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马体内全身性和中枢介导的血管紧张素II作用

Systemic and centrally mediated angiotensin II effects in the horse.

作者信息

Andersson B, Augustinsson O, Bademo E, Junkergård J, Kvart C, Nyman G, Wiberg M

出版信息

Acta Physiol Scand. 1987 Feb;129(2):143-9. doi: 10.1111/j.1748-1716.1987.tb08052.x.

DOI:10.1111/j.1748-1716.1987.tb08052.x
PMID:3577807
Abstract

The primary aim of the study was to evaluate the potential value of intravenous (i.v.) infusion of angiotensin II (AII) for phonocardiographic differential diagnosis of equine valvular insufficiency. Ten-minute AII infusions at 4.5-33 pmol kg-1 min-1 induced clear-cut dose-dependent rises in systemic arterial blood pressure (aBP), whereas the pulmonary aBP remained largely unaffected. It implies that i.v. infusion of AII at about 10 pmol kg-1 min-1 could be a valuable tool for the acoustic differentiation between mitral and tricuspid valvular dysfunction in the horse. The infusion at, and above 9 pmol kg-1 min-1 caused increased heart rate. This chronotrophic effect was not strictly dose-dependent and exhibited significant tachyphylaxis. Angiotensin II administration at, or above 9 pmol kg-1 min-1 was needed to induce an urge to drink, suggesting that angiotensin-induced thirst does not appear in the euhydrated horse until the octapeptide reaches supraphysiological blood concentration. Determinations of plasma aldosterone concentration (PA) revealed comparatively high morning control values (269 +/- 46 pmol-1). Three consecutive AII infusions with 10-min intervals and at increasing dosages caused a cumulative, almost fourfold elevation of PA. The PA pattern indicated that AII-induced hypersecretion of aldosterone continued for several minutes after the end of the infusions, but also showed that the metabolic clearance of the hormone took precedency of the secretion within 20 min post-infusion. In two of the horses a fall in PA occurred during a fourth, final infusion, indicating that in these instances the previous AII administration had impoverished the store of aldosterone available for release from the adrenal cortex.

摘要

该研究的主要目的是评估静脉输注血管紧张素II(AII)在马心脏瓣膜功能不全的心音图鉴别诊断中的潜在价值。以4.5 - 33 pmol kg⁻¹ min⁻¹的剂量输注AII 10分钟可引起体循环动脉血压(aBP)明显的剂量依赖性升高,而肺aBP基本不受影响。这表明以约10 pmol kg⁻¹ min⁻¹的剂量静脉输注AII可能是区分马二尖瓣和三尖瓣功能障碍的声学差异的有价值工具。输注剂量在9 pmol kg⁻¹ min⁻¹及以上会导致心率加快。这种变时效应并非严格的剂量依赖性,且表现出明显的快速耐受性。需要以9 pmol kg⁻¹ min⁻¹及以上的剂量给予血管紧张素II才能引起饮水欲望,这表明在水合正常的马中,直到八肽达到超生理血药浓度时血管紧张素诱导的口渴才会出现。血浆醛固酮浓度(PA)测定显示早晨对照值相对较高(269±46 pmol⁻¹)。以递增剂量每隔10分钟连续输注三次AII导致PA累积升高近四倍。PA模式表明,AII诱导的醛固酮分泌增多在输注结束后会持续几分钟,但也表明该激素的代谢清除在输注后20分钟内优先于分泌。在其中两匹马中,第四次也是最后一次输注期间PA出现下降,表明在这些情况下,先前给予的AII耗尽了肾上腺皮质可用于释放的醛固酮储备。

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