Enhanced osmotic responsiveness in angiotensin AT1a receptor deficient mice: evidence for a role for AT1b receptors.
Enhanced osmotic responsiveness in angiotensin AT1a receptor deficient mice: evidence for a role for AT1b receptors.
复制标题
血管紧张素 AT1a 受体缺陷小鼠的渗透反应性增强：AT1b 受体作用的证据。
DOI：
10.1113/expphysiol.2005.030643
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Morris,Mariana
中科院分区：
文献类型：
--
作者：
Chen,Yanfang;Chen,Hao;Morris,Mariana
Experiments were performed to study the role of angiotensin (Ang) AT1a and AT1b receptor subtypes in osmotic regulation of blood pressure using gene deletion and pharmacological methods. The cardiovascular effects of hypertonic saline (HS) or vasopressin (VP) delivered via vascular catheters were measured in AngAT1agene deletion (AT1a−/−) and control (AT1a+/+) mice. Blood pressure (BP) and heart rate (HR) were recorded in conscious mice using direct carotid catheters. Plasma osmolality and VP concentration were also measured. The major finding was that deletion of AT1a receptors resulted in enhanced BP response to osmotic stimulation. This was seen after acute HS injection (20 μl, 20% NaCl). The peak percentage change in mean arterial pressure (MAP) was 15.4 ± 1.9%versus28.1 ± 2.4% (AT1a+/+versusAT1a −/−, respectively). Losartan (AT1 antagonist), but not PD123319 (AT2 antagonist), inhibited the HS‐induced MAP response, specifically in AT1a−/− mice. Plasma osmolality and VP concentration were elevated after HS injection with no differences noted between groups. Vascular injection of VP (5 ng g−1) increased BP and HR, with similar MAP response between groups. Evidence shows that removal of Ang AT1a receptors results in a significant enhancement in the pressor response to acute osmotic stimulation. Studies of AT1 receptor blockade indicate that complementary Ang AT1b receptors, but not AT2 receptors, may be involved in the osmotic response.
