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Received date: August 26, 2017; Accepted date: September 12, 2017; Published date: September 19, 2017
Citation: Mangel A, Lothman K (2017) Emergence of a New Paradigm in Understanding the Cardiovascular System: Pulse Synchronized Contractions. Cardiovasc Pharm Open Access 6:220. doi: 10.4172/2329-6607.1000220
Copyright: © 2017 Mangel A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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• The large conduit arteries undergo rhythmic smooth muscle activation in synchrony with the cardiac cycle.
• The contractions are neurogenic and are denoted as pulse synchronized contractions (PSCs).
• PSCs are not a movement artifact from the pulse wave or heartbeat.
• The pacemaker for the PSCs is in the right atrium.
• The smooth muscle wall of large arteries can contract as fast as the heartbeat.
An increase in intracellular calcium activates contractions in muscle cells. Because smooth muscle cells are long, narrow-diameter cells, it was believed that an influx of calcium could serve as the sole source of activator calcium for contractions following changes in membrane potential. Therefore, no depolarization-mediated release of intracellularly stored calcium occurred (Figures 1-3).
Figure 3: In contrast to gastrointestinal muscle segments, incubation of aortic segments from rabbits in normal saline is electrically quiescent (upper trace). In calcium-free solution, a fast rhythmic electrical event is produced (lower trace), but the muscle segments remain mechanically quiescent .
• The prevailing hypothesis describing the behavior of the smooth muscle wall of the large arteries is that the wall does not contract in synchrony with the cardiac cycle but, rather, behaves as a passive elastic tube being rhythmically distended by pulsatile pressure changes. Neural input may modulate tone.
• Thus, it was believed that there was no vascular smooth muscle rhythmicity in synchrony with the cardiac cycle .
»» Extra-arterially recorded brachial pulses sometimes preceded intra-arterial pulses, suggesting arterial diameter varies in advance of pressure changes during the cardiac cycle.
»» The difference between the extra-arterially recorded and intra-arterially recorded pulse waves was abolished by stellate ganglion block, suggesting a neurally mediated event.
»» It was concluded that: “the behaviour of the artery in the pulse is contradictory to principles of passive elasticity but seem to provide evidence of active participation of the arterial wall….”
»» This series of papers has been largely ignored.
Based on the ability of the aortic smooth muscle wall to generate fast rhythmic electrical activity in calcium-free solution (Figure 3), we sought to determine if the aortic smooth muscle wall could potentially show fast rhythmic contractile activity in vivo (Figures 4 and 5).
Figure 4: Recording technique for measurement of contractile activity in the in vivo rabbit aorta. Configuration represents a segment of aorta having blood flow bypassed and tension (T) recorded from the bypassed segment. Pulse pressure changes (P) were recorded from the non-bypassed segment [9,10].
• Eliminate pulse wave (Figures 6 and 7)
Figure 6: Following bleeding of rabbits, PSCs continued. In this configuration, ventricular muscle contractions were also recorded and pacing of the ventricles occurred. These studies (a) eliminated the pulse wave as an artifact, as animals were bled; (b) eliminated cardiac contractions as an artifact, as following excision of the right atrium with ventricular contractions paced to supra baseline levels, PSCs were not produced; and (c) suggested the PSC pacemaker is in the right atrium as excision of the right, but not left atrium, abolished PSCs .
Figure 7: Shown above is an example of right atrial pacing in a bled rabbit. PSCs followed the pacing rate. In this and other animals, heart block developed with corresponding large amplitude ventricular contractions. This experiment supports both the pacemaker for PSCs residing in the right atrium and that PSCs are not secondary to a movement artifact from the heart .
• Eliminate cardiac contractility (Figures 6 and 7)
• Dispel prejudice that smooth muscle cannot “contract that fast” (Figure 8)
Figure 8: Electrical stimulation of the rat aorta in vivo produced contractions similar to PSCs. As PSCs are, these contractions were eliminated by the neural blocker tetrodotoxin (TTX). Black bars represent timing of stimulation .
|Dog||Coronary, femoral, carotid arteries|
To evaluate whether the arterial smooth muscle wall is capable of contracting at the frequency of the heartbeat, electrical stimulation of the aorta in vivo was performed (Figure 8).
• The smooth muscle wall of the large arteries is capable of undergoing rapid contractions (PSCs) at the rate of the heartbeat.
• The pacemaker for the PSCs is in the right atrium.
• Direct electrical stimulation of the nerves within the aorta yields similar contractile activity.
• PSCs represent a modified platform to understand the etiology of cardiovascular diseases allowing for the development of new therapeutic targets.