Sympathetic activation in the pathogenesis of hypertension and progression of organ damage

Giuseppe Mancia, Guido Grassi, Cristina Giannattasio, Gino Seravalle

Research output: Contribution to journalArticlepeer-review


Although animal models of hypertension have clearly shown that high blood pressure is associated with and is probably caused by an increase in sympathetic cardiovascular influences, a similar demonstration in humans has been more difficult to obtain for methodological reasons. There is now evidence, however, of increased sympathetic activity in essential hypertension. This article will review this evidence by examining data showing that plasma norepinephrine is increased in essential hypertension and that this is also the case for systemic and regional norepinephrine spillover, as well as for the sympathetic nerve firing rate in the skeletal muscle nerve district. Evidence will also be provided that sympathetic activation is a peculiar feature of essential hypertension, particularly in its early stages, with secondary forms of high blood pressure not usually characterized by an increased central sympathetic outflow. Humoral, metabolic, reflex, and central mechanisms are likely to be the factors responsible for the adrenergic activation characterizing hypertension, which may also promote the development and progression of the cardiac and vascular alterations that lead to hypertension-related morbidity and mortality, independent of blood pressure values. This represents the rationale for considering sympathetic deactivation one of the major goals of antihypertensive treatment.

Original languageEnglish
Pages (from-to)724-728
Number of pages5
Issue number4 II
Publication statusPublished - Oct 1999


  • Hypertension, essential
  • Hypertension, secondary
  • Hypertrophy
  • Nervous system, sympathetic
  • Norepinephrine
  • Pressoreceptors

ASJC Scopus subject areas

  • Internal Medicine


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