| Endothelial dysfunction in hypertension is independent from the etiology and from vascular structure. | |
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MedLine Citation:
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PMID: 9453325 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The aim of our study was to evaluate the relationships between endothelial function, small resistance artery structure, and blood pressure in patients with primary or secondary hypertension. Sixty subjects were included in the study: 9 patients with pheochromocytoma, 10 with primary aldosteronism, 17 with renovascular hypertension, and 13 with essential hypertension with 11 normotensive subjects who served as controls. Clinic and 24-hour ambulatory blood pressure (ABPM) were evaluated. All subjects were submitted to a biopsy of subcutaneous fat. Small resistance arteries were dissected and mounted on a micromyograph and the media/lumen ratio was calculated. A dose-response curve to acetylcholine was performed at cumulative concentrations from 10(-9) to 10(-5) mol/L. The vasodilator response to acetylcholine was similarly impaired in the four groups of hypertensive patients (ANOVA P<.05 versus normotensive controls), without any significant difference among them. In subcutaneous small arteries of patients with either primary aldosteronism or renovascular hypertension, a marked increase in media:lumen ratio was observed, while in patients with pheochromocytoma, the extent of vascular structural alterations was similar to that observed in essential hypertension. No significant correlation between media-lumen ratio or clinic blood pressure and maximum acetylcholine-induced vasodilatation was observed. On the contrary, a significant, albeit not very close, correlation between ABPM values and maximum acetylcholine-induced vasodilatation was observed (r=34, P<.05 with 24-hour systolic blood pressure, r=0.36, P<.05 with 24-hour diastolic blood pressure). In conclusion, endothelial dysfunction seems to be independent from the degree of vascular structural alterations and from the etiology of hypertension, and it is probably more linked to the hemodynamic load. |
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Authors:
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D Rizzoni; E Porteri; M Castellano; G Bettoni; M L Muiesan; G Tiberio; S M Giulini; G Rossi; G Bernini; E Agabiti-Rosei |
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Publication Detail:
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Type: In Vitro; Journal Article |
Journal Detail:
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Title: Hypertension Volume: 31 ISSN: 0194-911X ISO Abbreviation: Hypertension Publication Date: 1998 Jan |
Date Detail:
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Created Date: 1998-02-20 Completed Date: 1998-02-20 Revised Date: 2006-11-15 |
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: 335-41 Citation Subset: IM |
Affiliation:
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Semeiotica and Metodologia Medica, University of Brescia, Italy. damiano.rizzoni@schering-pl.it |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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pharmacology Adipose Tissue / blood supply Adrenal Gland Neoplasms / complications Aldosterone / blood Arterioles / drug effects, pathology, physiopathology* Blood Pressure* Cholesterol / blood Diastole Endothelium, Vascular / drug effects, pathology, physiopathology* Epinephrine / urine Female Humans Hyperaldosteronism / physiopathology Hypertension / etiology*, physiopathology* Hypertension, Renovascular / physiopathology* Male Middle Aged Nitroprusside / pharmacology Norepinephrine / urine Pheochromocytoma / complications Reference Values Regression Analysis Renin / blood Systole Triglycerides / blood Vascular Resistance |
| Chemical | |
Reg. No./Substance:
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0/Triglycerides; 15078-28-1/Nitroprusside; 51-41-2/Norepinephrine; 51-43-4/Epinephrine; 51-84-3/Acetylcholine; 52-39-1/Aldosterone; 57-88-5/Cholesterol; EC 3.4.23.15/Renin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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