• Title, Summary, Keyword: Vasopressin

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Analysis of Vasopressin-Induced $Ca^{2+}$ Increase in Rat Hepatocytes

  • Kim, Hyun-Sook;Fumikazu-Okajima;Im, Dong-Soon
    • Archives of Pharmacal Research
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    • v.26 no.1
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    • pp.64-69
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    • 2003
  • To analyze vasopressin-induced $Ca^{2+}$ increase in liver cells, rat hepatocytes were isolated and attached to collagen-coated cover slips. Using fura-2, a $Ca^{2+}$-sensing dye, changes in intracellular $Ca^{2+}$ concentration by vasopressin were monitored. Results in this communication suggested that vasopressin-induced $Ca^{2+}$ increase were composed of both $Ca^{2+}$ release from internal $Ca^{2+}$ stores and influx from the plasma membrane. The $Ca^{2+}$ influx consisted of two distinguishable components. One was dependent on the presence of vasopressin and the other was not. SK&F96365 blocked vasopressin-induced $Ca^{2+}$ influx in a dose-dependent manner. Vasopressin-induced $Ca^{2+}$ release from internal stores diminished in a primary culture of hepatocytes according to the culture time. However, changes in vasopressin-induced $Ca^{2+}$ influx across the plasma membrane differed from changes in the $Ca^{2+}$ release from internal stores, suggesting two separate signalings from receptor activation to internal stores and to the plasma membrane.

Melanin-dispersing Effect of Vasopressin on Frog Skin Melanocyte (Vasopressin의 멜라닌 확산작용에 대하여)

  • Hong, Seung-Kil
    • The Korean journal of physiology & pharmacology
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    • v.7 no.2
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    • pp.59-66
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    • 1973
  • It has been reported that vasopressin disperse the melanophore granule of frog skin. The author used hypophysectomized and adrenergic receptor blockaded animals in order to define the mechanism of vasopressin on the melanopore pigment of frog skin. The Rana niglomaculata which could be found in the Seoul area were used on this experiment. The amount of the following drugs were injected into the lymphatic sac of the frog; vaospressin $(0.05\;{\mu}g/g\;B.W.)$, dibenzylin $(0.05\;{\mu}g/g\;B.W.)$, and propranolol $(0.01\;{\mu}g/g\;B.W.)$. The following results were observed; 1. Vasopressin dispersed the melanin granules of melanocyte of frog skin. 2. The melanin granule dispersion activity of vasopressin was observed on the hypophysectomized frog. 3. The melanin granule dispersion was observed on the adrenergic receptor blockaded frog with dibenzylin or propranolol respectively, especially the later one was found to be more obvious. 4. The melanin granule dispersion was observed on the frog which was injected with vasopressin after alpha-receptor or beta-receptor blockade and the later one was found to be more obvious. 5. The melanin granule dispersion was more effective with the blockade of beta-receptor after the treatment with vasopressin on hypophysectomized frog.

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The Effects of Prolactin and Vasopressin on the Regulation of Amniotic Fluid Volume and Its $Na^{+}$ Concentration through the Membrane Surrounding Amniotic Fluid

  • Kim, Dong-Wook;Kim, Sang-Jeong;Sung, Ho-Kyung
    • The Korean journal of physiology & pharmacology
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    • v.29 no.1
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    • pp.81-89
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    • 1995
  • The effects of prolactin and vasopressin on the regulation of amniotic fluid (AF) volume and its $Na^{+}$ concentration $([Na^{+}])$ through the membrane surrounding the AF during increase in AF volume due to fetal urination were studied. About 70% of AF volume was replaced with normal isotonic saline solution. Isotonic saline solution (0.5 ml) containing Censored and LiCl was introduced into each amniotic sac. Vasopressin (25 ng/ml) or prolactin (1 mg/ml) of AF was then injected into experimental amniotic sac. The concentrations of Congored, $Li^{+}$, and $Na^{+}$ were measured at 30 and 60 min intervals after injection. Af samples with decreased Censored concentration ([CR]) during the period of 30 - 60 min were analyzed. The percentage change of $[Na^{+}]$ and the rate of $Li^{+}$ movement during this period were calculated, and the effects of vasopressin and prolactin on them were evaluated. Fellowing results were obtained: 1. The rate of reduction of [CR] in the AF was retarded by vasopressin or prolactin injection. 2. The rate of reduction of $[Li^{+}]$ in the AF was also retarded by vasopressin or prolactin injection. 3. The rate of reduction of $[Li^{+}]$ in the AF was less retarded by vasopressin than that of [CR]. 4. $[Na^{+}]$ changed to approach to the normal level, but this was markedly retarded by prolactin injection. 5. Direction of $Li^{+}$ movement was correlated with the change in $[Na^{+}]$ but it always moved out of the amniotic sac even when the $[Na^{+}]$ increased in vasopressin injected AF. From the above results, it is suggested that vasopressin in the AF triggers the fetus to urinate, and then the membranes surrounding the AF regulate osmolarity by efflux of $Na^{+}$. We suggest that prolactin facilitates water outflow across the amniotic membrane during increase in AF volume, in contrast to a constant volume, whereas regulation of $[Na^{+}]$ is partly restricted by prolactin.

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Diuretic Action of Vasopressin (바소프레신의 이뇨작용)

  • Go, Seok-Tae;Yun, Jae-Gyeong;Yu, Gang-Jun
    • YAKHAK HOEJI
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    • v.40 no.4
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    • pp.468-477
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    • 1996
  • Vasopressin which is an antidiuretic hormone in human body produced the diuretic action in dog. This study was investigated in order to certify the diuretic action and to search out the mechanism of the action on the vasopressin. Vasopressin, when given in a dose of 10.0mU/kg, bolus+1.0mU/kg/min intravenously, exhibited the increase of urine flow(Vol), renal plasma flow(RPF), osmolar clearance (Cosm) and amounts of sodium and potassium excreted in urine ($E_{Na},\;E_K$), the decrease of reabsorption rate of sodium and potassium in renal tubules ($R_{Na},\;R_K$), and then elevated the mean arterial pressure(MAP). Vasopressin given in a increased dose to 30.0mU/kg, bolus+1.0mU/kg/min intravenously elicited the same aspect with that exhibited by a small dose in changes of Vol. and all renal function and potentiated the change rates, whereas this time MAP did not change at all when compared with control value. Vasopressin, when administered into a renal artery, did not induce the changes of Vol and all renal function in experimental (administered) kidney, but increased slightly the Vol, glomerular filtration rate(GFR), $E_{Na},\;and\;E_K$ expected the no change of $R_{Na}\;and\;R_K$ in the control (not administered) kidney. Vasopressin, when infused into carotid artery, showed the increase of Vol. GFR, $E_{Na},\;and\;E_K$ and no change of $R_{Na}\;and\;R_K$ in a dose of 1/5 of intravenous dose. Diuretic action of vasopressin administered into carotid artery was not influenced by renal denervation. Above results suggest that vasopressin produced diuretic action by hemodynamic changes in dogs. These hemodynamic changes may be mediated by central endogenous substances not associated with renal nerve.

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Analysis of vasopressin-induced Ca2+ influx in rat hepatocytes

  • Kim, Hyun-Sook;Im, Dong-Soon
    • Proceedings of the PSK Conference
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    • pp.271.2-271
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    • 2002
  • To analyze vasopressin-induced Ca$\sub$2+/ influx in liver cells, rat hepatocytes were isolated and attached to collagen-coated cover slips. Using fura-2, a Ca$\sub$2+/-sensing dye, changes in intracellular Ca$\sub$2+/ concentration by vasopressin were monitored. Results in this communication suggested that vasopressin-induced Ca$\sub$2+/ influx consists of two distinguishable components. One was present for a short time and the other was for a long time until it happened. (omitted)

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Study on the Change of Catecholamine, Arginine Vasopressin and V1 Vasopressin Receptor Release in the Stressed Rat Brain

  • Kim, Tae-Gyun;Kim, Jee-Hee;Kim, Seung-Hee;Kang, Seog-Youn;Ki, Kyung-Chung;Huh, Young-Buhm;Lee, Song-Deuk
    • Proceedings of the Korean Society of Applied Pharmacology
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    • pp.85-85
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    • 1997
  • 스트레스가 유발된 랫드의 대뇌에서 Vasopressin-catecholamine pathway의 활성도를 알아보기 위해 면역화학염색법으로 vasopressin 호르몬의 분비와 catecholamine의 생성변화를 tyrosine hydroxylase (TH) 효소의 발현변화로 규명하고, arginine vasopressin (AVP)과 V1 vasopressin receptor의 유전자 발현변화를 in situ hybridization 방법을 이용하여 살펴보았다. 수컷 SD rat를 7시간동안 stress cage에 넣어 16$\pm$1$^{\circ}C$의 물에 수침구속 스트레스를 준 후 대조군과 함께 관류고정하여 brain을 적출하였다. Brain의 hypothalamus 부위를 중심으로하여 동결절편하여 면역조직화학 염색과 in situ hybridization을 시행하였다. TH 면역조직화학 염색에서 대뇌의 줄무늬체 부위의 꼬리조가비핵에서와 시상하부 부위의 내측등쪽시상하부와 흑색질부위에서 스트레스군이 대조군에 비해 TH 면역염색성이 증가되어 관찰되었으나 시상하부 부위의 시삭위핵, 뇌실주위핵, 뇌실옆핵에서는 두 군간의 큰 면역염색성의 차이는 보이지 않았다. AVP 면역조직화학 염색에서는 시삭위핵에 많은 수의 AVP 양성 신경세포체들이 밀집되어 있으며 뇌실옆핵에서는 스트레스군에서 AVP 면역염색성이 약간 증가되어 관찰되었으나 신경섬유의 분포양상은 비슷하였다. 중간융기에서는 모두 강한 염색성의 신경섬유들이 관찰되어 두 군간에 큰 차이는 없었다. AVP 유전자에 대한 in situ hybridization 결과 시삭위핵의 신경세포에서 AVP mRNA 양성반응을 관찰할 수 있었으나 다른 시상하부핵에서는 관찰할 수 없었으며, V1 vasopressin receptor에 대한 in situ hybridization 결과는 두 군의 대뇌에서 모두 양성반응을 관찰할 수 없었으며 V1 vasopressin receptor 유전자의 조직별 발현정도와 스트레스에 의한 발현량 조절을 관찰할 필요가 있다고 사료된다.

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Treatment of Vasodilatory Shock after Cardiac Surgery : Low Dose Arginine Vasopressin Therapy - Three cases report - (개심술후 발생한 Vasodilatory Shock의 치료 : Arginine Vasopressin의 소량투여요법 - 3례 보고 -)

  • 이교준;김해균;정은규;김도형;강두영;이응석
    • The Korean Journal of Thoracic and Cardiovascular Surgery
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    • v.35 no.3
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    • pp.227-230
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    • 2002
  • The vasodilatory shock after cardiopulmonary bypass is defined as the condition involving severe and persistent form of hypotension, tachycardia, normal or increased cardiac output and decreased systemic vascular resistance. Because of the unsuccessful response to infusion of fluids or catecholamine vasopressors, a sustained systemic shock state occurs and results in a high morbidity and mortality. We successfully treated this syndrome of 3 patients after open heart surgery with low dose of arginine vasopressin(AVP). Therefore, we report these cases with a review of related articles.

Arginine Vasopressin Therapy of Vasodilatory Shock after Cardiopulmonary Bypass - Two cases- (체외 순환 후 발생한 혈관 확장성 쇼크에 대한 바소프레신 투여요법 -2예 보고-)

  • Ahn Young-Chan;Park Chul-Hyun;Lee Jae-ik;Jeon Yang-Bin;Park Kook-Yang
    • The Korean Journal of Thoracic and Cardiovascular Surgery
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    • v.39 no.1
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    • pp.60-63
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    • 2006
  • Vasodilatory shock has been implicated in life-threatening complications after cardiac surgery. This syndrome may result from the vasopressin deficiency following cardiopulmonary bypass (CPB), which do not respond to fluids or usual intravenous inotropes. We used arginine-vasopressin in adults with vasodilatory shock coming on cardiopulmonary bypass. Therefore, we report these cases with a review of articles.

Effect of Diet and Water Intake on Aquaporin 2 Function

  • Kim, Jun-Mo;Kim, Tae-Hee;Wang, Tong
    • Childhood Kidney Diseases
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    • v.20 no.1
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    • pp.11-17
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    • 2016
  • Appropriate control of diet and water intake is important for maintaining normal blood pressure, fluid and electrolyte homeostasis in the body. It is relatively understood that the amount of sodium and potassium intake directly affects blood pressure and regulates ion transporters; Na and K channel functions in the kidney. However, little is known about whether diet and water intake regulates Aquaporin (AQP) function. AQPs, a family of aquaporin proteins with different types being expressed in different tissues, are important for water absorption by the cell. Water reabsorption is a passive process driven by osmotic gradient and water permeability is critical for this process. In most of the nephron, however, water reabsorption is unregulated and coupled to solute reabsorption, such as AQP1 mediated water absorption in the proximal tubule. AQP2 is the only water channel founded so far that can be regulated by hormones in the kidney. AQP2 expressed in the apical membrane of the principal cells in the collecting tubule can be regulated by vasopressin (antidiuretic hormone) controlling the final volume of urine excretion. When vasopressin binds to its receptor on the collecting duct cells, it stimulates the translocation of AQP2 to the membrane, leading to increased water absorption via this AQP2 water channel. However, some studies also indicated that the AQP2 is also been regulated by vasopressin independent mechanism. This review is focused on the regulation of AQP2 by diet and the amount of water intake on salt and water homeostasis.

Effects of Centrally Administered Angiotensin ll Receptor Antagonists on the Cardiovascular and Hormonal Responses to Hemorrhage in Conscious SHR

  • Seo, Il-Sook;Yang, Eun-Kyoung;Park, Jae-Sik;Kim, Hyeong-Jin;Lee, Won-Jung
    • The Korean journal of physiology & pharmacology
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    • v.27 no.2
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    • pp.217-225
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    • 1993
  • The role of endogenous brain angiotensin ll (Ang ll) in mediating the cardiovascular and vasopressin responses to hemorrhage was assessed in conscious spontaneously hypertensive rats (SHR), and normotensive Wistar-Kyoto (WKY) rats. Artificial cerebrospinal fluid (aCSF) with or without losartan (DuP 753), a specific Ang ll receptor subtype I $(AT_1)$ antagonist and saralasin, a combined $AT_1/AT_2$ antagonist was administered into the cerebral lateral ventricle. Hemorrhage was performed at a rate of 3 ml/kg/min far 5 min. Intracerebroventricular administration of losartan and saralasin had no effect on the basal blood pressure. However, in response to acute hemorrhage, central Ang ll antagonists produced a remarkably greater fall in blood pressure, a reduced tachycardia, and an enhanced renin release compared with the aCSF control experiment in SHR, but effected no significant change in WKY rats. Central Ang ll-blocked SHR showed significantly lower blood pressure and heart rate during the recovery period than the aCSF control rats. Vasopressin release tallowing the hemorrhage was attenuated by icv Ang ll antagonists: the effect was more pronounced in SHR than in WKY rats. Centrally administered losartan and saralasin produced remarkably similar effects on the cardiovascular function and vasopressin responses to hemorrhage. These data suggest that brain Ang ll acting primarily through AT, receptors plays an important physiological role in mediating rapid cardiovascular regulation and vasopressin release in response to hemorrhage especially in Hypertensive rats.

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