Pathophysiologie der Adipositas-assoziierten Hypertonie

Zusammenfassung

Die Pathophysiologie der Adipositas-assoziierten Hypertonie ist ein multifaktorielles Geschehen. Im Zentrum dieser Vorgänge steht ein erhöhtes Herzminutenvolumen (HMV) mit begleitendem Anstieg des peripheren vaskulären Widerstands. Die Zunahme des HMV ist Folge einer Vermehrung des intravasalen Volumens, hervorgerufen durch eine Stimulation der renalen Natriumretention. Diese Prozesse werden maßgeblich durch eine verstärkte Aktivität des sympathischen Nervensystems (SNS), die Aktivierung des Renin-Angiotensin-Aldosteron-Systems (RAAS) und strukturelle Nierenveränderungen verursacht. Wichtige Mediatoren der SNS-Aktivierung bei Adipositas sind Hyperinsulinämie, erhöhte Plasmaleptinspiegel und obstruktive Schlafapnoe. Die Aktivierung des RAAS ist wesentlich durch die verstärkte Aktivität eines lokalen RAAS in der zunehmenden Fettmasse verursacht. Zusätzlich rückt die Bedeutung des perivaskulären Fetts als vasoaktives Gewebe zunehmend in den Mittelpunkt der heutigen Untersuchungen. Eine Dysregulation der sekretorischen Funktion des perivaskulären Fetts könnte ein wichtiger pathophysiologischer Faktor bei der Entstehung der Adipositas-assoziierten Hypertonie sein. Eine pharmakologische Intervention zur Behandlung der Adipositas-assoziierten Hypertonie sollte sich an den genannten Prinzipien orientieren.

Summary

The pathophysiology of obesity-associated hypertension is a multifactorial process. An increased cardiac output has been identified as an important pathophysiological mediator accompanied by augmented peripheral vascular resistance. The enhanced cardiac output likely results from plasma volume expansion due to enhanced renal sodium retention. These processes are mainly mediated by activation of the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone-system (RAAS) during obesity as well as by structural kidney changes. Important stimulators of SNS-activity have been described in obesity including hyperinsulinemia, increased plasma leptin levels, and obstructive sleep apnea. Exaggerated RAAS activation might be attributed to an enhanced activity of a local RAAS in the incremental adipose tissue mass. In addition, perivascular fat is gaining increased attention as a vasoactive tissue. A dysregulated secretory function of perivascular fat might be an important pathophysiological initiator during the development of obesity-associated hypertension. A pharmacological treatment strategy for obesity-associated hypertension absolutely requires the integration of these pathophysiological principles.

Schlüsselwörter

Adipositas-assoziierte Hypertonie - sympathisches Nervensystem - Renin-Angiotensin-Aldosteron-System

Keywords

Obesity-associated hypertension - sympathetic nervous system - renin-angiotensin-aldosterone-system

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