Tags

Type your tag names separated by a space and hit enter

Type 5 phosphodiesterase inhibition by sildenafil abrogates acute smoking-induced endothelial dysfunction.
Am J Hypertens 2004; 17(11 Pt 1):1040-4AJ

Abstract

BACKGROUND

Endothelial dysfunction is a key early event in the process of atherosclerosis and a risk factor for cardiovascular events. Sildenafil, an effective oral treatment for patients with erectile dysfunction, inhibits cGMP degradation by specific type 5 phosphodiesterase (PDE) inhibition. Sildenafil has been shown to improve vascular function, however, the effect of type 5 PDE inhibition on acute smoking-induced endothelial dysfunction is unknown.

METHODS

We studied the effect of 50 mg of sildenafil on acute smoking-induced endothelial dysfunction in 14 male smokers according to a randomized, placebo-controlled, cross-over design. Endothelial function was evaluated with flow-mediated dilatation (FMD) of the brachial artery using high-resolution ultrasonography.

RESULTS

Sildenafil abolishes the decrease in FMD of the brachial artery that is induced acutely by smoking (placebo/smoking session: from 4.56% +/- 0.60% to 2.80% +/- 0.43%, sildenafil/smoking session: from 3.83% +/- 0.64% to 4.33% +/- 0.47%, ie, improvement of 51%, P < .05). This was associated with no reversal effect of sildenafil on smoking-induced decrease in resting brachial artery diameter and with a partial reversal of the smoking-induced decrease in hyperemic brachial artery diameter (placebo/smoking session: from 4.68 +/- 0.13 mm to 4.53 +/- 0.15 mm, sildenafil/smoking session: from 4.72 +/- 0.12 mm to 4.64 +/- 0.13 mm, ie, improvement of 1.5%, P < .005).

CONCLUSIONS

The present study shows, for the first time, that type 5 PDE inhibition with sildenafil abrogates the smoking-induced acute decrease in FMD of the brachial artery. These findings may have clinical implications given the detrimental consequences of smoking and the strategic role of normal endothelial function.

Authors+Show Affiliations

Cardiovascular and Sexual Health Unit, First Department of Cardiology, Athens Medical School, Hippokration Hospital, Athens, Greece. cvlachop@otenet.grNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial

Language

eng

PubMed ID

15533731

Citation

Vlachopoulos, Charalambos, et al. "Type 5 Phosphodiesterase Inhibition By Sildenafil Abrogates Acute Smoking-induced Endothelial Dysfunction." American Journal of Hypertension, vol. 17, no. 11 Pt 1, 2004, pp. 1040-4.
Vlachopoulos C, Tsekoura D, Alexopoulos N, et al. Type 5 phosphodiesterase inhibition by sildenafil abrogates acute smoking-induced endothelial dysfunction. Am J Hypertens. 2004;17(11 Pt 1):1040-4.
Vlachopoulos, C., Tsekoura, D., Alexopoulos, N., Panagiotakos, D., Aznaouridis, K., & Stefanadis, C. (2004). Type 5 phosphodiesterase inhibition by sildenafil abrogates acute smoking-induced endothelial dysfunction. American Journal of Hypertension, 17(11 Pt 1), pp. 1040-4.
Vlachopoulos C, et al. Type 5 Phosphodiesterase Inhibition By Sildenafil Abrogates Acute Smoking-induced Endothelial Dysfunction. Am J Hypertens. 2004;17(11 Pt 1):1040-4. PubMed PMID: 15533731.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Type 5 phosphodiesterase inhibition by sildenafil abrogates acute smoking-induced endothelial dysfunction. AU - Vlachopoulos,Charalambos, AU - Tsekoura,Dorothea, AU - Alexopoulos,Nikolaos, AU - Panagiotakos,Demosthenes, AU - Aznaouridis,Konstantinos, AU - Stefanadis,Christodoulos, PY - 2004/05/02/received PY - 2004/06/11/revised PY - 2004/06/29/accepted PY - 2004/11/10/pubmed PY - 2005/2/23/medline PY - 2004/11/10/entrez SP - 1040 EP - 4 JF - American journal of hypertension JO - Am. J. Hypertens. VL - 17 IS - 11 Pt 1 N2 - BACKGROUND: Endothelial dysfunction is a key early event in the process of atherosclerosis and a risk factor for cardiovascular events. Sildenafil, an effective oral treatment for patients with erectile dysfunction, inhibits cGMP degradation by specific type 5 phosphodiesterase (PDE) inhibition. Sildenafil has been shown to improve vascular function, however, the effect of type 5 PDE inhibition on acute smoking-induced endothelial dysfunction is unknown. METHODS: We studied the effect of 50 mg of sildenafil on acute smoking-induced endothelial dysfunction in 14 male smokers according to a randomized, placebo-controlled, cross-over design. Endothelial function was evaluated with flow-mediated dilatation (FMD) of the brachial artery using high-resolution ultrasonography. RESULTS: Sildenafil abolishes the decrease in FMD of the brachial artery that is induced acutely by smoking (placebo/smoking session: from 4.56% +/- 0.60% to 2.80% +/- 0.43%, sildenafil/smoking session: from 3.83% +/- 0.64% to 4.33% +/- 0.47%, ie, improvement of 51%, P < .05). This was associated with no reversal effect of sildenafil on smoking-induced decrease in resting brachial artery diameter and with a partial reversal of the smoking-induced decrease in hyperemic brachial artery diameter (placebo/smoking session: from 4.68 +/- 0.13 mm to 4.53 +/- 0.15 mm, sildenafil/smoking session: from 4.72 +/- 0.12 mm to 4.64 +/- 0.13 mm, ie, improvement of 1.5%, P < .005). CONCLUSIONS: The present study shows, for the first time, that type 5 PDE inhibition with sildenafil abrogates the smoking-induced acute decrease in FMD of the brachial artery. These findings may have clinical implications given the detrimental consequences of smoking and the strategic role of normal endothelial function. SN - 0895-7061 UR - https://www.unboundmedicine.com/medline/citation/15533731/Type_5_phosphodiesterase_inhibition_by_sildenafil_abrogates_acute_smoking_induced_endothelial_dysfunction_ L2 - https://academic.oup.com/ajh/article-lookup/doi/10.1016/j.amjhyper.2004.06.027 DB - PRIME DP - Unbound Medicine ER -