Re: Heusser et al: Elevation of sympathetic activity by eprosartan in young male subjects [1] (multiple letters)

Heinz Rupp*, Karsten Heusser, Jan Vitkovsky, Walter Raasch, Roland E. Schmieder, Hans P. Schobel

*Corresponding author for this work


Heusser et al1 examined effects of the angiotensin I receptor blocker eprosartan on the sympathetic nervous system in humans. The authors wrote in the Limitations of the Study section that “... only young men with arterial BP <160/100 mm Hg were tested.” In reality, the subject population was normotensive. Table 1 in their article, which lists subjects' characteristics, shows that systolic arterial pressure was 127.0 and diastolic arterial pressure 76.0 mm Hg. By indicating value of <160/100 mm Hg the authors implied that they tested subjects with mild hypertension. In fact, they looked at effects of an antihypertensive drug in a normotensive population. The authors concluded that eprosartan “caused augmented central neural vasoconstrictor outflow paralleled by increased plasma levels of norepinephrine, which casts doubt on its ability to dampen norepinephrine release from peripheral sympathetic nerve endings in humans.” The authors did not, however, provide data for proving the absence of inhibitory presynaptic effects. In contrast, they actually showed that eprosartan reduces norepinephrine influences. In the experiments on mental stress, heart rate was significantly lowered, which occurred in addition to a putatively increased basal sympathetic outflow and the increased sympathetic activity due to the stress. Also, blood pressure values were reduced, but not significantly. Eprosartan did not induce hypotension in the normotensive study population, given that sympathetic outflow was increased. The untreated level of muscle sympathetic nerve activity was very low, however, and the nerve firing rate on eprosartan, although increasing a little, remained at the bottom end of the normal range. Furthermore, the treatment period of 1 week was too short for excluding a residual compensatory sympathetic response. Also the hypothesis that the elevation of plasma angiotensin II caused the augmented central sympathetic outflow could hold only for normotensive individuals. In patients with chronic renal failure, enalapril and losartan reduced sympathetic hyperactivity (Klein et al2). Furthermore, addition of valsartan to an ACE inhibitor improved cardiac sympathetic nerve activity (Kasama et al3).
Original languageEnglish
JournalAmerican Journal of Hypertension
Issue number3
Pages (from-to)281-283
Number of pages3
Publication statusPublished - 01.03.2004


Dive into the research topics of 'Re: Heusser et al: Elevation of sympathetic activity by eprosartan in young male subjects [1] (multiple letters)'. Together they form a unique fingerprint.

Cite this