Department of Biological Sciences, California State University San Marcos, 333 S. Twin Oaks Valley Road, San Marcos, CA 92096, United States of America.
Department of Biology, Texas Lutheran University, 1000 W. Court St., Seguin, TX 78155, United States of America.
Comp Biochem Physiol A Mol Integr Physiol. 2021 Sep;259:110977. doi: 10.1016/j.cbpa.2021.110977. Epub 2021 May 10.
Developmental hypoxia has been shown to result in significant changes in cardiovascular development of American alligators and common snapping turtles. These include similar effects on cardiac mass and aspects of cardiovascular function. However, given the distant phylogenetic relationship between crocodilians and chelonians, we hypothesized that snapping turtles would also exhibit differences in the effects of developmental hypoxia on cardiovascular regulation. This hypothesis was based in part on prior studies that documented differences in plasticity of vagal tone on the heart between alligators and snapping turtles incubated in hypoxic conditions. To test this hypothesis, we investigated how 10% O exposure over final 80% of incubation altered the heart rate and blood pressure response to two chemical manipulations of the "chemoreflex" in common snapping turtles at 70% and 90% of incubation. NaCN injections produced a dose dependent bradycardia that was mediated by cholinergic receptor stimulation. This reflex was relatively unaffected by hypoxic incubation conditions in snapping turtle embryos. Injections of the 5-HT agonist phenylbiguanide (PBG) caused a pronounced bradycardia that decreased in intensity at 90% of incubation in embryos from the normoxic group while the heart rate response was unchanged in the hypoxic group. This differs from the previously reported diminished heart rate response of embryonic alligators incubated in 10% O, suggesting plasticity in this chemoreflex response differs between the species. Our data also indicate the cardiovascular response is mediated by a secondary cholinergic receptor stimulation however the inability of ganglionic blockade to inhibit the PBG response leaves the location of the receptors antagonized by PBG in question in embryonic snapping turtles. Primarily, our findings refute the hypothesis that hypoxic incubation decreases the "chemoreflex' response of snapping turtle embryos.
发育性缺氧已被证明会导致美洲鳄和普通 snapping 龟的心血管发育发生重大变化。这些变化包括对心脏质量和心血管功能方面的相似影响。然而，鉴于鳄鱼和龟鳖类动物在系统发育上的遥远关系，我们假设 snapping 龟也会表现出发育性缺氧对心血管调节的影响的差异。这一假设部分基于先前的研究，该研究记录了在缺氧条件下孵化的鳄鱼和 snapping 龟之间迷走神经张力对心脏的可塑性存在差异。为了验证这一假设，我们研究了在孵化的最后 80%期间暴露于 10% O 如何改变心率和血压对 common snapping 龟在孵化的 70%和 90%时两种“化学反射”化学处理的反应。NaCN 注射产生了剂量依赖性的心动过缓，这是由胆碱能受体刺激介导的。这种反射在 snapping 龟胚胎的缺氧孵化条件下相对不受影响。5-HT 激动剂苯并胍（PBG）的注射引起明显的心动过缓，在来自正常氧组的胚胎中，90%的孵化时强度降低，而在缺氧组中，心率反应不变。这与先前报道的在 10% O 中孵化的胚胎鳄的心率反应减弱不同，表明物种之间这种化学反射反应的可塑性不同。我们的数据还表明，心血管反应是由次级胆碱能受体刺激介导的，但是神经节阻断不能抑制 PBG 反应，这使得 PBG 拮抗的受体在 embryonic snapping 龟中存在问题。主要是，我们的发现反驳了缺氧孵化会降低 snapping 龟胚胎“化学反射”反应的假设。
