The cardioinhibitor and cardioaccelerator centers in the medulla control the heart rate and the force of contraction. These centers are regulated by signals from the carotid sinus as well as from stretch receptors in the heart. Follow the interactions beginning with increased arterial blood pressure.
The carotid sinus (CS) is stimulated as blood pressure (BP) increases --a direct relationship (solid arrow). Stimulatory impulses (solid line) from the sinus lead to the cardioinhibitor centers (CI). This center sends simultaneous inhibitory signals (dashed lines) to two locations: to the pacemaker (heart rate (HR)) via the vagus nerve (V) and to the medullary cardioaccelerator center (CA).
Notice that the pacemaker (HR) has dual innervation. It has inhibitory neurons (dashed line) from the cardioinhibitor center (CI) via the vagus nerve(V). It also has stimulatory neurons (solid line) from the cardioaccelerator center (CA) center via the cardiac nerves (CN).
Simultaneous stimulation does indeed occur but they do not rise and fall together-- this could stop the heart! Instead, as the carotid sinus (CS) increases heart rate (HR) it simultaneously decreases impulses from the cardioaccelerator center (CA). When the cardioinhibitor center is decreasing heart rate it is also decreasing the ability of the cardioaccelerator center to increase heart rate!
Decreased heart rate leads to deceased cardiac output which then leads to decreased arterial blood pressure. We've returned to the beginning where arterial blood pressure was increasing-- negative feedback, homeostasis at work.
Stimulatory neurons (solid lines) simultaneously increase the heart rate (HR) and the contractility (C). The neurons involved run from the cardioaccelerator center (CA) via the cardiac nerves (CN) .
The number of cross-bridges that can form within myofilaments in cardiac contractile cells is dependent on the concentration of calcium ions. About 80% of cytoplasmic calcium is pumped into the sarcoplasmic reticulum between each contraction. The actual amount stored is increased by allowing more calcium into the cell from the interstitial fluid. (This is discussed in detail in the 'Cardiac Contractile Cell Tutorial'.) The end effect is that increased contractility (C) empties the heart more completely leaving less residual blood-- end systolic volume (ESV) behind.
Increased venous return (VR) stretches the heart causing stretch receptors to send stimulatory signals to the cardioaccelerator center (CA) via the glossopharyngeal nerve (GP) (solid line). This results in increased activity of this center resulting in increased heart rate and force of contraction (contractility).
Last update: 7/14/2005