| Tissue-type plasminogen activator release in healthy subjects and hypertensive patients: relationship with beta-adrenergic receptors and the nitric oxide pathway. | |
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MedLine Citation:
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PMID: 18574075 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The relationship between adrenergic stimuli and NO in modulating tissue-type plasminogen activator (t-PA) release from endothelial cells was investigated in normotensive subjects and essential hypertensive patients. Sympathetic activation, a well-known stimulus for endogenous fibrinolysis, is also involved in the determination of cardiovascular risk in essential hypertension. However, the existence of cross-talk between adrenergic stimuli and NO availability in modulating t-PA release is not well established yet. We assessed the release of t-PA in the forearm microcirculation of 58 normotensive subjects (mean age: 47+/-9 years) and 44 essential hypertensive patients (mean age: 48+/-11 years) under specific intra-arterial adrenergic stimuli. Intrabrachial infusion of epinephrine (0.1 to 0.3 microg/100 mL per minute) induced greater t-PA release in normotensive subjects as compared with essential hypertensive patients (P<0.05). However, inhibition of NO synthase with N(G)-monomethyl-L-arginine (100 microg/100 mL per minute) infusion blunted epinephrine-induced t-PA release in normotensive subjects (P<0.05) but not in essential hypertensive patients. In normotensive subjects, t-PA release by epinephrine was not affected by phentolamine (8 microg/100 mL per minute) coinfusion and was abolished in the presence of propanolol (10 microg/100 mL per minute). Intrabrachial isoproterenol (0.03 microg/100 mL per minute) induced a significant increase in t-PA release (P<0.01), an effect blunted by N(G)-monomethyl-L-arginine (P<0.05). In essential hypertensive patients, the response to isoproterenol was impaired as compared with normotensive subjects and was unaffected by N(G)-monomethyl-L-arginine coinfusion. In conclusion, the results of the present study demonstrate that adrenergic-induced t-PA release is mediated by beta-adrenoreceptors via a mechanism involving the NO pathway. Our results show an impaired adrenergic-stimulated t-PA release among essential hypertensive patients, probably mediated via a reduced NO availability. This impaired fibrinolytic activity might contribute to the increased cardiovascular risk associated with hypertension. |
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Authors:
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Chiara Giannarelli; Agostino Virdis; Ferdinando De Negri; Emiliano Duranti; Armando Magagna; Lorenzo Ghiadoni; Antonio Salvetti; Stefano Taddei |
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Publication Detail:
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Type: Journal Article Date: 2008-06-23 |
Journal Detail:
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Title: Hypertension Volume: 52 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2008 Aug |
Date Detail:
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Created Date: 2008-07-24 Completed Date: 2008-08-22 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 314-21 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine, University of Pisa, Via Roma, 67, 56100 Pisa, Italy. c.giannarelli@int.med.unipi.it |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Aged Analysis of Variance Case-Control Studies Epinephrine / pharmacology Female Humans Hypertension / blood*, diagnosis Infusions, Intra-Arterial Male Middle Aged Nitric Oxide / metabolism* Probability Receptors, Adrenergic, beta / analysis, metabolism* Reference Values Sensitivity and Specificity Signal Transduction / drug effects, physiology Tissue Plasminogen Activator / analysis, metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Receptors, Adrenergic, beta; 10102-43-9/Nitric Oxide; 51-43-4/Epinephrine; EC 3.4.21.68/Tissue Plasminogen Activator |
| Comments/Corrections | |
Comment In:
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Hypertension. 2008 Aug;52(2):218-9
[PMID:
18574069
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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