Autoregulation

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Autoregulation is a process within many biological systems, resulting from an internal adaptive mechanism that works to adjust (or mitigate) that system's response to stimuli. While most systems of the body show some degree of autoregulation, it is most clearly observed in the kidney, the heart, and the brain.[1] Perfusion of these organs is essential for life, and through autoregulation the body can divert blood (and thus, oxygen) where it is most needed.

Cerebral autoregulation[edit]

More so than most other organs, the brain is very sensitive to increased or decreased blood flow, and several mechanisms (metabolic, myogenic, and neurogenic) are involved in maintaining an appropriate cerebral blood pressure. Brain blood flow autoregulation is abolished in several disease states such as traumatic brain injury,[2] stroke,[3] brain tumors, or persistent abnormally high CO2 levels.[4][5]

Homeometric autoregulation[edit]

Homeometric autoregulation, in the context of the circulatory system, is the heart's ability to increase contractility and restore stroke volume when afterload increases.[6] This is in contrast to heterometric regulation.

Coronary circulatory autoregulation[edit]

Since the heart is a very aerobic organ, needing oxygen for the efficient production of ATP & Creatine Phosphate from fatty acids (and to a smaller extent, glucose & very little lactate), the coronary circulation is auto regulated so that the heart receives the right flow of blood & hence sufficient supply of oxygen. If a sufficient flow of oxygen is met and the resistance in the coronary circulation rises (perhaps due to vasoconstriction), then the coronary perfusion pressure (CPP) increases proportionally, to maintain the same flow. In this way, the same flow through the coronary circulation is maintained over a range of pressures. This part of coronary circulatory regulation is known as auto regulation and it occurs over a plateau, reflecting the constant blood flow at varying CPP & resistance. The slope of a CBF (coronary blood flow) vs. CPP graph gives 1/Resistance.

Renal autoregulation[edit]

Regulation of renal blood flow is important to maintaining a stable glomerular filtration rate (GFR) despite changes in systemic blood pressure (within about 80-180 mmHg). In a mechanism called tubuloglomerular feedback, the kidney changes its own blood flow in response to changes in sodium concentration. The sodium chloride levels in the urinary filtrate are sensed by the macula densa cells at the end of the ascending limb. When sodium levels are moderately increased, the macula densa releases ATP[7] and reduces prostaglandin E2 release[8] to the juxtaglomerular cells nearby. The juxtaglomerular cells in the afferent arteriole constrict, and juxtaglomerular cells in both the afferent and efferent arteriole decrease their renin secretion. These actions function to lower GFR. Further increase in sodium concentration leads to the release of nitric oxide, a vasodilating substance, to prevent excessive vasoconstriction.[8] In the opposite case, juxtaglomerular cells are stimulated to release more renin, which stimulates the renin-angiotensin system, producing angiotensin II which constricts the efferent arteriole and increases GFR.

Autoregulation of genes[edit]

This is so-called "steady-state system". An example is a system in which a protein P that is a product of gene G "positively regulates its own production by binding to a regulatory element of the gene coding for it,"[9] and the protein gets used or lost at a rate that increases as its concentration increases. This feedback loop creates two possible states "on" and "off". If an outside factor makes the concentration of P increase to some threshold level, the production of protein P is "on", i.e. P will maintain its own concentration at a certain level, until some other stimulus will lower it down below the threshold level, when concentration of P will be insufficient to make gene G express at the rate that would overcome the loss or use of the protein P. This state ("on" or "off") gets inherited after cell division, since the concentration of protein a usually remains the same after mitosis. However, the state can be easily disrupted by outside factors. [9]

See also[edit]

References[edit]

  1. ^ Autoregulation
  2. ^ Figaji, Anthony A.; Eugene Zwane; A. Graham Fieggen; Andrew C. Argent; Peter D. Le Roux; Peter Siesjo; Jonathan C. Peter (2009). "Pressure autoregulation, intracranial pressure, and brain tissue oxygenation in children with severe traumatic brain injury". Journal of Neurosurgery. Pediatrics 4 (5): 420–428. doi:10.3171/2009.6.PEDS096. ISSN 1933-0715. PMID 19877773. 
  3. ^ Budohoski K. P., Czosnyka M., Kirkpatrick P. J., Smielewski P., Pickard J. D. (2013). "Clinical relevance of cerebral autoregulation following subarachnoid haemorrhage". Nat. Rev. Neurol 9 (3): 152–63. doi:10.1038/nrneurol.2013.11. 
  4. ^ Paulson, O. B.; S. Strandgaard; L. Edvinsson (1990). "Cerebral autoregulation". Cerebrovascular and Brain Metabolism Reviews 2 (2): 161–192. ISSN 1040-8827. PMID 2201348. 
  5. ^ Panerai, R. B.; S. T. Deverson; P. Mahony; P. Hayes; D. H. Evans (1999). "Effect of CO2 on dynamic cerebral autoregulation measurement". Physiological Measurement 20 (3): 265. doi:10.1088/0967-3334/20/3/304. ISSN 0967-3334. Retrieved 2015-01-24. 
  6. ^ Sarnoff SJ, Mitchell JH, Gilmore JP, Remensnyder JP (1960). "Homeometric autoregulation in the heart" (PDF). Circulation Research 8 (5): 1077–1091. doi:10.1161/01.res.8.5.1077. PMID 13746560. 
  7. ^ Bell, P. Darwin; Peter Komlosi, Zhi-Ren Zhang (2009). "ATP as a mediator of macula densa cell signalling". Purinergic Signalling 5 (4): 461–471. doi:10.1007/s11302-009-9148-0. ISSN 1573-9538. PMC 2776136. PMID 19330465. Retrieved 2015-01-24. 
  8. ^ a b Komlosi, P.; A. Fintha; P. D. Bell (2004). "Current mechanisms of macula densa cell signalling". Acta Physiologica Scandinavica 181 (4): 463–469. doi:10.1111/j.1365-201X.2004.01319.x. ISSN 0001-6772. PMID 15283759. 
  9. ^ a b Jablonka E., Lachmann M., Lamb M.J. (1992). "Evidence, Mechanisms and Models for the Inheritance of Acquired Characters". Journal of Theoretical Biology: 245–268. doi:10.1016/s0022-5193(05)80722-2.