Re Heusser et al elevation of sympathetic activi

Authors: Rupp Heinz

Publish Date: 2004/03/01

Volume: 17, Issue: 3, Pages: 281-281

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Abstract

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 1270 and diastolic arterial pressure 760 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 populationThe 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 significantlyEprosartan 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

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