The vasopressin response to centrally administered hypertonic solutions in the conscious rat.
The vasopressin response to centrally administered hypertonic solutions in the conscious rat.
复制标题
加压素对清醒大鼠集中施用高渗溶液的反应。
DOI：
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发表时间：
1990
期刊：
影响因子：
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通讯作者：
R. Windle
中科院分区：
文献类型：
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作者：
T. Wells;M. Forsling;R. Windle
1.脑室内（I. C. V.）在清醒大鼠第三脑室背侧（D_3V）和腹侧（V_3V）注射等渗和高渗溶液，观察加压素（AVP）释放和平均动脉压（MAP）对脑脊液（CSF）渗透压升高的反应。2. D3 V注射高渗氯化钠溶液与血浆AVP浓度和MAP的浓度依赖性一过性增加相关。3. D3 V注射5微升0.85 M氯化钠引起血浆AVP和催产素浓度增加7倍，但对血浆ACTH浓度无影响。D3 V注射溶于0.15 M氯化钠的1.11 M甘露醇对血浆AVP浓度或MAP无影响。然而，D3 V注射0.746 M甘露醇的0.4 M氯化钠溶液引起血浆AVP显著一过性升高，但对MAP无影响。4. V3 V注射5微升0.85 M氯化钠引起血浆AVP浓度的长期增加和MAP的短暂增加。V3 V注射5 μ l溶于0.15 M氯化钠的1.11 M甘露醇引起血浆AVP浓度等量但短暂的增加，但对MAP无影响。5. D3 V注射0.85 M氯化钠的升压作用不受V1（升压）受体拮抗剂（β-巯基-β，β-环戊亚甲基丙酰1，O-Me-Tyr 2，Arg 8）-加压素既往给药的影响。6.这些结果表明，促肾上腺皮质激素诱导的AVP分泌可能是由钠受体和β受体介导的，虽然反应的表达可能取决于CSF中钠的“容许”浓度的维持。7.也似乎升压效应不是由于血浆AVP浓度增加，而仅仅是由于CSF钠浓度升高。
1. Intracerebroventricular (I.C.V.) injections of isotonic and hypertonic solutions into the dorsal (D3V) and ventral (V3V) third ventricle were employed to examine the release of vasopressin (AVP) and the mean arterial pressure (MAP) response to elevated cerebrospinal fluid (CSF) osmolality in the conscious rat. 2. The D3V injection of hypertonic sodium chloride solution was associated with a concentration‐dependent, transient increase in plasma AVP concentration and MAP. 3. The D3V injection of 5 microliters 0.85 M‐sodium chloride elicited a 7‐fold increase in plasma AVP and oxytocin concentrations, but had no effect on plasma ACTH concentration. The D3V injection of 1.11 M‐mannitol in 0.15 M‐sodium chloride had no effect on plasma AVP concentration or MAP. However, the D3V injection of 0.746 M‐mannitol in 0.4 M‐sodium chloride elicited a significant transient increase in plasma AVP, but had no effect on MAP. 4. The V3V injection of 5 microliters 0.85 M‐sodium chloride elicited a prolonged increase in plasma AVP concentration and a transient increase in MAP. The V3V injection of 5 microliters 1.11 M‐mannitol in 0.15 M‐sodium chloride elicited an equal, but transient, increase in plasma AVP concentration, but had no effect on MAP. 5. The pressor effect of a D3V injection of 0.85 M‐sodium chloride was unaffected by prior administration of the V1 (pressor) receptor antagonist (beta‐mercapto‐beta,beta‐cyclopentamethylene propionyl1, O‐Me‐Tyr2, Arg8)‐vasopressin. 6. These results indicate that osmotically induced AVP secretion may be mediated by both sodium receptors and osmoreceptors, although expression of the response may depend upon the maintenance of a ‘permissive’ concentration of sodium in the CSF. 7. It appears also that the pressor effect is not due to increased plasma AVP concentration, but only results from elevation of the CSF sodium concentration.