{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/23416"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/23416","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Modulation of calcium channel expression in cardiac myocytes of rats during growth hormone-induced growth or normal postnatal development","abstract":"Voltage-dependent Ca$\\sp{2+}$ currents of cardiac myocytes were studied using patch-clamp techniques. T-type Ca$\\sp{2+}$ current density of atrial myocytes was found to be positively correlated with the plasma growth hormone levels and the growth rate of atrial myocytes in normally developing Sprague-Dawley rats, adult Wistar-Furth rats made to reenter an active growth phase following implantation of a growth hormone-secreting tumor, and mutant dwarf rats with retarded growth due to a specific deficiency in pituitary growth hormone synthesis. The voltage and time dependent activation and inactivation of T-type Ca$\\sp{2+}$ current are not changed in spite of the changes in T-current density. The unchanged macroscopic current properties and constant single T-channel current suggest that the change in T-current density is likely due to a change in membrane density of T-type Ca$\\sp{2+}$ channels rather than a change in the channel protein itself. Though atrial T-current density increases when plasma growth hormone levels are high, it is difficult to prove the involvement of growth hormone in regulating Ca$\\sp{2+}$ channel expression because of the complication from other hormones and growth factors. It is also possible that the correlation between atrial T-current density and plasma growth hormone levels is merely accidental. The up-regulation of T-type Ca$\\sp{2+}$ channel density during active growth is specific for atrial myocytes, since T-type Ca$\\sp{2+}$ current is not induced in ventricular myocytes from the tumor-bearing rats. High T-current density during the period of active growth of atrial myocytes supports the idea that T-type Ca$\\sp{2+}$ channels may have some role in embryonic/postnatal development in certain tissues. L-type Ca$\\sp{2+}$ channels are regulated in a different way. In contrast to T-type Ca$\\sp{2+}$ current, L-type Ca$\\sp{2+}$ current density remains constant in both atrial and ventricular cells from rats during either normal postnatal development in young rats or induced active growth in adult rats bearing growth hormone-secreting tumors. The constant L-current density may be important to keep up Ca$\\sp{2+}$ influx with increased cell size to support normal cardiac contraction.","abstract_html":"Voltage-dependent Ca$\\sp{2+}$ currents of cardiac myocytes were studied using patch-clamp techniques. T-type Ca$\\sp{2+}$ current density of atrial myocytes was found to be positively correlated with the plasma growth hormone levels and the growth rate of atrial myocytes in normally developing Sprague-Dawley rats, adult Wistar-Furth rats made to reenter an active growth phase following implantation of a growth hormone-secreting tumor, and mutant dwarf rats with retarded growth due to a specific deficiency in pituitary growth hormone synthesis. The voltage and time dependent activation and inactivation of T-type Ca$\\sp{2+}$ current are not changed in spite of the changes in T-current density. The unchanged macroscopic current properties and constant single T-channel current suggest that the change in T-current density is likely due to a change in membrane density of T-type Ca$\\sp{2+}$ channels rather than a change in the channel protein itself. Though atrial T-current density increases when plasma growth hormone levels are high, it is difficult to prove the involvement of growth hormone in regulating Ca$\\sp{2+}$ channel expression because of the complication from other hormones and growth factors. It is also possible that the correlation between atrial T-current density and plasma growth hormone levels is merely accidental. The up-regulation of T-type Ca$\\sp{2+}$ channel density during active growth is specific for atrial myocytes, since T-type Ca$\\sp{2+}$ current is not induced in ventricular myocytes from the tumor-bearing rats. High T-current density during the period of active growth of atrial myocytes supports the idea that T-type Ca$\\sp{2+}$ channels may have some role in embryonic/postnatal development in certain tissues. L-type Ca$\\sp{2+}$ channels are regulated in a different way. In contrast to T-type Ca$\\sp{2+}$ current, L-type Ca$\\sp{2+}$ current density remains constant in both atrial and ventricular cells from rats during either normal postnatal development in young rats or induced active growth in adult rats bearing growth hormone-secreting tumors. The constant L-current density may be important to keep up Ca$\\sp{2+}$ influx with increased cell size to support normal cardiac contraction.","abstract_has_math":true,"creators":["Xu, Xiao Ping"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Physiology","degree_department":null,"school":null,"contributors":["Best, Philip M."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-05-07T14:13:24Z","date_published":"2011-05-07T14:13:24Z","updated_at":"2026-07-22T22:25:21Z","subjects":["Biology, Animal Physiology"],"languages":["eng"],"rights":["Copyright 1992 Xu, Xiao Ping"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9215913","(UMI)AAI9215913"],"render_values":[{"text":"AAI9215913","href":null,"code":true},{"text":"(UMI)AAI9215913","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/23416","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Best, Philip M."]},{"key":"dc:creator","label":"Author","values":["Xu, Xiao Ping"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2011-05-07T14:13:24Z","10000-01-01","1992"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Physiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Animal Physiology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 1992 Xu, Xiao Ping"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9215913","(UMI)AAI9215913","http://hdl.handle.net/2142/23416"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Voltage-dependent Ca$\\sp{2+}$ currents of cardiac myocytes were studied using patch-clamp techniques. T-type Ca$\\sp{2+}$ current density of atrial myocytes was found to be positively correlated with the plasma growth hormone levels and the growth rate of atrial myocytes in normally developing Sprague-Dawley rats, adult Wistar-Furth rats made to reenter an active growth phase following implantation of a growth hormone-secreting tumor, and mutant dwarf rats with retarded growth due to a specific deficiency in pituitary growth hormone synthesis. The voltage and time dependent activation and inactivation of T-type Ca$\\sp{2+}$ current are not changed in spite of the changes in T-current density. The unchanged macroscopic current properties and constant single T-channel current suggest that the change in T-current density is likely due to a change in membrane density of T-type Ca$\\sp{2+}$ channels rather than a change in the channel protein itself. Though atrial T-current density increases when plasma growth hormone levels are high, it is difficult to prove the involvement of growth hormone in regulating Ca$\\sp{2+}$ channel expression because of the complication from other hormones and growth factors. It is also possible that the correlation between atrial T-current density and plasma growth hormone levels is merely accidental. The up-regulation of T-type Ca$\\sp{2+}$ channel density during active growth is specific for atrial myocytes, since T-type Ca$\\sp{2+}$ current is not induced in ventricular myocytes from the tumor-bearing rats. High T-current density during the period of active growth of atrial myocytes supports the idea that T-type Ca$\\sp{2+}$ channels may have some role in embryonic/postnatal development in certain tissues. L-type Ca$\\sp{2+}$ channels are regulated in a different way. In contrast to T-type Ca$\\sp{2+}$ current, L-type Ca$\\sp{2+}$ current density remains constant in both atrial and ventricular cells from rats during either normal postnatal development in young rats or induced active growth in adult rats bearing growth hormone-secreting tumors. The constant L-current density may be important to keep up Ca$\\sp{2+}$ influx with increased cell size to support normal cardiac contraction.","Made available in DSpace on 2011-05-07T14:13:24Z (GMT). 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T-type Ca$\\sp{2+}$ current density of atrial myocytes was found to be positively correlated with the plasma growth hormone levels and the growth rate of atrial myocytes in normally developing Sprague-Dawley rats, adult Wistar-Furth rats made to reenter an active growth phase following implantation of a growth hormone-secreting tumor, and mutant dwarf rats with retarded growth due to a specific deficiency in pituitary growth hormone synthesis. The voltage and time dependent activation and inactivation of T-type Ca$\\sp{2+}$ current are not changed in spite of the changes in T-current density. The unchanged macroscopic current properties and constant single T-channel current suggest that the change in T-current density is likely due to a change in membrane density of T-type Ca$\\sp{2+}$ channels rather than a change in the channel protein itself. Though atrial T-current density increases when plasma growth hormone levels are high, it is difficult to prove the involvement of growth hormone in regulating Ca$\\sp{2+}$ channel expression because of the complication from other hormones and growth factors. It is also possible that the correlation between atrial T-current density and plasma growth hormone levels is merely accidental. The up-regulation of T-type Ca$\\sp{2+}$ channel density during active growth is specific for atrial myocytes, since T-type Ca$\\sp{2+}$ current is not induced in ventricular myocytes from the tumor-bearing rats. High T-current density during the period of active growth of atrial myocytes supports the idea that T-type Ca$\\sp{2+}$ channels may have some role in embryonic/postnatal development in certain tissues. L-type Ca$\\sp{2+}$ channels are regulated in a different way. In contrast to T-type Ca$\\sp{2+}$ current, L-type Ca$\\sp{2+}$ current density remains constant in both atrial and ventricular cells from rats during either normal postnatal development in young rats or induced active growth in adult rats bearing growth hormone-secreting tumors. The constant L-current density may be important to keep up Ca$\\sp{2+}$ influx with increased cell size to support normal cardiac contraction.","Made available in DSpace on 2011-05-07T14:13:24Z (GMT). No. of bitstreams: 2 license.txt: 4922 bytes, checksum: 910b249b4beec47e7ab768910c8f966f (MD5) 9215913.pdf: 4348605 bytes, checksum: f289efa7e92137c370193a2d6fb50567 (MD5) Previous issue date: 1992","Item marked as restricted to the 'UIUC Users [automated]' Group (id=2) by Howard Ding (hding2@illinois.edu) on 2011-05-07T15:04:20Z Item is restricted indefinitely.","Restriction data tranferred 2014-07-01T11:30:43-05:00 Original Data Group with Access UIUC Users [automated] Release Date: none Reason: ETDs are only available to UIUC Users without author permission","ETDs are only available to UIUC Users without author permission","U of I Only"],"dc:identifier":["AAI9215913","(UMI)AAI9215913","http://hdl.handle.net/2142/23416"],"dc:language":["eng"],"dc:rights":["Copyright 1992 Xu, Xiao Ping"],"dc:subject":["Biology, Animal Physiology"],"dc:title":["Modulation of calcium channel expression in cardiac myocytes of rats during growth hormone-induced growth or normal postnatal development"],"dc:type":["text"],"thesis:degree_discipline":["Physiology"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois at Urbana-Champaign"]},"updated_at":"2026-07-22T22:25:21Z"}