{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/77678"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/77678","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Sympathetic Innervation of the Rat Adrenal Cortex and Its Effects on the Compensatory Adrenal Cortical Growth Response to Unilateral Adrenalectomy (Catecholamine, Endocrine, Splanchnic Nerve, Cell Proliferation)","abstract":"Histofluorescence techniques were used to demonstrate that rat adrenal cortex is innervated by catecholaminergic nerve fibers which enter the adrenal in arterial plexuses and distribute among zona glomerulosa cells. Ultrastructurally, axonal varicosities containing small (30-60 nm) dense-cored vesicles abut on glomerulosa cells and blood vessels. This innervation was eliminated after neonatal sympathectomy with guanethidine or 6-hydroxydopamine, but unaffected by splanchnic nerve ligation or suprarental ganglion extirpation. Sympathetic innervation was shown to mediate compensatory adrenal cortical growth, a cell proliferation response which occurs in the remaining adrenal after unilateral adrenalectomy. In unilaterally adrenalectomized, sympathectomized rats the characteristic increase in adrenal weight in the remaining adrenal was attenuated and not accompanied by the usual increase in DNA content. The effects of sympathectomy on compensatory adrenal growth were not attributable to suppression of the renin-angiotensin system because direct inhibition of angiotensin II and III synthesis with Enalapril (20 mg/kg orally) did not affect compensatory adrenal growth. Furthermore, potassium-induced stimulation of aldosterone secretion did not prevent the increase in adrenal DNA content associated with compensatory growth. Compensatory adrenal growth was observed in animals treated with the (beta)-blockers propranolol (10 or 25 mg/kg) and Sotalol (25 or 50 mg/kg), although vehicle-injected animals failed to show the response. These results suggested that (beta)-adrenergic receptor blockade released a stress-related inhibition of the compensatory adrenal growth response. Adrenal DNA content was increased after 7 days of propranolol treatment suggesting that basal adrenal cortical cell proliferation may also be under inhibitory sympathetic (or central) (beta)-adrenergic inhibition. We propose that peripheral (beta)-adrenergic activity inhibits the adrenal cell proliferation but unilateral adrenalectomy may cause disinhibition, thereby triggering the compensatory adrenal growth response.","abstract_html":"Histofluorescence techniques were used to demonstrate that rat adrenal cortex is innervated by catecholaminergic nerve fibers which enter the adrenal in arterial plexuses and distribute among zona glomerulosa cells. Ultrastructurally, axonal varicosities containing small (30-60 nm) dense-cored vesicles abut on glomerulosa cells and blood vessels. This innervation was eliminated after neonatal sympathectomy with guanethidine or 6-hydroxydopamine, but unaffected by splanchnic nerve ligation or suprarental ganglion extirpation. Sympathetic innervation was shown to mediate compensatory adrenal cortical growth, a cell proliferation response which occurs in the remaining adrenal after unilateral adrenalectomy. In unilaterally adrenalectomized, sympathectomized rats the characteristic increase in adrenal weight in the remaining adrenal was attenuated and not accompanied by the usual increase in DNA content. The effects of sympathectomy on compensatory adrenal growth were not attributable to suppression of the renin-angiotensin system because direct inhibition of angiotensin II and III synthesis with Enalapril (20 mg/kg orally) did not affect compensatory adrenal growth. Furthermore, potassium-induced stimulation of aldosterone secretion did not prevent the increase in adrenal DNA content associated with compensatory growth. Compensatory adrenal growth was observed in animals treated with the (beta)-blockers propranolol (10 or 25 mg/kg) and Sotalol (25 or 50 mg/kg), although vehicle-injected animals failed to show the response. These results suggested that (beta)-adrenergic receptor blockade released a stress-related inhibition of the compensatory adrenal growth response. Adrenal DNA content was increased after 7 days of propranolol treatment suggesting that basal adrenal cortical cell proliferation may also be under inhibitory sympathetic (or central) (beta)-adrenergic inhibition. We propose that peripheral (beta)-adrenergic activity inhibits the adrenal cell proliferation but unilateral adrenalectomy may cause disinhibition, thereby triggering the compensatory adrenal growth response.","abstract_has_math":false,"creators":["Kleitman, Naomi"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Neuroscience","degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-05-14T15:20:50Z","date_published":"2015-05-14T15:20:50Z","updated_at":"2026-07-22T22:26:11Z","subjects":["Biology, Neuroscience"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(UMI)AAI8521805"],"render_values":[{"text":"(UMI)AAI8521805","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/77678","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Kleitman, Naomi"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-05-14T15:20:50Z","10000-01-01","1985"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Neuroscience"]},{"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, Neuroscience"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/77678","(UMI)AAI8521805"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Histofluorescence techniques were used to demonstrate that rat adrenal cortex is innervated by catecholaminergic nerve fibers which enter the adrenal in arterial plexuses and distribute among zona glomerulosa cells. Ultrastructurally, axonal varicosities containing small (30-60 nm) dense-cored vesicles abut on glomerulosa cells and blood vessels. This innervation was eliminated after neonatal sympathectomy with guanethidine or 6-hydroxydopamine, but unaffected by splanchnic nerve ligation or suprarental ganglion extirpation. Sympathetic innervation was shown to mediate compensatory adrenal cortical growth, a cell proliferation response which occurs in the remaining adrenal after unilateral adrenalectomy. In unilaterally adrenalectomized, sympathectomized rats the characteristic increase in adrenal weight in the remaining adrenal was attenuated and not accompanied by the usual increase in DNA content. The effects of sympathectomy on compensatory adrenal growth were not attributable to suppression of the renin-angiotensin system because direct inhibition of angiotensin II and III synthesis with Enalapril (20 mg/kg orally) did not affect compensatory adrenal growth. Furthermore, potassium-induced stimulation of aldosterone secretion did not prevent the increase in adrenal DNA content associated with compensatory growth. Compensatory adrenal growth was observed in animals treated with the (beta)-blockers propranolol (10 or 25 mg/kg) and Sotalol (25 or 50 mg/kg), although vehicle-injected animals failed to show the response. These results suggested that (beta)-adrenergic receptor blockade released a stress-related inhibition of the compensatory adrenal growth response. Adrenal DNA content was increased after 7 days of propranolol treatment suggesting that basal adrenal cortical cell proliferation may also be under inhibitory sympathetic (or central) (beta)-adrenergic inhibition. We propose that peripheral (beta)-adrenergic activity inhibits the adrenal cell proliferation but unilateral adrenalectomy may cause disinhibition, thereby triggering the compensatory adrenal growth response.","Made available in DSpace on 2015-05-14T15:20:50Z (GMT). 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Ultrastructurally, axonal varicosities containing small (30-60 nm) dense-cored vesicles abut on glomerulosa cells and blood vessels. This innervation was eliminated after neonatal sympathectomy with guanethidine or 6-hydroxydopamine, but unaffected by splanchnic nerve ligation or suprarental ganglion extirpation. Sympathetic innervation was shown to mediate compensatory adrenal cortical growth, a cell proliferation response which occurs in the remaining adrenal after unilateral adrenalectomy. In unilaterally adrenalectomized, sympathectomized rats the characteristic increase in adrenal weight in the remaining adrenal was attenuated and not accompanied by the usual increase in DNA content. The effects of sympathectomy on compensatory adrenal growth were not attributable to suppression of the renin-angiotensin system because direct inhibition of angiotensin II and III synthesis with Enalapril (20 mg/kg orally) did not affect compensatory adrenal growth. Furthermore, potassium-induced stimulation of aldosterone secretion did not prevent the increase in adrenal DNA content associated with compensatory growth. Compensatory adrenal growth was observed in animals treated with the (beta)-blockers propranolol (10 or 25 mg/kg) and Sotalol (25 or 50 mg/kg), although vehicle-injected animals failed to show the response. These results suggested that (beta)-adrenergic receptor blockade released a stress-related inhibition of the compensatory adrenal growth response. Adrenal DNA content was increased after 7 days of propranolol treatment suggesting that basal adrenal cortical cell proliferation may also be under inhibitory sympathetic (or central) (beta)-adrenergic inhibition. We propose that peripheral (beta)-adrenergic activity inhibits the adrenal cell proliferation but unilateral adrenalectomy may cause disinhibition, thereby triggering the compensatory adrenal growth response.","Made available in DSpace on 2015-05-14T15:20:50Z (GMT). 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