Endothelium-dependent nitric oxide and hyperpolarization-mediated venous relaxation pathways in rat inferior vena cava

Raffetto JD, Yu P, Reslan OM, et al (Brigham and Women’s Hosp, Boston, MA) J Vasc Surg 55:1716-1725, 2012^§

Abstract

Introduction

The vascular endothelium plays a major role in the control of arterial tone; however, its role in venous tissues is less clear. The purpose of this study was to determine the role of endothelium in the control of venous function and the relaxation pathways involved.

Methods

Circular segments of inferior vena cava (IVC) from male Sprague–Dawley rats were suspended between two wires and isometric contraction to phenylephrine (Phe; 10⁻⁵ M) and 96 mM KCl was measured. Acetylcholine (Ach; 10⁻¹⁰ to 10⁻⁵ M) was added and the percentage of venous relaxation was measured. To determine the role of nitric oxide (NO) and prostacyclin (PGI₂), vein relaxation was measured in the presence of the nitric oxide synthase inhibitor N_ω-nitro-L-arginine methyl ester (L-NAME; 3 × 10⁻⁴ M) and the cyclooxygenase inhibitor indomethacin (10⁻⁵ M). To measure the role of hyperpolarization, vein relaxation was measured in the presence of K⁺ channel activator cromakalim (10⁻¹¹ to 10⁻⁶ M), and the nonselective K⁺ channel blocker tetraethylammonium (TEA; 10⁻³ M). To test for the contribution of a specific K⁺ channel, the effects of K⁺ channel blockers: glibenclamide (adenosine triphosphate [ATP]-sensitive K_ATP, 10⁻⁵ M), 4-aminopyridine (4-AP; voltage-dependent K_v, 10⁻³ M), apamin (small conductance Ca²⁺-dependent SK_Ca, 10⁻⁷ M), and iberiotoxin (large conductance Ca²⁺-dependent BK_Ca, 10⁻⁸ M) on Ach-induced relaxation were tested.

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