Aortic Body Chemoreceptors Regulate Coronary Blood Flow in Conscious Control and Hypertensive Sheep

Abstract

Background: Peripheral arterial chemoreceptors monitor the chemical composition of arterial blood and include both the carotid and aortic bodies (ABs). While the role of the carotid bodies has been extensively studied, the physiological role of the ABs remains relatively under-studied, and its role in hypertension is unexplored. We hypothesized that activation of the ABs would increase coronary blood flow in the normotensive state and that this would be mediated by the parasympathetic nerves to the heart. In addition, we determined whether the coronary blood flow response to stimulation of the ABs was altered in an ovine model of renovascular hypertension. Methods: Experiments were conducted in conscious and anesthetized ewes instrumented to record arterial pressure, coronary blood flow, and cardiac output. Two groups of animals were studied, one made hypertensive using a 2 kidney one clip model (n=6) and a sham-clipped normotensive group (n=6). Results: Activation of the ABs in the normotensive animals resulted in a significant increase in coronary blood flow, mediated, in part by a cholinergic mechanism since it was attenuated by atropine infusion. Activation of the ABs in the hypertensive animals also increased coronary blood flow ( P <0.05), which was not different from the normotensive group. Interestingly, the coronary vasodilation in the hypertensive animals was not altered by blockade of muscarinic receptors but was attenuated after propranolol infusion. Conclusions: Taken together, these data suggest that the ABs play an important role in modulating coronary blood flow and that their effector mechanism is altered in hypertension.

Dissecting the contributions of the peripheral chemoreflex and myocardial hypoxia to fetal heart rate decelerations in near‐term fetal sheep

“…Furthermore, coronary artery blood flow increases markedly during fetal hypoxaemia (Court et al., 1984; Itskovitz et al., 1991; Jensen et al., 1987a; Thornburg & Reller, 1999), which is important in maintaining myocardial oxygen consumption and substrate supply during moderate hypoxaemia (Fisher et al., 1982). Increased coronary perfusion is attributable, in part, to peripheral chemoreflex‐mediated parasympathetic stimulation, at least in adults (Feigl, 1969; Pen et al., 2022). This might be another mechanism through which vagal activation is cardioprotective.…”

Sympathetic transduction of cardiac sympathetic nerve activity in healthy, conscious sheep

“…Baseline recordings of BP, CoBF, CO and CSNA were made on resting, conscious and healthy animals ( n = 10) for up to 1 h. As a control for the propranolol infusions, a 10 mL saline bolus was administered first, before 30 mL of saline was infused over 90 min at a rate of 20 mL h –1 in accordance with previous studies conducted in sheep (Pachen et al., 2021a, b; Pen et al., 2022). These recordings were taken to determine transduction analysis as detailed below.…”

“…In healthy animals, baseline levels of cardiac SNA (CSNA) are low compared to other organs such as the kidney (Ramchandra et al., 2009) and heart rate (HR) is under greater parasympathetic control during resting conditions. In addition, CSNA has also been shown to alter baseline coronary artery blood flow (CoBF) in response to various autonomic reflexes (Pachen et al., 2021a, b; Pen et al., 2022). However, whether baseline levels of CSNA in the resting conscious animal are transduced to alter HR and/or CoBF is unknown and this was the focus of the present study.…”