Vascular smooth muscle contraction involves multiple signal-transduction pathways, the interrelations of which are not completely understood. Our objectives in this project were to compare the effects of phenylephrine (alpha1-adrenergic agonist, angiotensin II (AT1 agonist), clonidine (alpha2-adrenergic agonist) and moxondine (alpha2- adrenergic /I1-imidazoline agonist) on contraction in the rat-tail artery. Functionally, all these agonists cause contraction, but biochemically there are differences in how the result is achieved. We wanted to determine the role of protein kinase C (PKC) in the functional regulation between AT1 and alpha1-adrenergic receptor pathways. In addition, we were interested in elucidating the effects of moxonidine on the rat-tail artery. Our study demonstrates that the alpha1-adrenergic receptor is the major receptor for mediating contraction in the rat-tail artery. The postsynaptic alpha2-adrenergic receptor also plays a significant role in rat-tail artery contraction, but to a lesser extent than the alpha1-adrenergic receptors. Similarly, AT1 receptors are involved in rat-tail artery contraction, but to a lesser extent than the adrenergic receptors. I1 receptors were not found in rat-tail artery contraction. The data also suggest that PKC plays a greater role in the contractile response mediated by AT1 receptor than the alpha1-adrenergic receptor. The AT1 receptor response seems to affect PLD, resulting in PKC effects downstream. We finally, show that moxonidine, a known I1/alpha2-adrenergic agonist, mediates rat-tail artery contraction via the activation of alpha2-and alpha1-adrenergic receptors, and not via specific imidazoline receptors.
","abstract_html":"<p>Vascular smooth muscle contraction involves multiple signal-transduction pathways, the interrelations of which are not completely understood. Our objectives in this project were to compare the effects of phenylephrine (alpha<sub>1</sub>-adrenergic agonist, angiotensin II (AT<sub>1 </sub>agonist), clonidine (alpha<sub>2</sub>-adrenergic agonist) and moxondine (alpha<sub>2</sub>- adrenergic /I<sub>1</sub>-imidazoline agonist) on contraction in the rat-tail artery. Functionally, all these agonists cause contraction, but biochemically there are differences in how the result is achieved. We wanted to determine the role of protein kinase C (PKC) in the functional regulation between AT<sub>1 </sub>and alpha<sub>1</sub>-adrenergic receptor pathways. In addition, we were interested in elucidating the effects of moxonidine on the rat-tail artery. Our study demonstrates that the alpha<sub>1</sub>-adrenergic receptor is the major receptor for mediating contraction in the rat-tail artery. The postsynaptic alpha<sub>2</sub>-adrenergic receptor also plays a significant role in rat-tail artery contraction, but to a lesser extent than the alpha<sub>1</sub>-adrenergic receptors. Similarly, AT<sub>1</sub> receptors are involved in rat-tail artery contraction, but to a lesser extent than the adrenergic receptors. I<sub>1</sub> receptors were not found in rat-tail artery contraction. The data also suggest that PKC plays a greater role in the contractile response mediated by AT<sub>1</sub> receptor than the alpha<sub>1</sub>-adrenergic receptor. The AT<sub>1</sub> receptor response seems to affect PLD, resulting in PKC effects downstream. We finally, show that moxonidine, a known I<sub>1</sub>/alpha<sub>2</sub>-adrenergic agonist, mediates rat-tail artery contraction via the activation of alpha<sub>2</sub>-and alpha<sub>1</sub>-adrenergic receptors, and not via specific imidazoline receptors.</p>","abstract_has_math":false,"creators":["George, Oommen K."],"institution":null,"degree_name":"Doctor of Philosophy (PhD)","degree_level":"Dissertation","degree_discipline":"Physiology","degree_department":null,"school":null,"contributors":["Ramon R. Gonzalez, Jr","Lincoln P. Edwards","Raymond G. Hall, Jr.","George T. Javor","Robert W. Teel"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2003,"date_issued":"2003-06-01T07:00:00Z","date_published":"2003-06-01T07:00:00Z","updated_at":"2026-07-24T02:53:31Z","subjects":["Physiology","Muscle, Smooth -- drug effects -- dissertations; Receptors, Angiotensin -- metabolism; Vasoconstrictor Agents -- pharmacology."],"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/856","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Ramon R. Gonzalez, Jr","Lincoln P. Edwards","Raymond G. Hall, Jr.","George T. Javor","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/856"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Vascular smooth muscle contraction involves multiple signal-transduction pathways, the interrelations of which are not completely understood. Our objectives in this project were to compare the effects of phenylephrine (alpha1-adrenergic agonist, angiotensin II (AT1 agonist), clonidine (alpha2-adrenergic agonist) and moxondine (alpha2- adrenergic /I1-imidazoline agonist) on contraction in the rat-tail artery. Functionally, all these agonists cause contraction, but biochemically there are differences in how the result is achieved. We wanted to determine the role of protein kinase C (PKC) in the functional regulation between AT1 and alpha1-adrenergic receptor pathways. In addition, we were interested in elucidating the effects of moxonidine on the rat-tail artery. Our study demonstrates that the alpha1-adrenergic receptor is the major receptor for mediating contraction in the rat-tail artery. The postsynaptic alpha2-adrenergic receptor also plays a significant role in rat-tail artery contraction, but to a lesser extent than the alpha1-adrenergic receptors. Similarly, AT1 receptors are involved in rat-tail artery contraction, but to a lesser extent than the adrenergic receptors. I1 receptors were not found in rat-tail artery contraction. The data also suggest that PKC plays a greater role in the contractile response mediated by AT1 receptor than the alpha1-adrenergic receptor. The AT1 receptor response seems to affect PLD, resulting in PKC effects downstream. We finally, show that moxonidine, a known I1/alpha2-adrenergic agonist, mediates rat-tail artery contraction via the activation of alpha2-and alpha1-adrenergic receptors, and not via specific imidazoline receptors.
"]},{"key":"dc:title","label":"Title","values":["Comparison of Receptor Efficacies on Vascular Smooth Muscle Contraction"]}]}],"canonical_facts":{"dc:contributor":["Ramon R. Gonzalez, Jr","Lincoln P. Edwards","Raymond G. Hall, Jr.","George T. Javor","Robert W. Teel"],"dc:creator":["George, Oommen K."],"dc:description.abstract":["Vascular smooth muscle contraction involves multiple signal-transduction pathways, the interrelations of which are not completely understood. Our objectives in this project were to compare the effects of phenylephrine (alpha1-adrenergic agonist, angiotensin II (AT1 agonist), clonidine (alpha2-adrenergic agonist) and moxondine (alpha2- adrenergic /I1-imidazoline agonist) on contraction in the rat-tail artery. Functionally, all these agonists cause contraction, but biochemically there are differences in how the result is achieved. We wanted to determine the role of protein kinase C (PKC) in the functional regulation between AT1 and alpha1-adrenergic receptor pathways. In addition, we were interested in elucidating the effects of moxonidine on the rat-tail artery. Our study demonstrates that the alpha1-adrenergic receptor is the major receptor for mediating contraction in the rat-tail artery. The postsynaptic alpha2-adrenergic receptor also plays a significant role in rat-tail artery contraction, but to a lesser extent than the alpha1-adrenergic receptors. Similarly, AT1 receptors are involved in rat-tail artery contraction, but to a lesser extent than the adrenergic receptors. I1 receptors were not found in rat-tail artery contraction. The data also suggest that PKC plays a greater role in the contractile response mediated by AT1 receptor than the alpha1-adrenergic receptor. The AT1 receptor response seems to affect PLD, resulting in PKC effects downstream. We finally, show that moxonidine, a known I1/alpha2-adrenergic agonist, mediates rat-tail artery contraction via the activation of alpha2-and alpha1-adrenergic receptors, and not via specific imidazoline receptors.
"],"dc:identifier":["https://scholarsrepository.llu.edu/etd/856"],"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 -- drug effects -- dissertations; Receptors, Angiotensin -- metabolism; Vasoconstrictor Agents -- pharmacology."],"dc:title":["Comparison of Receptor Efficacies on Vascular Smooth Muscle Contraction"],"thesis:degree_discipline":["Physiology"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Doctor of Philosophy (PhD)"]},"updated_at":"2026-07-24T02:53:31Z"}