Myogenic mechanism
The myogenic mechanism is how
The smooth muscle of the blood vessels reacts to the stretching of the muscle by opening ion channels, which cause the muscle to depolarize, leading to muscle contraction. This significantly reduces the volume of blood able to pass through the lumen, which reduces blood flow through the blood vessel. Alternatively when the smooth muscle in the blood vessel relaxes, the ion channels close, resulting in vasodilation of the blood vessel; this increases the rate of flow through the lumen.
This system is especially significant in the
Myogenic mechanisms in the kidney are part of the autoregulation mechanism which maintains a constant renal blood flow at varying arterial pressure. Concomitant autoregulation of glomerular pressure and filtration indicates regulation of preglomerular resistance. Model and experimental studies were performed to evaluate two mechanisms in the kidney, myogenic response and tubuloglomerular feedback. A mathematical model showed good autoregulation through a myogenic response, aimed at maintaining a constant wall tension in each segment of the preglomerular vessels. Tubuloglomerular feedback gave rather poor autoregulation. The myogenic mechanism showed 'descending' resistance changes, starting in the larger arteries, and successively affecting downstream preglomerular vessels at increasing arterial pressures. This finding was supported by micropuncture measurements of pressure in the terminal interlobular arteries. Evidence that the mechanism was myogenic was obtained by exposing the kidney to a subatmospheric pressure of 40 mmHg; this led to an immediate increase in renal resistance, which could not be prevented by denervation or various blocking agents.[2]
Bayliss effect
Bayliss effect or Bayliss myogenic response is a special manifestation of the
Increased contraction increases the
This effect is independent of nervous mechanisms, which is controlled by the sympathetic nervous system.
The overall effect of the myogenic response (Bayliss effect) is to decrease blood flow across a vessel after an increase in blood pressure.
History
The Bayliss effect was discovered by physiologist Sir William Bayliss in 1902.[5]
Proposed mechanism
When the endothelial cell in the
Unstable Membrane Potentials
Many cells have
Slow wave potentials
Slow-wave potentials are unstable resting membrane potentials that continuously cycle through depolarization- and repolarization phases. However, not every cycle reaches depolarization threshold and thus an action potential (AP) will not always fire. Owing to temporal summation (depolarization potentials spaced closely together in time so that they summate), however, cell membrane depolarization will periodically reach depolarization threshold and an action potential will fire, triggering contraction of the myocyte.[citation needed]
Pacemaker potentials
Pacemaker potentials are unstable cell membrane potentials that reach depolarization threshold with every depolarization/repolarization cycle. This results in AP's being fired according to a set rhythm. Cardiac pacemaker cells, a type of cardiac myocyte in the SA node of heart, are an example of cells with a pacemaker potential.[citation needed]
Stretch
This mechanism involves the opening of mechanically-gated Ca2+ channels when some myocytes are stretched. The resulting influx of Ca2+ ions lead to the initiation of excitation-contraction coupling and thus contraction of the myocyte.[citation needed]
See also
References
- ISBN 978-1-947172-04-3.
- PMID 2681599.
- ISBN 0-340-76376-0.[page needed]
- ISBN 963-242-726-2.[page needed]
- PMID 16992618.