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Am J Physiol Heart Circ Physiol 279: H1600-H1608, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 4, H1600-H1608, October 2000

Effect of hypercholesterolemia on Ca2+-dependent K+ channel-mediated vasodilatation in vivo

Richmond W. Jeremy and Hugh McCarron

Department of Medicine, University of Sydney, Sydney, New South Wales 2006, Australia

Nitric oxide (NO)-mediated and NO-independent mechanisms of endothelium-dependent vasodilatation involve Ca2+-dependent K+ (KCa) channels. We examined the role in vivo of KCa channels in NO-independent vasodilatation in hypercholesterolemia. Hindlimb vascular conductance was measured at rest and after aortic injection of ACh, bradykinin (BK), and sodium nitroprusside in anesthetized control and cholesterol-fed rabbits. Conductances were measured before and after treatment with the NO synthase antagonist Nomega -nitro-L-arginine methyl ester (L-NAME, 10 mg/kg) or KCa blockers tetraethylammonium (30 mg/kg), charybdotoxin (10 µg/kg), and apamin (50 µg/kg). The contribution of NO to basal conductance was greater in control than in cholesterol-fed rabbits [2.2 ± 0.4 vs. 1.1 ± 0.3 (SE) ml · min-1 · kg-1 · 100 mmHg-1, P < 0.05], but the NO-independent KCa channel-mediated component was greater in the cholesterol-fed than in the control group (1.1 + 0.4 vs. 0.3 ± 0.1 ml · min-1 · kg-1 · 100 mmHg-1, P < 0.05). Maximum conductance response to ACh and BK was less in cholesterol-fed than in control rabbits, and the difference persisted after L-NAME (ACh: 7.7 ± 0.7 vs. 10.1 ± 0.5 ml · min-1 · kg-1 · 100 mmHg-1, P < 0.005). Blockade of KCa channels with tetraethylammonium or charybdotoxin + apamin almost completely abolished L-NAME-resistant vasodilatation after ACh or BK. The magnitude of KCa-mediated vasodilatation after ACh or BK was impaired in hypercholesterolemic rabbits. Vasodilator responses to nitroprusside did not differ between groups. In vivo, hypercholesterolemia is associated with an altered balance between NO-mediated and NO-independent KCa channel contributions to resting vasomotor tone and impairment of both mechanisms of endothelium-dependent vasodilatation.

cholesterol; endothelium; microcirculation; endothelium-derived factors


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