The left ventricle increases contractility in response to baroreceptor unloading, which is sympathetically mediated in the anesthetized rat

• Published in: Journal of applied physiology (1985) Vol. 137; no. 1; pp. 136 - 144
• Main Authors: Stewart, Liam C, Wainman, Liisa, Ahmadian, Mehdi, Duffy, Jennifer, Seethaler, Rudolph, Mueller, Patrick J, Eves, Neil D, West, Christopher R
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.07.2024
• Subjects: Anesthesia; Animals; Arterial Pressure - drug effects; Arterial Pressure - physiology; Atropine; Atropine - pharmacology; Autonomic nervous system; Baroreceptors; Baroreflex - drug effects; Baroreflex - physiology; Blood pressure; Blood Pressure - drug effects; Blood Pressure - physiology; Heart Ventricles - drug effects; Load distribution; Male; Muscle contraction; Myocardial Contraction - drug effects; Myocardial Contraction - physiology; Parasympathetic nervous system; Pressoreceptors - drug effects; Pressoreceptors - physiology; Propanolamines; Rats; Rats, Wistar; Reflexes; Servocontrol; Sympathetic Nervous System - drug effects; Sympathetic Nervous System - physiology; Unloading; Ventricles (cerebral); Ventricular Function, Left - drug effects; Ventricular Function, Left - physiology; baroreflex; parasympathetic nervous system; cardiac contractility; sympathetic nervous system
• DOI: 10.1152/japplphysiol.00722.2023
• ISSN: 8750-7587; 1522-1601

Contemporary discussion of the baroreflex includes the efferent vascular-sympathetic and cardiovagal arms. Since sympathetic postganglionic neurons also innervate the left ventricle (LV), it is often assumed that the LV produces a sympathetically mediated increase in contractility during baroreceptor unloading, but this has not been characterized using a load-independent index of contractility. We aimed to determine ) whether LV contractility increases in response to baroreceptor unloading and ) whether such increases are mediated via the sympathetic or parasympathetic arm of the autonomic nervous system. Ten male Wistar rats were anesthetized (urethane) and instrumented with arterial and LV pressure-volume catheters to measure mean arterial pressure (MAP) and load-independent LV contractility [maximal rate of increase in pressure adjusted to end-diastolic volume (PAdP/d )], respectively. Rats were placed in a servo-controlled lower-body negative pressure (LBNP) chamber to reduce MAP by 10% for 60 s to mechanically unload baroreceptors under control conditions. LBNP was repeated in each animal following infusions of cardiac autonomic blockers using esmolol (sympathetic), atropine (parasympathetic), and esmolol + atropine. Under control conditions, PAdP/d increased during baroreceptor unloading (26 ± 6 vs. 31 ± 9 mmHg·s ·μL , = 0.031). During esmolol, there was no increase in LV contractility during baroreceptor unloading (11 ± 2 vs. 12 ± 2, = 0.125); however, during atropine, there was an increase in LV contractility during baroreceptor unloading (26 ± 6 vs. 31 ± 9, = 0.019). During combined esmolol and atropine, there was a small increase in contractility versus control (13 ± 3 vs. 15 ± 4, = 0.046). Our results demonstrate that, in anesthetized rats, LV contractility increases in response to baroreceptor unloading, which is largely sympathetically mediated. This study empirically demonstrates a sympathetically mediated increase in LV contractility in response to baroreceptor unloading using a load-independent index of cardiac contractility in the anesthetized rat.