Sind Sekretionsprodukte der Fettzellen für die Adipositas-assoziierte Hypertonie verantwortlich?

St. Engeli

doi:10.1055/s-0037-1618611

Adipositas - Ursachen, Folgeerkrankungen, Therapie, Table of Contents

Adipositas - Ursachen, Folgeerkrankungen, Therapie 2007; 01(02): 74-78
DOI: 10.1055/s-0037-1618611

Hypertonie bei Adipositas

Schattauer GmbH

Sind Sekretionsprodukte der Fettzellen für die Adipositas-assoziierte Hypertonie verantwortlich?

Role of secreted molecules from fat cells for obesityassociated hypertension

St. Engeli

¹Franz-Volhard-Centrum für Klinische Forschung, Charité Campus Buch, Berlin

› Author Affiliations

Abstract

Zusammenfassung

Adipozyten bilden eine Vielzahl von Molekülen, die direkt in die kardiovaskuläre Regulation eingreifen können (Angiotensin II, NO, Prostazyklin, nicht veresterte Fettsäuren, Adiponektin, Sauerstoffradikale, Leptin, und adipose-derived relaxing factors) oder indirekt die Aktivität kreislaufregulatorischer Mediatoren beeinflussen (Aldosteron, Kortisol, atriales natriuretisches Peptid, ADMA). Als pathophysiologisches Prinzip bei der Adipositas-assoziierten Hypertonie wird ein komplexes Ungleichgewicht zwischen diesen vielzähligen Fettzellprodukten angenommen, das in gesteigerter vaskulärer Reaktivität, endothelialer Dysfunktion, gesteigerter Sympathikusaktivität und Salzsensitivität resultiert. Die günstige Beeinflussung dieses Ungleichgewichts durch Reduktion des Körpergewichts wurde insbesondere für das Renin-Angiotensin-Aldosteron-System nachgewiesen. Von besonderer Bedeutung für die zukünftige Forschung wird es sein, die spezifische Rolle des perivaskulären Fettgewebes bei der Entstehung der Adipositas-assoziierten Hypertonie aufzuklären, da bislang nur die großen subkutanen und viszeralen Fettgewebedepots untersucht wurden.

Summary

Adipocytes produce a number of molecules with direct vascular activity (e. g. angiotensin II, NO, prostacyclin, nonesterified fatty acids, adiponectin, radical oxygen species, leptin, and adipose-derived relaxing factors). Other adipocyte-derived products indirectly act on vascular regulation by influencing cardiovascular mediators (e. g. aldosterone, cortisol, atrial natriuretic peptide, ADMA). The pathophysiology of obesity-associated hypertension can be explained in part by a complex imbalance between these adipocytederived molecules that leads to enhanced vascular reactivity, endothelial dysfunction, increased activity of the sympathetic nervous system and salt sensitivity. A beneficial effect of weight loss on this imbalance was described especially for the renin-angiotensin-aldosterone system. During the last decade, only the role of large subcutaneous and visceral adipose tissue depots was studied. In the near future, an additional research focus will be on the specific role of perivascular adipose tissue for the development of obesity-associated hypertension.

Schlüsselwörter

Renin-Angiotensin-Aldosteron System - 11β-Hydroxysteroid-Dehydrogenase 1 - asymmetrisches Dimethylarginin - oxidativer Stress

Keywords

Renin-angiotensin-aldosterone system - 11β-Hydroxysteroid-Dehydrogenase 1 - asymmetrical dimethylarginine - oxidative stress

Full Text

References

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