Epinephrine breakdown

Stimulation of glycogen breakdown involves consumption of molecules of ATP at three different steps in the hormone-sensitive adenylyl cyclase cascade (Figure 15.19). Note that the cascade mechanism is a means of chemical amplification, because the binding of just a few molecules of epinephrine or glucagon results in the synthesis of many molecules of cyclic / MP, which, through the action of c/ MP-dependent protein kinase, can activate many more molecules of phosphorylase kinase and even more molecules of phosphorylase. For example, an extracellular level of 10 to 10 M epinephrine prompts the for-... 

Epinephrine is a signal that energy is needed immediately. It stimulates breakdown of glycogen, fat, and protein. 

Thus, epinephrine causes a rapid response toward net glycogen breakdown to provide for the energy needs of muscle. 

A dose of 1 at 30 mg/kg increased the effects of intravenous doses of epinephrine at 5 g/kg and of dl-noreplnephrine at 10 ug/kg on both blood flow and blood pressure. Intravenous phenoxybenzamine at 15 mg/kg plus tolazollne at 2 mg/kg prevented almost completely the actions of I on blood pressure and blood flow Intravenous reserpine at 2 mg/kg increased markedly the effects of I at 30 mg/kg on blood pressure and peripheral resistance, but converted the usual immediate, small, temporary increase in blood flow into an immediate, small, temporary decrease. These various responses would be expected from either a mild sympathomimetic amine or an inhibitor of the breakdown of endogenous catecholamines Indeed, I at 10 M, was found to inhibit the monoamlneoxldase of the rat s liver. If the dose of I used in these experiments were distributed into the same fraction of the body water as that estimated for the human body,the concentration in the plasma would be about 9 times that stated above as the effective concentration for inhibiting the mono amine oxIdase. It is possible that inhibition of monoamlneoxldase by I plays a part in inducing the effects of the oxime on blood vessels and blood pressure. It is possible also that I interferes with reuptake of catecholamines by nerve endings this possibility seems not to have been explored. 

Local anesthetics are frequently coadministered with vasoconstrictor molecules such as epinephrine. Normally, they are applied or injected locally and then taken up by local blood vessels into the systemic circulation, ultimately leading to their metabolic breakdown. The co-administration of a vasoconstrictor decreases the systemic absorption of the local anesthetic, thereby increasing its effective half-life in the area of administration and decreasing the probability of systemic toxicity (i.e., cardiac toxicity) secondary to systemic distribution. 

Glucagon or epinephrine decreases [fructose 2,6-bisphosphate]. The hormones do this by raising [cAMP] and bringing about phosphorylation of the bifunctional enzyme that makes and breaks down fructose 2,6-bisphosphate. Phosphorylation inactivates PFK-2 and activates FBPase-2, leading to breakdown of fructose 2,6-bisphosphate. Insulin increases [fructose 2,6-bisphosphate] by activating a phosphoprotein phosphatase that dephosphorylates (activates) PFK-2. 

In muscle, epinephrine stimulates glycogen breakdown and glycolysis, providing ATP to support contraction. 

Glucagon causes an increase in blood glucose concentration in several ways (Table 23-4). Like epinephrine, it stimulates the net breakdown of liver glycogen... 

Hormonal control Glycogen metabolism is tightly controlled by hormones. When blood glucose by epinephrine levels fall, glucagon is secreted by the a cells of the pancreas and acts on the and glucagon liver to stimulate glycogen breakdown to glucose which is then released into... 

The breakdown of fatty acids in (3-oxidation (see Topic K2) is controlled mainly by the concentration of free fatty acids in the blood, which is, in turn, controlled by the hydrolysis rate of triacylglycerols in adipose tissue by hormone-sensitive triacylglycerol lipase. This enzyme is regulated by phosphorylation and dephosphorylation (Fig. 5) in response to hormonally controlled levels of the intracellular second messenger cAMP (see Topic E5). The catabolic hormones glucagon, epinephrine and norepinephrine bind to receptor proteins on the cell surface and increase the levels of cAMP in adipose cells through activation of adenylate cyclase (see Topic E5). The cAMP allosterically activates... 

Gs Epinephrine, glucagon Adenylyl cyclase Glycogen/fat breakdown... 

The neurotransmitter action of epinephrine is terminated by reuptake into the neuron that released it, or breakdown to inactive metabolites by the enzymes catechol-O-methyl transferase (COMT) and monoamine oxidase (MAO). The second messenger effects inside the cell are terminated by enzymes that break down cAMP, and by phosphatases that reverse the action of the kinases by removing phosphates. 

The action of epinephrine illustrates the principles by which cyclic AMP mediates hormone action. Epinephrine is the flight or fight hormone that the adrenal glands release in response to stress. The hormone causes an increase in blood pressure and the breakdown of... 

If the interaction occurs, emitted light intensity will decrease at 476 nm and increase at 527 nm on addition of epinephrine to cells expressing the fusion proteins. If the interaction does not occur, the wavelength of the emitted light will remain at 476 nm. There are several reasons why this might fail for example, the fusion proteins (1) are inactive or otherwise unable to interact, (2) are not translocated to their normal subcellular location, or (3) are not stable to proteolytic breakdown. 

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