The following points highlight the top six effects of Catecholamines. The effects are:- 1. Effects on Carbohydrate Metabolism 2. Effects on Lipid Metabolism 3. Effects on Protein Metabolism 4. Thermeogenesis 5. Effects on cardiovascular system 6. Effects on Smooth Muscles.
1. Effects on Carbohydrate Metabolism:
(i) Adrenaline increases blood glucose level by enhancing hepatic glycogenolysis on binding to β2 and α1 receptors on the hepatocyte membrane. NE has little effect on blood glucose.
(ii) Adrenaline increases blood glucose by stimulating hepatic gluconeogenesis, on binding to hepatic β2-receptors.
In skeletal and cardiac muscles, the β2 effect of epinephrine enhances glycolysis, but in smooth muscles, the α1-effect of epinephrine leads to enhanced glycolysis.
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Catecholamines inhibit pancreatic insulin secretion by β-cells through α1 effects. On the other hand, catecholamines are stimulatory to glucagon secretion through an action on β-ARs of pancreatic a cells. Thus, during stress, elevated level of E would be stimulatory to many physiological processes that would elevate blood glucose levels.
2. Effects on Lipid Metabolism:
In adipose tissues, lipolysis is stimulated in response to catecholamine action. Both E and NE can increase cAMP that activates hormone sensitive lipase, triglyceride lipase, which metabolize fats into free fatty acids and glycerol.
The free fatty acids thus released into blood are then taken up directly by certain tissues (brain, cardiac muscle) as sources of energy or these may be used by liver for the synthesis of glucose. In some cases, catecholamines may reduce lypolysis by decreasing the intracellular cAMP level through α2 effect.
3. Effects on Protein Metabolism:
Through the β-effect epinephrine may decrease the release of amino acids from skeletal muscles. As a result, lactate, glycerol and glucose levels would be increased and additional gluconeogenic substrates might not be needed.
4. Thermeogenesis:
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Epinephrine increases O2 consumption, BMR and body temperature. It is suggested that, during fasting, suppression of sympathetic activity may conserve calories by decreasing metabolism and heat production, whereas, during feeding, the increased sympathetic activity may expend the excess calories.
It has also been suggested that cold exposure stimulates brown adipose tissue growth by increasing the release of NE from sympathetic nerves. That neurohormone also activates mitosis in brown apipose tissue cells via β-receptors.
5. Effects on Cardiovascular System:
Catecholomines increase the rate and frequency of contraction and increase the irritability of the myocardium by activating myocardial β receptors. The release of catecholamines can increase heart rate and cardiac output and cause peripheral vasoconstriction—all lead to an increase in blood pressure.
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All such events are modulated by reflex mechanisms. Although NE, in the usual doses will have these effects, the effect of E may vary depending on the smooth muscle tone of the vascular system at the time.
For example, in an individual with a reduction in vascular tone, the mean blood pressure would be expected to increase. The central organisation of the sympathetic nervous system is such that its normal regulatory effects are quite discrete in contrast to periods of stress, when stimulation may be rather generalized and accompanied by release of catecholamines into the circulation.
6. Effects on Smooth Muscles:
Catecholamines also regulate smooth muscle activity in tissues other than blood vessels. Epinephrine relaxes smooth muscles of urinary bladder, bronchioles and gastrointestinal wall. It causes contraction of smooth muscles of bladder sphincter, dilator pupillae, spleen, pilomotor muscles, and both pregnant and non-pregnant human uteri.
Norepinephrine does not relax vascular and bronchial smooth muscles and it has weaker inhibitory effects than epinephrine on other smooth muscles.