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-induced relaxation. It can be concluded that the vascular smooth muscle contains an endogenous hyperpolarization mechanism that regulates initial changes in arterial tone. Higher arterial tension causes the release of NO and another hyperpolarization factor from the endothelium which function to further regulate arterial tone.
","abstract_html":"<p>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 K<sub>Ca++</sub>-dependent hyperpolarization with tetraethylammonium (TEA), or K<sub>ATP</sub> hyperpolarization with BaCl<sub>2</sub> 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 BaCl<sub>2</sub> 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 BaCl<sub>2</sub> 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, BaCl<sub>2</sub>, 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-induced relaxation. It can be concluded that the vascular smooth muscle contains an endogenous hyperpolarization mechanism that regulates initial changes in arterial tone. Higher arterial tension causes the release of NO and another hyperpolarization factor from the endothelium which function to further regulate arterial tone.</p>","abstract_has_math":false,"creators":["Geary, Greg G."],"institution":null,"degree_name":"Doctor of Philosophy (PhD)","degree_level":"Dissertation","degree_discipline":"Physiology","degree_department":null,"school":null,"contributors":["Ramon R. Gonzales, Jr.","George Maeda","Robert W. Teel","Raymond G. Hall, Jr.","Marvin A. Peters"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":1994,"date_issued":"1994-06-01T07:00:00Z","date_published":"1994-06-01T07:00:00Z","updated_at":"2026-07-24T02:53:44Z","subjects":["Physiology","Muscle, Smooth, Vascular -- drug effects; Rats; Endothelium-Derived Relaxing Factor -- pharmacology Electronic Stimulation; Muscle Relaxation; Arteries -- physiology"],"languages":["English"],"rights":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://scholarsrepository.llu.edu/etd/1382","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Ramon R. Gonzales, Jr.","George Maeda","Robert W. 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The author retains all other copyrights."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarsrepository.llu.edu/etd/1382"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["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-induced relaxation. It can be concluded that the vascular smooth muscle contains an endogenous hyperpolarization mechanism that regulates initial changes in arterial tone. Higher arterial tension causes the release of NO and another hyperpolarization factor from the endothelium which function to further regulate arterial tone.
"]},{"key":"dc:title","label":"Title","values":["An Intramural, Tension-modulating Reflex in the Rat Caudal Artery"]}]}],"canonical_facts":{"dc:contributor":["Ramon R. Gonzales, Jr.","George Maeda","Robert W. Teel","Raymond G. Hall, Jr.","Marvin A. Peters"],"dc:creator":["Geary, Greg G."],"dc:description.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-induced relaxation. It can be concluded that the vascular smooth muscle contains an endogenous hyperpolarization mechanism that regulates initial changes in arterial tone. Higher arterial tension causes the release of NO and another hyperpolarization factor from the endothelium which function to further regulate arterial tone.
"],"dc:identifier":["https://scholarsrepository.llu.edu/etd/1382"],"dc:language":["English"],"dc:rights":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."],"dc:subject":["Physiology","Muscle, Smooth, Vascular -- drug effects; Rats; Endothelium-Derived Relaxing Factor -- pharmacology Electronic Stimulation; Muscle Relaxation; Arteries -- physiology"],"dc:title":["An Intramural, Tension-modulating Reflex in the Rat Caudal Artery"],"thesis:degree_discipline":["Physiology"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Doctor of Philosophy (PhD)"]},"updated_at":"2026-07-24T02:53:44Z"}