The Anrep effect is nothing but a self-regulation method in which the contracting ability of the heart muscles increases with after-load. After-load is the pressure against which the heart must pump the blood during systole (the contraction of the ventricle). After-load is just proportional to the average pressure in the artery. This was experimentally determined that as the after-load increases, it causes a proportional linear increase in the ventricular entropy (an agent that changes muscle contractions) as well.
There are a few terms that need to be stated here before studying the Anrep effect, the terms are as follows-
- Systole – that part of the cardiac cycle in which the heart muscles contract after refilling with the blood.
- Diastole – that face of the cardiac cycle in which the muscles of the heart relax and allows the blood to be filled in.
- Cardiac cycle – cardiac cycle starts with the ending of one Heartbeat to the starting of the next it consists of two phases systole and diastole systole the contraction and diastole the relaxation of the heart muscles also called as cardiac muscles.
- Auricles – the auricles are two in number its work is to increase the volume of the Atrium.
- Ventricles – A ventricle is one of two large chambers whose work is to collect and expel the blood that is received from an atrium.
- Aorta – it is the main artery that carries the blood away from the heart to the whole body and this is how through aorta blood is provided or is transported to different parts of the body.
The ‘Anrep effect’ is named after a Russian physiologist Sir Gleb von Anrep, who first described it in 1912. The Anrep effect allows the heart to compensate or overcome for an increased end contraction volume and the decreased stroke volume; which usually occurs when the blood pressure in the aorta increases. If the Anrep effect would not have been there, even an increase in the blood pressure in aorta would create a decrease in the stroke volume that would create a major problem to the ideal blood circulation in the human body.
The phenomenon is observed in denervated hearts (the one that has lost its breve supply) and also observed in isolated cardiac muscle, as well as in intact hearts. As stated above, if there is a sudden increase in the pressure in the aorta it causes an abrupt increase in the end-diastolic volume of the left ventricle. This leads to an initial increase in the contractile force of the ventricle via the Frank-Starling mechanism. It is also observed that if the increased after-load is maintained for 10-15 minutes further, then the force of contraction also increases further, and in the case of the intact heart, the end-diastolic volume begins to decrease. The functional significance of the Anrep effect is that the increased entropy compensates for the increased volume of the end-systole slightly and there is a decrease in the stroke volume caused by the increase in after-load.
The mechanisms mainly responsible for the initial response and the delayed response may appear to be different. The initial increase in the force of contraction is largely due to increased troponin C (myocytes of the heart) sensitivity to calcium and the delayed response involves not only one but several mechanisms that promote more release of calcium by the sarcoplasmic reticulum (these are the structures that store calcium and releases then when required).
Somewhere it has been demonstrated that angiotensin II (used to treat hypertension as a result of shock) also maybe aldosterone (help in body’s ability to regulate blood pressure) are implicated in the increase in the contraction of heart muscles following greater afterload. Though the heart is under continuous nervous, hormonal, and physiological influence. In spite of this fact, the cardiac muscle has inbuilt mechanisms to adapt our cardiac output to changes in outside, bodily as well as hemoglobin conditions. An increase in left ventricular end-diastolic volume (EDV), which may be caused by either increasing resistance in the aorta to ejection, immediately leads to a more powerful contraction.
There is a well-known mechanism called the Frank-Starling mechanism that allows the heart to increase its output after a rise in preload or to maintain it despite a greater afterload. The release of angiotensin II or endothelin type-I is mainly responsible for the heart cells (also called as myocytes) hypertrophy, and when for some reason there is the blockade of angiotensin II or due to some factors angiotensin ll is not released, it abolishes the Anrep effect and in these cases, we see that the heart muscles do not undergo Anrep effect.
It is also seen that angiotensin II and endothelin type-I have a one-way direction that is both vary in the same degree and an upstream process, as the inhibition of endothelin type-I receptors eventually results in the blockade of angiotensin II release. The Anrep effect is not related to any other genomic mechanisms as for the mechanical response to occur a very brief period is required.
Hence, we can say that there is enough evidence to suggest that the Anrep effect takes place only after a series of events, with the release of Angiotensin II thereafter starting this molecular and biological phenomenon, and it tends to end with an increase in the Ca releases. It is very interesting to know that 50 years after Anrep reported his phenomenon, another scientist named ‘Sarnoff’ coined the word “autoregulation”, a term aiming mainly that the mechanism resides in the myocardium itself.