Hindsight: Metabolic Effects of Valsartan

Saturday, October 13, 2012

Prof. Dr. med. Jens Jordan, Institut für Klinische Pharmakologie, Medizinische Hochschule Hannover, Germany

Prof. Dr. med. Jens Jordan, Institut für Klinische Pharmakologie, Medizinische Hochschule Hannover, Germany

Given my interest in the adipose tissue renin angiotensin and our findings that this system may have metabolic effects, in 2005, my colleague Jens Jordan and I published the results of a small randomised controlled trial comparing the hemodynamic effects of the angiotensin receptor type 1 (AT-1) blocker valsartan to the beta-blocker atenolol in around 70 obese patients with mild to moderate uncomplicated essential hypertension. (Journal of Hypertension, 2005)

Participants were treated with valsartan at a maximal dose of 160 mg/day or with atenolol at a maximal dose of 100 mg/day for 13 weeks. Hydrochlorothiazide at doses of 12.5-25 mg was added in patients with blood pressure > 140/90 mmHg on monotherapy.

As expected, blood pressure levels dropped significantly and similarly with both treatments.

Although we did not see any effects on body weight, lipid levels or hsCRP, insulin resistance, as assessed by homeostasis model assessment for insulin resistance (HOMA-IR) improved with valsartan but not with atenolol.

From this study we concluded that, while both beta-receptor and AT1-receptor blockers, particularly in combination with low-dose diuretics, effectively lower blood pressure in obese hypertensives, treatment with AT1-receptor blockers may have beneficial effects on glucose homeostasis, particularly in obese hypertensives, given their profoundly increased diabetes risk.

Over time, this small study together with evidence from much larger studies has certainly added to the evidence suggesting that blockers of the renin-angiotensin system should be considered first line therapy for hypertension in obese patients.

AMS
Boston, MA