An Intramural, Tension-modulating Reflex in the Rat Caudal Artery
type: CreativeWork
description: Electrical field stimulation (EES) of preconstricted arteries causes relaxation. This relaxation is of either neuronal, vascular smooth muscle, and/or endothelial origins. We have shown that EFS-induced relaxation of intact, phenylephrine (PE) preconstricted rat tail artery (RTA) rings was dependent upon the extracellular concentration of Ca++. Inhibiting either nitric oxide (NO) synthesis with N-nitro-L-arginine methyl ester (L-NAME), or the synthesis of cyclic guanosine monophosphate (cGMP) with methylene blue (MB) reduced the EFS-induced relaxation. In addition, inhibition of KCa++-dependent hyperpolarization with tetraethylammonium (TEA), or KATP hyperpolarization with BaCl2 or glibenclamide also reduced EFS-induced relaxation. L-arginine reversed the effect of L-NAME. When either MB and KCl, L-NAME and KCl, or L-NAME and BaCl2 were used, the EFS-induced relaxation was completely inhibited. The EFS-induced relaxation was not inhibited by tetrodotoxin, a voltage-operated Na+ channel antagonist. EFS-induced relaxation was partially inhibited by endothelium denuding. The remaining EFS-induced relaxation in the denuded RTA was inhibited by BaCl2 and KCl. EFS-induced relaxation in the intact, KCl preconstricted RTA was inhibited by L-NAME and MB. Effluent from freshly isolated, bovine aortic endothelial cells (BAEC) exposed to EES relaxed denuded RTA and could be blocked by L-NAME, MB, KCl, and TEA. L-arginine reversed the effect of L-NAME as in the ring experiments. EFS-induced relaxation of intact, pressurized, and PE preconstricted RTA was frequency and voltage-dependent, and inhibited by either L-NAME, BaCl2, or the voltage-operated Ca++ channel antagonist diltiazem. As in all the other studies, L-arginine reversed the effect of L-NAME. Membrane potential recordings of EFS-induced relaxation showed a mean membrane hyperpolarization of -20 mV simultaneously with relaxation. A positive correlation was shown to exist between the initial level of tone and the EFS-ind…
abstract: Electrical field stimulation (EES) of preconstricted arteries causes relaxation. This relaxation is of either neuronal, vascular smooth muscle, and/or endothelial origins. We have shown that EFS-induced relaxation of intact, phenylephrine (PE) preconstricted rat tail artery (RTA) rings was dependent upon the extracellular concentration of Ca++. Inhibiting either nitric oxide (NO) synthesis with N-nitro-L-arginine methyl ester (L-NAME), or the synthesis of cyclic guanosine monophosphate (cGMP) with methylene blue (MB) reduced the EFS-induced relaxation. In addition, inhibition of KCa++-dependent hyperpolarization with tetraethylammonium (TEA), or KATP hyperpolarization with BaCl2 or glibenclamide also reduced EFS-induced relaxation. L-arginine reversed the effect of L-NAME. When either MB and KCl, L-NAME and KCl, or L-NAME and BaCl2 were used, the EFS-induced relaxation was completely inhibited. The EFS-induced relaxation was not inhibited by tetrodotoxin, a voltage-operated Na+ channel antagonist. EFS-induced relaxation was partially inhibited by endothelium denuding. The remaining EFS-induced relaxation in the denuded RTA was inhibited by BaCl2 and KCl. EFS-induced relaxation in the intact, KCl preconstricted RTA was inhibited by L-NAME and MB. Effluent from freshly isolated, bovine aortic endothelial cells (BAEC) exposed to EES relaxed denuded RTA and could be blocked by L-NAME, MB, KCl, and TEA. L-arginine reversed the effect of L-NAME as in the ring experiments. EFS-induced relaxation of intact, pressurized, and PE preconstricted RTA was frequency and voltage-dependent, and inhibited by either L-NAME, BaCl2, or the voltage-operated Ca++ channel antagonist diltiazem. As in all the other studies, L-arginine reversed the effect of L-NAME. Membrane potential recordings of EFS-induced relaxation showed a mean membrane hyperpolarization of -20 mV simultaneously with relaxation. A positive correlation was shown to exist between the initial level of tone and the EFS-ind…
author: Geary, Greg G.
language: English
keywords: Physiology, Muscle, Smooth, Vascular -- drug effects; Rats; Endothelium-Derived Relaxing Factor -- pharmacology Electronic Stimulation; Muscle Relaxation; Arteries -- physiology
date published: 1994-06-01T07:00:00Z
date modified: 2026-07-24T02:53:44Z
provider: Loma Linda University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Loma Linda University