<P> This is in contrast to heterometric regulation, governed by the Frank - Starling law, which results from a more favorable positioning of actin and myosin filaments in cardiomyocytes as a result of changing fiber lengths . </P> <P> 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 . </P> <P> 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 and reduces prostaglandin E2 release 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 . In the opposite case, juxtaglomerular cells are stimulated to release more renin, which stimulates the renin--angiotensin system, producing angiotensin I which is converted by Angio - Tensin Converting Enzyme (ACE) to angiotensin II . Angiotensin II then causes preferential constriction of the efferent arteriole of the glomerulus and increases the GFR . </P> <P> 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," 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 . </P>

Autoregulatory increase of blood flow to a tissue