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Abstract

In essential hypertensive patients (EH) the altered endothelium (END)-dependent vasodilation (VD) is characterized by a reduced nitric oxide (NO) availability and in these patients END-dependent VD induced by bradykinin (BDK) is mediated by a compensatory production of EDHF sensitive to ouabain (OUA), a Na+-K+ ATPase inhibitor.

To evaluate whether Ca-antagonist Lercanidipine (LER) can restore NO availability, in n= 15 EH (age 51.4±6.5 years) we evaluated the effect of 3 months of therapy with oral LER (10-20 mg/die) on forearm blood flow changes (FBF, strain-gauge venous plethysmography) induced by intrabrachial infusion of BDK (5, 15, 50 ng/100ml/min), at baseline (saline 0.2 ml/100 ml/min), during L-NMMA (100 μg/100ml/min), a NO-synthase inhibitor, or OUA (0.72 μg/100ml/min). These infusions were repeated in the presence of vitamin (Vit) C (8 mg/100ml/min), an antioxidant. VD to sodium nitroprusside (SNP:1, 2, 4 μg/100ml/min) was also evaluated. Finally, plasma lipoperoxides (LOOH) and antioxidant plasma capacity (FRAP) were measured, by colorimetric assay.

At baseline VD to BDK (FBF%:98±41, 224±58, 343±88), not modified by L-NMMA (FBF%:83±35, 224±61, 370±82), was reduced (p<0.05) by OUA (FBF%: 27±17, 80±35, 152±50). Vit C increased (p<0.05) VD to BDK (FBF%: 208±60, 376±90, 553±120), restored the inhibiting activity of L-NMMA (FBF%: 70±41, 165±51, 242±81) and reversed the inhibiting effect of OUA (FBF%:229±72, 388±86, 557±113). LER, which reduced BP from 152±5/98±3 to 135±5/85±2 mmHg (p<0.05), while not modifying response to SNP (FBF% basale: 98±40, 234±62, 353±85;LER : 106±40, 232±62, 343±83), potentiated (p<0.01) VD to BDK (FBF%: 166±41, 342±129, 482±158), restored the inhibiting effect of L-NMMA (FBF%: 51±40, 131±71, 205±81) reversing the inhibitory effect of OUA (FBF%: 141±53, 351±220, 478±298). Moreover, after LER, Vit C did not change either VD to BDK (FBF%:168±42, 322±85, 484±131) or the inhibitory effect of L-NMMA. Finally, LER enhanced FRAP (from 305±32 to 430±146 mmol/L, p<0.01) and reduced LOOH (from 4.8±3.3 to 2.6±2 μmol/L, p<0.001). In EH treatment with LER normalised END-dependent VD restoring NO availability, probably through an antioxidant effect.

Nitric Oxide, Essential Hypertension, Calcium Antagonist
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© American Journal of Hypertension, Ltd. 2002
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