Both the autonomic nervous system and the neuroendocrine system are activated by osmotic stimulation (OS) evoking cardiovascular effects. The current study investigated the mechanisms involved in the cardiovascular responses evoked by an acute osmotic stimulus with intraperitoneal (i.p.) injection of either isotonic (0.15 M NaCl) or hypertonic saline (0.6 M NaCl) in conscious rats. Hypertonic saline increased mean arterial pressure (MAP) and heart rate (HR) for 30 min, as well as plasma osmolality and sodium content. Urinary sodium and urinary volume were also increased. Pretreatment with the ganglion blocker pentolinium (i.v.) did not affect the pressor response, but significantly decreased the tachycardic response caused by OS. Pretreatment with the V1-vasopressin receptor antagonist dTyr(CH2)5(Me)AVP (i.v.) reduced the pressor response, without affecting the tachycardic response evoked by the hypertonic OS. Neither the pressor nor the tachycardic response to OS was affected by pretreatment with either the oxytocin receptor antagonist atosiban or the α1-antagonist prazosin. Pretreatment with the β1-antagonist atenolol had no effect on the pressor response, but markedly decreased the tachycardic response evoked by OS. Results indicate that i.p. hypertonic OS-evoked pressor response is mediated by the release of vasopressin, with a minor influence of the vascular sympathetic input.LAY SUMMARYIncreased plasma osmolality, such as that observed during dehydration or salt intake, is a potent stimulus yielding to marked cardiovascular and neuroendocrine responses. The intraperitoneal (i.p.) injection of hypertonic saline solution is a commonly used animal model to cause a sustained increase in plasma osmolality, leading to a cardiovascular response characterized by sustained blood pressure and heart increases, whose systemic mechanisms were presently studied. Our findings indicate that the pressor response to the i.p. osmotic stimulus (OS) is mediated mainly by the release of vasopressin into the blood circulation with a minor or even the noninvolvement of the vascular sympathetic nervous system, whereas activation of the sympathetic-cardiac system mediates the tachycardic response to OS.

中文翻译：

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清醒大鼠急性渗透刺激引起的心血管效应的机制。

自主神经系统和神经内分泌系统均通过引起心血管作用的渗透刺激（OS）来激活。目前的研究调查了在清醒大鼠中通过腹膜内（ip）注射等渗（0.15 M NaCl）或高渗盐水（0.6 M NaCl）引起的急性渗透刺激引起的心血管反应的机制。高渗盐水可增加30分钟的平均动脉压（MAP）和心率（HR），以及血浆渗透压和钠含量。尿钠和尿量也增加。用神经节阻滞剂喷妥林（iv）进行预处理不会影响升压反应，但会显着降低OS引起的心动过速反应。用V1-加压素受体拮抗剂dTyr（CH2）5（Me）AVP（iv）进行预处理可降低升压反应，而不会影响高渗OS引起的心动过速反应。催产素受体拮抗剂阿托西班或α1拮抗剂哌唑嗪预处理均不会影响对OS的升压或心动过速反应。用β1拮抗剂阿替洛尔进行预处理对升压反应没有影响，但显着降低了OS引起的心动过速反应。结果表明，腹膜后加压素的释放是由腹膜高渗OS引起的升压反应介导的，而对血管交感神经输入的影响较小.LAY概述血浆渗透压的升高（例如在脱水或食盐期间观察到的渗透压升高）是一种有效的刺激，产生显着的心血管和神经内分泌反应。腹膜内（ip ）注射高渗盐溶液是引起血浆渗透压持续升高的常见动物模型，导致心血管反应以持续血压升高和心脏增加为特征，目前正在研究其全身机制。我们的研究结果表明，对ip渗透刺激（OS）的升压反应主要是通过血管加压素释放到血液循环中而介导的血管交感神经系统轻微甚至不参与介导的，而交感心脏系统的激活介导对OS的心动过速反应。