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The left ventricle increases contractility in response to baroreceptor unloading, which is sympathetically mediated in the anesthetized rat.
- Source :
-
Journal of applied physiology (Bethesda, Md. : 1985) [J Appl Physiol (1985)] 2024 Jul 01; Vol. 137 (1), pp. 136-144. Date of Electronic Publication: 2024 May 30. - Publication Year :
- 2024
-
Abstract
- 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 1 ) whether LV contractility increases in response to baroreceptor unloading and 2 ) 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 t <subscript>max</subscript> )], 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 t <subscript>max</subscript> increased during baroreceptor unloading (26 ± 6 vs. 31 ± 9 mmHg·s <superscript>-1</superscript> ·μL <superscript>-1</superscript> , P = 0.031). During esmolol, there was no increase in LV contractility during baroreceptor unloading (11 ± 2 vs. 12 ± 2, P = 0.125); however, during atropine, there was an increase in LV contractility during baroreceptor unloading (26 ± 6 vs. 31 ± 9, P = 0.019). During combined esmolol and atropine, there was a small increase in contractility versus control (13 ± 3 vs. 15 ± 4, P = 0.046). Our results demonstrate that, in anesthetized rats, LV contractility increases in response to baroreceptor unloading, which is largely sympathetically mediated. NEW & NOTEWORTHY 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.
- Subjects :
- Animals
Male
Rats
Blood Pressure physiology
Blood Pressure drug effects
Arterial Pressure physiology
Arterial Pressure drug effects
Atropine pharmacology
Anesthesia
Propanolamines
Rats, Wistar
Myocardial Contraction physiology
Myocardial Contraction drug effects
Pressoreceptors physiology
Pressoreceptors drug effects
Baroreflex physiology
Baroreflex drug effects
Sympathetic Nervous System physiology
Sympathetic Nervous System drug effects
Heart Ventricles drug effects
Ventricular Function, Left physiology
Ventricular Function, Left drug effects
Subjects
Details
- Language :
- English
- ISSN :
- 1522-1601
- Volume :
- 137
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Journal of applied physiology (Bethesda, Md. : 1985)
- Publication Type :
- Academic Journal
- Accession number :
- 38813608
- Full Text :
- https://doi.org/10.1152/japplphysiol.00722.2023