Is the cardiovascular chemoreflex response to NaCN plastic in embryonic American alligators, Alligator mississippiensis

Developmental environments can modify organismal phenotypes via epigenetic mechanisms, and phenotypic changes can first become evident during embryonic or fetal life. Phenotypic plasticity of the cardiovascular system has been suggested to be particularly susceptible to environmentally induced phenotypic changes, in part due to its early and essential function during development. Prior studies using egg-laying reptiles as models have revealed that cardiovascular phenotypes can be altered by low developmental oxygen (hypoxia). Hypoxia for embryonic American alligators, Alligator mississippiensis, alters the morphological and physiological cardiovascular phenotype. For example, incubation in 10% O 2 produces embryonic alligators with relatively larger hearts, that are hypotensive, that are bradycardic and have a blunted cardiovascular response to phenylbiguanide (a chemoreflex-inducing compound). While the cardiovascular chemoreflex has been demonstrated to be plastic, the capacity of embryonic alligators to modulate this reflex was unknown. The main objective of this study was to determine the capacity of embryonic alligators chronically incubated in normoxia (21% O 2 ) or hypoxia (10% O 2 ) to respond to another chemoreflex-inducing agent, Sodium cyanide (NaCN) and modulate that reflex during prolonged exposure to 10% O 2 . Our first study demonstrated that the embryonic alligator cardiovascular response to NaCN injections consisted of an initial rapid decrease in heart rate followed by a secondary increase in arterial blood pressure. Chronic normoxic (21% O 2 ) or chronic hypoxic incubation (10% O 2 ) did not affect the intensity of heart rate or blood pressure response to NaCN in embryonic alligators at both points of incubation studied (70% and 90% of incubation). Our second study demonstrated that ganglionic blockade with hexamethonium chloride inhibited or dampened the NaCN bradycardic response, indicating the bradycardia was mediated via a reflex loop. Our third study demonstrated that the cardiovascular response to an Injection a NaCN during a 1 hr exposure to 10% O 2 caused similar cardiovascular responses to those measured prior to the hypoxic exposure. Based on the data, embryonic alligators exhibit a cardiovascular chemoreflex that is elicited by NaCN but lack the capacity to modulate this reflex during exposure to 10% O 2 . Finally, the cardiovascular response to NaCN does not display the plasticity previously reported for the chemoreflex inducing agent phenylbiguanide in embryonic alligators. Funding for the project was provided to D.A.C. II by the National Science Foundation OS 1755187. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

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Journal
Physiology
Published
2025-05-01
DOI
https://doi.org/10.1152/physiol.2025.40.s1.0234
Primary Topic
Physiological and biochemical adaptations
Type
article
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article

Is the cardiovascular chemoreflex response to NaCN plastic in embryonic American alligators, Alligator mississippiensis

John Eme, Dane A. Crossley, Kevin B. Tate, Ruth M. Elsey et al.
Physiology
Physiological and biochemical adaptations
article

Is the cardiovascular chemoreflex response to NaCN plastic in embryonic American alligators, Alligator mississippiensis

John Eme, Dane A. Crossley, Kevin B. Tate, Ruth M. Elsey, G Batista, Audrey Keneda
article en

Abstract

Developmental environments can modify organismal phenotypes via epigenetic mechanisms, and phenotypic changes can first become evident during embryonic or fetal life. Phenotypic plasticity of the cardiovascular system has been suggested to be particularly susceptible to environmentally induced phenotypic changes, in part due to its early and essential function during development. Prior studies using egg-laying reptiles as models have revealed that cardiovascular phenotypes can be altered by low developmental oxygen (hypoxia). Hypoxia for embryonic American alligators, Alligator mississippiensis, alters the morphological and physiological cardiovascular phenotype. For example, incubation in 10% O 2 produces embryonic alligators with relatively larger hearts, that are hypotensive, that are bradycardic and have a blunted cardiovascular response to phenylbiguanide (a chemoreflex-inducing compound). While the cardiovascular chemoreflex has been demonstrated to be plastic, the capacity of embryonic alligators to modulate this reflex was unknown. The main objective of this study was to determine the capacity of embryonic alligators chronically incubated in normoxia (21% O 2 ) or hypoxia (10% O 2 ) to respond to another chemoreflex-inducing agent, Sodium cyanide (NaCN) and modulate that reflex during prolonged exposure to 10% O 2 . Our first study demonstrated that the embryonic alligator cardiovascular response to NaCN injections consisted of an initial rapid decrease in heart rate followed by a secondary increase in arterial blood pressure. Chronic normoxic (21% O 2 ) or chronic hypoxic incubation (10% O 2 ) did not affect the intensity of heart rate or blood pressure response to NaCN in embryonic alligators at both points of incubation studied (70% and 90% of incubation). Our second study demonstrated that ganglionic blockade with hexamethonium chloride inhibited or dampened the NaCN bradycardic response, indicating the bradycardia was mediated via a reflex loop. Our third study demonstrated that the cardiovascular response to an Injection a NaCN during a 1 hr exposure to 10% O 2 caused similar cardiovascular responses to those measured prior to the hypoxic exposure. Based on the data, embryonic alligators exhibit a cardiovascular chemoreflex that is elicited by NaCN but lack the capacity to modulate this reflex during exposure to 10% O 2 . Finally, the cardiovascular response to NaCN does not display the plasticity previously reported for the chemoreflex inducing agent phenylbiguanide in embryonic alligators. Funding for the project was provided to D.A.C. II by the National Science Foundation OS 1755187. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

PhysiologyVol. 40(S1)
University of North Texas (US), Louisiana Department of Wildlife and Fisheries (US), California State University, San Marcos (US)
Openalex Percentile: Top 84%
Physiological and biochemical adaptations
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