Mechanismen des gesteigerten sympathikotonus bei essentieller hypertonie

Translated title of the contribution: Mechanisms of sympathetic augmentation in essential hypertension

M. P. Schlaich, E. Lambert, D. M. Kaye, M. D. Esler

Research output: Contribution to journalArticle

Abstract

Background: There is strengthening evidence that essential hypertension is commonly neurogenic, initiated and sustained by sympathetic nervous system overactivity. Potential mechanisms include increased central sympathetic outflow, altered norepinephrine (NE) neuronal reuptake, diminished arterial baroreflex dampening of sympathetic nerve traffic and sympathetic neuromodulation by angiotensin II. Methods and results: To address this issue, we used microneurography and radiotracer dilution methodology to measure regional sympathetic activity in 22 hypertensive patients and 11 normotensive control subjects. The NE transport inhibitor desipramine was infused to directly assess the potential role of impaired neuronal NE reuptake. To evaluate possible angiotensin-sympathetic neuromodulation, the relation of arterial and coronary sinus plasma concentrations of angiotensin II to sympathetic activity was investigated. Hypertensive patients displayed increased muscle sympathetic nerve activity and elevated total systemic, cardiac and renal NE spillover. Cardiac neuronal NE reuptake was decreased in hypertensive subjects. In response to desipramine, both the reduction of fractional transcardiac 3[H]NE extraction and the increase in cardiac NE spillover were less pronounced in hypertensive patients. Arterial baroreflex control of sympathetic nerve traffic was not diminished in hypertensive subjects. Angiotensin ii plasma concentrations were similar in both groups and were not related to indices of sympathetic activation. Conclusions: Increased rates of sympathetic nerve firing and reduced neuronal ne reuptake both contribute to sympathetic activation in hypertension, whereas a role for dampened arterial baroreflex restraint on sympathetic nerve traffic and a peripheral neuromodulating influence of angiotensin ii seem to be excluded.

Translated title of the contributionMechanisms of sympathetic augmentation in essential hypertension
Original languageGerman
Pages (from-to)45-51
Number of pages7
JournalNieren- und Hochdruckkrankheiten
Volume34
Issue number2
Publication statusPublished - Feb 2005
Externally publishedYes

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