Abstract
Central hypovolemia, defined as diminished blood volume in the heart and pulmonary vascular bed, is still an unresolved problem from a therapeutic point of view. The development of pharmaceutical agents targeted at specific angiotensin II receptors, such as the non-peptidergic AT2-receptor agonist compound 21, is yielding many opportunities to uncover more knowledge about angiotensin II receptor profiles and possible therapeutic use. Cardiovascular, anti-inflammatory, and neuroprotective therapeutic use of compound 21 have been suggested. However, there has not yet been a focus on the use of these agents in a hypovolemic setting. We argue that the latest debates on the effect of angiotensin II during hypovolemia might guide for future studies, investigating the effect of such agents during experimentally simulated central hypovolemia. The purpose of this review is to examine the role of angiotensin II during episodes of central hypovolemia. To examine this, we reviewed results from studies with three experimental models of simulated hypovolemia: head up tilt table test, lower body negative pressure, and hemorrhage of animals. A systemic literature search was made with the use of PubMed/MEDLINE for studies that measured variables of the renin–angiotensin system or its effect during simulated hypovolemia. Twelve articles, using one of the three models, were included and showed a possible organ-protective effect and an effect on the sympathetic system of angiotensin II during hypovolemia. The results support the possible organ-protective vasodilatory role for the AT2-receptor during hypovolemia on both the kidney and the splanchnic tissue.
Highlights
Central hypovolemia, defined as diminished blood volume in the heart and pulmonary vasculary bed [1], is a potentially life-threatening condition that left untreated leads to hemorrhagic shock [2]
The purpose of this review is to examine the role of angiotensin II during episodes of central hypovolemia
Explaining the accentuated orthostatic response of losartan has lead to two general areas of interest for analysis of angiotensin II’s effect during episodes of experimentally simulated central hypovolemia
Summary
Central hypovolemia, defined as diminished blood volume in the heart and pulmonary vasculary bed [1], is a potentially life-threatening condition that left untreated leads to hemorrhagic shock [2]. The therapeutic strategy for central hypovolemia is debated and still unresolved [3, 4]. Expanding our knowledge about the hormones that act to stabilize the hemodynamic conditions during hypovolemia is essential to proposing new therapeutic strategies. During World War II, an increase in the interest in hypovolemic shock gave rise to a large body of research on the hemodynamic effects of central hypovolemia [5,6,7,8]. This research shed light on many of the well-known hemodynamic effects of central hypovolemia and developed the broadly used experimental models for simulating central hypovolemia.
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