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Abstract

Vascular endothelial dysfunction can be demonstrated in essential hypertension, and reversing this abnormality is an attractive therapeutic objective. We tested whether this could be achieved by blocking the AT1 receptor and compared this with calcium channel blockade.

12 hypertensives [mean age 60 (SD 8) years] with a mean ambulatory blood pressure of 154(10)/97(6) mmHg were randomized following a 2-week placebo (baseline) run-in period in a single blind crossover fashion to 8 week treatment period with either valsartan or amlodipine, separated by 2-week placebo washout period. Forearm venous occlusion plethysmography and intra-arterial infusions of acetylcholine (ACh) and NG-monomethyl-L-arginine (L-NMMA) were used to assess stimulated and basal endothelium-dependent nitric oxide (NO) release, respectively. Sodium nitroprusside (SNP) was used as endothelium-independent NO (control vasodilator).

Valsartan and amlodipine each lowered the clinic blood pressure to the same extent (Table). The vasodilatory response to ACh was significantly increased with valsartan but remained unchanged with amlodipine. The response to SNP was not different between treatments suggesting that the endothelium-independent pathway was unaffected. Valsartan and amlodipine similarly increased the vasoconstrictive response to L-NMMA (Table).

VariableBaselineAmlodipineValsartan
Office SBP (mmHg)162 ± 13139 ± 11**139 ± 6**
Office DBP (mmHg)103 ± 989 ± 6**86 ± 6**
ACh (%ΔFBF)185.6(34)210(54)301(47)*
SNP (%ΔFBF)209(32)207(31)209(37)
L-NMMA (%ΔFBF)-26.4(3)-42(5)**-43(6)**
VariableBaselineAmlodipineValsartan
Office SBP (mmHg)162 ± 13139 ± 11**139 ± 6**
Office DBP (mmHg)103 ± 989 ± 6**86 ± 6**
ACh (%ΔFBF)185.6(34)210(54)301(47)*
SNP (%ΔFBF)209(32)207(31)209(37)
L-NMMA (%ΔFBF)-26.4(3)-42(5)**-43(6)**
*

p<0.05 versus baseline;

**

p<0.001 versus baseline.[table]

VariableBaselineAmlodipineValsartan
Office SBP (mmHg)162 ± 13139 ± 11**139 ± 6**
Office DBP (mmHg)103 ± 989 ± 6**86 ± 6**
ACh (%ΔFBF)185.6(34)210(54)301(47)*
SNP (%ΔFBF)209(32)207(31)209(37)
L-NMMA (%ΔFBF)-26.4(3)-42(5)**-43(6)**
VariableBaselineAmlodipineValsartan
Office SBP (mmHg)162 ± 13139 ± 11**139 ± 6**
Office DBP (mmHg)103 ± 989 ± 6**86 ± 6**
ACh (%ΔFBF)185.6(34)210(54)301(47)*
SNP (%ΔFBF)209(32)207(31)209(37)
L-NMMA (%ΔFBF)-26.4(3)-42(5)**-43(6)**
*

p<0.05 versus baseline;

**

p<0.001 versus baseline.[table]

Valsartan, an AT1 receptor antagonist, increased both stimulated and basal endothelial nitric oxide release whereas for the same degree of blood pressure control, amlodipine had no effect on stimulated NO release. Thus, AT1 receptor blockade may offer superior vascular protection in hypertension.

Table legend:

SBP/DBP systolic and diastolic blood pressure (SD); FBF=Forearm Blood Flow (SEM)

amlodipine, nitric oxide, valsartan
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© American Journal of Hypertension, Ltd. 2001
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