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신장에서 V2 - 수용체를 통한 옥시토신의 aquaporin - 2 발현 조절
전은실(Un Sil Jeon),나기영(Ki Young Na),오윤규(Yoon Kyu Oh),한진석(Jin Suk Han),이정상(Jung Sang Lee),주권욱(Kwon Wook Joo),김진(Jin Kim),김근호(Gheun Ho Kim) 대한내과학회 2002 대한내과학회지 Vol.62 No.3
Background: Oxytocin is a nonapeptide hormone secreted from posterior pituitary gland and has a very similar structure to vasopressin. The aquaporin-2 (AQP2) water channel is predominantly expressed in the kidney and plays a key role in regulation of water permeability of mammalian collecting duct, exerted by both short-term and long-term vasopressin action. We speculated that oxytocin may be involved in some part of vasopressin-independent urinary concentrating mechanism by regulating AQP2 trafficking in the kidney. Methods: This study was undertaken to investigate whether and how the acute stimulation of oxytocin induces changes in AQP2 localization in the kidney. Immunohistochemistry and semiquantitative immunoblotting of AQP2 were carried out from Sprague-Dawley rat kidneys after a single intraperitoneal injection of oxytocin with or without pretreatment of a vasopressin-2 receptor (V2R) antagonist. Results: Urinary cAMP excretion was increased by oxytocin administration. Immuno- histochemistry of inner medullary collecting duct (IMCD) revealed that AQP2 was shifted from diffuse cytoplasmic localization in controls to the apical and basolateral membrane domains in oxytocin-treated rats. This pattern of AQP2 redistribution was noted in connecting tubule, cortical collecting duct and outer medullary collecting duct as in IMCD, although the tendency to basolateral localization was somewhat less. Semiquantitative immunoblotting of membrane fractions of whole kidney homogenates was also used t o assess redistribution of AQP2. The band density ratio of theplasma membrane-rich fraction over cyoplasmic vesicle- rich fraction was higher in oxytocin- treated rat s than in controls (3.64 ±0.60 vs. 1.09 ±0.14, p<0.05>. Regarding the receptor pathway of oxytocin action in the kidney, we found that pretreatment with a V2 R ant antagonist (OPC- 31260) blocked redistribution of AQP2 which was induced by oxytocin. Conclusion: In conclusion, oxytocin induces a V2 R- mediated redistribution of AQP2- containing cytoplasmic vesicles t o both apical and basolateral plasma membrane domains in r at kidney. Oxytocin may be one of the facts or that accounts for vasopressin - independent AQP2 t argeting in the kidney.(Korean J Med 62:268-277, 2002)
Oxytocin에 의한 내수질집합관의 cAMP 생성 및 요배설의 변화
한진석(Jin Suk Han),이정상(Jung Sang Lee),김강석(Kang Seock Kim),허우성(Woo Seong Huh),김연수(Yon Su Kim),전은실(Un Sil Jeon),주권욱(Kwon Wook Joo),안규리(Curie Ahn),김성권(Suhnggwon Kim),이중건(Jung Geon Lee),나기영(Ki Young Na),정우경 대한신장학회 2000 Kidney Research and Clinical Practice Vol.19 No.1
N/A Oxytocin, like vasopressin, has been known to act in the IMCD by the activation of adenylyl cyclase through V2 receptor, but the exact mechanism of its action remains to be elucidated. To prove whether oxytocin is involved in the activation of adenylyl cyclase in the renal collecting duct, we measured the cAMP production and urinary cAMP excretion rate. After single IMCD segments of Sprague-Dawley rats were microdissected and treated with different con- centrations of vasopressin(10pM, 10nM) and oxytocin (10pM, 10nM), cAMP production was measured. Urinary cAMP excretion rate was measured after dehydration and intraperitoneal injection of vasopressin and oxytocin. The results are as follows. 1) cAMP production in single IMCD was significantly increased in vasopressin group(10pM: 48,9±4.7(mean±SE), 10nM:94.6±5.3fmol/mm) and oxy-tocin group(10pM: 11.3±2.9, 10nM: 65.7±6.1fmol/mm) compared with that in the control(3.2±0.2fmol/ mm). 2) Urine volume was significantly decreased in dehydration group(40±7μl/hour) and vasopressin group(420±120μl/hour), but urine volume of oxytocin group(1,480±230μl/hour) was not different from that of control(1,550±120μl/hour). Urine osmolality was significantly increased in all experimental groups(control: 737.0±132.6, dehydration group : 2,463.9± 412.5, vasopressin group : 1,702±412.5, oxytocin group 1,293.4±117.9mOsm/kg). Urinary cAMP excretion rate was significantly increased in dehydration group(4,149.5±1,072.3pmol/hour) and oxytocin group(4,843.3±2,341.8pmol/hour), but not in vasopressin group(1,358.1±690.2pmol/hour), compared with that in control(49±10.7pmoVhour). These results suggest that oxytacin has anti-diuretic effect by the activation of adenylyl cyclase through V2 receptor.
만성신부전에서 염류코르티코이드 투여가 포타시움 평형과 요 암모늄 배설에 미치는 효과
한진석(Jin Suk Han),이정상(Jung Sang Lee),김강석(Kang Seock Kim),허우성(Woo Seong Huh),전은실(Un Sil Jeon),이서진(Seo Jin Lee),주권욱(Kwon Wook Joo),김성권(Suhnggwon Kim),진호준(Ho Jun Chin),조윤숙(Yun Suk Cho) 대한신장학회 2000 Kidney Research and Clinical Practice Vol.19 No.2
N/A Mineralocorticoids influences on acid-base homeo-stasis by the regulation of urine acidification. But its mechanism of acion is not well known in human. This study compared the acid-base status and the indices of urine acidification before and after mineralocorticoid administration in human, and analyzed the effect of mineralocorticoids on human acid-base homeostasis. We administered 9a-fludrocortisone in 6 chronic renal failure patients and 6 normal controls 0.5mg daily for 7 days. The results were as following ' 1) After administration of 9a-fludrocortisone in patients group, serum aldosterone level changed from 120.2±71.0pg/mL to 44.8±32.2pg/mL(mean±SD, p< 0.05). Serum HCO- level was not changed. Urine ammonium excretion was incresed from 24.6±12.3 mmol/day to 43.7±19.0(p<0.05), but there were no change in urine pH and urine anion gap, Serum potassium level decreased from 5.5±0.7mBq/L to 4.1±0.5mEq/L(p<0.05), and TTKG increased from 3.9 to 8.9(p<0.05). 2) After administration of 9a-fludrocortisone in control group, serum aldosterone level changed from 99.7±44.5pg/mL to 25.1±3 mL(p<0.05). Serum HCO- level was not changed. Urine ammonium ex-cretion was incresed from 44.3±21.6mmoVday to 76.3±19.6(p<0.05), but there were no change in urine pH and urine anion gap. Serum potassium level decreased from 4.8±0.5mEq/L to 3.9±0.2mHq/L(p< 0.05), but there was no change in TTKG. 3) No patient or control showed any discomfort after 9-fludrocortisoneadministration, and there was no elevation in diastolic blood pressure, increase in body weight, electrolyte abnormality. In summary, after 9α-fludrocortisane administration, urinary ammonium excretion increased in both patients and control group, and this phenomenon occured with correction of hyperkalemia without urine pH change. This result implies urinary ammonium excretion increase by mineralocorticoid. In human increase in renal distal acidification by mineralocorticoid is due to increase in renal ammo- niagenesis rather than stimulation on proton excretion.
급성 포르피리아 발작중 발생한 심한 저나트륨혈증 1 예
정철원(Chul Won Jung),전은실(Un Sil Jeon),정우경(Woo Kyung Chung),김원석(Won Seog Kim),조종태(Jong Tai Cho),안규리(Cu Rie Ahn),한진석(Jin Suk Han),김성권(Suhng Gwon Kim),이정상(Jung Sang Lee) 대한내과학회 1995 대한내과학회지 Vol.49 No.2
Hepatic porphyria shows impaired heme biosynthesis predominantly in the liver and usually presents with abdominal pain, vomiting, photosensitivity and neurologic abnormalities and sometimes with hyponatremia accompanied by syndrome of inappropriate antidiuretic hormone secretion(SIADH). We report a case seemed to be a hereditary coproporphyria presenting with acute abdominal pain and vomiting. She had severe hyponatremia with the feature of SIADH and peripheral neuropathy which was provoked by the ingestion of alcohol, poor oral intake and by the administration of imipramine. She was thought to have hereditary coproporphyria by the clinical feature, stool porphyrin and quantitation of the 24 hour urine δ-aminolevulinic acid, porpho-bilinogen and porphyrins. Supportive treatment with NaCI infusion and propranolol resulted in symptomatic recovery and she was discharged after education of precipitating factors.
일반연제 발표 : 기능검사로 진단된 Gitelman Syndrome 환자 신조직의 Na-C1 Cotransporter(NCCT) 결손
장혜련 ( Jang Hye Lyeon ),이재욱 ( Lee Jae Ug ),주권욱 ( Ju Gwon Ug ),김근호 ( Kim Geun Ho ),전은실 ( Jeon Eun Sil ),안규리 ( An Gyu Li ),한진석 ( Han Jin Seog ),김성권 ( Kim Seong Gwon ),이정상 ( Lee Jeong Sang ),김진 ( Kim Jin 대한신장학회 2003 춘계학술대회 초록집 Vol.22 No.1