ϩ 3.4 Ϯ 0.8 for rats fed control diet. RGZ did not affect feed or water intake, but rats treated with high-dose RGZ had decreased urine volume (by 22%), sodium excretion (44%), kidney weight (9%), and creatinine clearance (35%). RGZ increased whole kidney protein abundance of the ␣-1 subunit of Na-K-ATPase, the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2), the sodium hydrogen exchanger (NHE3), the aquaporins 2 and 3, and endothelial nitric-oxide synthase. We conclude that both increases in renal tubule transporter abundance and a decrease in glomerular filtration rate likely contribute to the RGZ-induced sodium retention.

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“…Evidence for a role for eNOS in affecting blood pressure is quite strong (Forte et al, 1997;Kelm, 2003). Disruption of eNOS gene in mice leads to hypertension (Forte et al, 1997).…”

Section: Rgz Reduces Map and Increases Renal Namentioning

confidence: 99%

Rosiglitazone Activates Renal Sodium- and Water-Reabsorptive Pathways and Lowers Blood Pressure in Normal Rats

Song

Knepper²,

Hu³

et al. 2003

J Pharmacol Exp Ther

125

122

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“…GCs inhibit NOS synthesis [21••] and may lead to increased BP by reduction in peripheral vasodilation [26]. Similarly, GCs inhibit the production of prostacyclin, another potent vasodilator in the vascular endothelium [27].…”

Section: Effects On Vasodilator Actionmentioning

confidence: 99%

Glucocorticoid excess and hypertension

Baid

Nieman

2004

Current Science Inc

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Cushing's syndrome is a rare disorder characterized by chronic, excess glucocorticoid exposure. Hypertension is one of the most discriminating features of the disease, as it is present in 80% of patients. Patients with Cushing's syndrome have a mortality rate four times that of the general population, most likely secondary to an increased number of cardiovascular risk factors, including hypertension. In this article, we review several pathogenetic mechanisms of glucocorticoid-induced hypertension, including the role of sodium/water and mineralocorticoid excess, as well as involvement of the vasculature and kidney. Although treatment of hypertension with available antihypertensive medications is only moderately successful, after cure of Cushing's syndrome, approximately 30% of patients have persistent hypertension.

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“…It is involved in a number of physiological functions in the body such as blood pressure regulation (Kelm, 2003), neurotransmission (Yun et al, 1996), inhibition of platelet adhesion (Riddell and Owen, 1999), vasodilatation (Moncada et al, 1991), wound healing (Witte and Barbul, 2002) and nonspecific immune response to infection (Sasaki et al, 1998). There are direct chemical reactions in which NO interacts directly with biological molecules.…”

Section: Introductionmentioning

confidence: 99%

Antibacterial and bactericidal activity of nitric oxide-releasing natural zeolite

Narin

Albayrak

Ülkü

2010

Applied Clay Science

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The zeolitic tuff from Gördes (Western Anatolia) was used as adsorbent for nitric oxide (NO) storage and release purposes. The NO loading of the zeolite was performed under 20 mL min − 1 NO flow at 30°C and then the zeolite was purged with inert gas in order to remove the species that were reversibly adsorbed and in the gas phase (desorption). The total and reversible adsorption capacities of the zeolite were determined from the adsorption and desorption breakthrough curves, respectively. The NO-loaded zeolite exhibited antibacterial and bactericidal activities against Gram-negative (Escherichia coli) and Gram-positive bacteria (Bacillus subtilis) under physiological conditions. From the NO release kinetics, the diffusion coefficient of NO in the zeolite particle was determined.

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The L-arginine-nitric oxide pathway in hypertension

Cited by 40 publications

References 97 publications

Rosiglitazone Activates Renal Sodium- and Water-Reabsorptive Pathways and Lowers Blood Pressure in Normal Rats

Rosiglitazone Activates Renal Sodium- and Water-Reabsorptive Pathways and Lowers Blood Pressure in Normal Rats

Glucocorticoid excess and hypertension

Antibacterial and bactericidal activity of nitric oxide-releasing natural zeolite

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