Adrenaline physiological effects

Epinephrine is also known as adrenaline and is a hormone with profound physiological effects designed to prepare the body for fight or flight... 

Catecholamines. The catecholamines, epinephrine (EPl adrenaline) (85), norepinephrine (NE noradrenaline) (86) (see Epinephrine and norepinephrine), and dopamine (DA) (2), are produced from tyrosine by the sequential formation of L-dopa, DA, NE, and finally EPl. EPl and NE produce their physiological effects via CC- and -adrenoceptors, a-Adrenoceptors can be further divided into CC - and a2-subtypes which in turn are divided... 

Ahlquist, in 1948, first proposed that noradrenaline could produce its diverse physiological effects by acting on different populations of adrenoceptors, which he termed a and ft receptors. This classification was based upon the relative selectivity of adrenaline for the a receptors and isoprenaline for the ft receptors drugs such as phentolamine were found to be specific antagonists of the a, and propranolol for the ft receptors. 

Adrenaline is synthesised in the adrenal medulla and at sympathetic nerve endings from phenylalanine and metabolised by oxidation (monoamine oxidase MAO) or conjugation (catechol 0-methyl transferase COMT). It is excreted in the urine as vanillylmandelic acid. Its main physiological effects are at pi and a adrenoceptors, with less marked effects at (P2... 

ADRENAL MEDULLA HORMONES. Adrenaline (epinephrine) and its immediate biological precursor noradrenaline (norepinephrine, levartei-nol) are the principal hormones of the adult adrenal medulla. See Fig.l. Some of the physiological effects produced by adrenaline arc contraction of the dilator muscle of the pupil of the eye (mydriasis), relaxation of the smooth muscle of the bronchi constriction of most small blood vessels dilation of some blood vessels, notably those in skeletal muscle increase in heart rate and force of ventricular conlraction relaxation of the smooth muscle of the intestinal tract and either contraction or relaxation, or both, of uterine smooth muscle. Electrical stimulation of appropriate sympathetic (adrenergic) nerves can produce all the aforementioned effects with exception of vasodilation in skeletal muscle. 

The source of the ergot strongly influences the type of alkaloids present, as well as the clinical picture of ergotism [171]. The ergot alkaloids have three types of physiological effects they cause contraction of smooth muscle, they block the action of serotonin and adrenaline, and they act on the hypothalamic-pituitary system to inhibit the secretion of prolactin. These properties have led to their being used to induce uterine contractions, to relieve migraine headaches, and to treat prolactin-dependent disorders. 

The multiple drug effects on smooth muscles are also little understood. Thus, isoprenaline relaxes and adrenaline and noradrenaline contract the isolated rat aorta, but all three catecholamines increase cyclic AMP formation [61]. Adrenaline induces relaxation and prostaglandin Ei contraction in the estrogen-treated rat isolated myometrium, but both adrenaline and prostaglandin Ei elevate the cyclic AMP level in the tissue [62]. An example of a critical evaluation of the evidence linking cyclic AMP to a physiological effect (cardiac contractility) is that of Sobel and Mayer [63]. 

The adrenal medulla secretes adrenaline (80%) and noradrenaline (20%). They have similar physiological effects, which augment activation of the sympathetic nervous system. 

Antagonism occurs when the action of one drug opposes the action of another. The two drugs simply have opposite pharmacodynamic effects, e.g. histamine and adrenaline on the bronchi exhibit physiological or functional antagonism or they compete reversibly for the same drug receptor, e.g. flumazenil and benzodiazepines exhibit competitive antagonism. 

Adrenergic mechanisms have a role in the physiological control of plasma potassium concentration. The biochemical pump that shifts potassium into cells is activated by the P -adrenoceptor agonists (adrenaline, salbutamol, isoprenaline) and can cause hypokalaemia. Pj-adrenoceptor antagonists block the effect. 

By using a drug with opposite effects, e.g. histamine constricts bronchi, causes vasodilatation and increases capillary permeability. Adrenaline (epinephrine), by activating a and adrenoceptors, produces opposite effects — referred to as physiological antagonism. 

Adrenaline and noradrenaline can both give rise to melanins (c/. below). An intermediate in such a transformation of adrenaline is adrenochrome, a molecule stabilized by resonance (359). Adrenochrome has a powerful effect on the maturation of reticulocytes (281) and might play a part in normal physiological processes. The extent to which adrenaline is converted to adrenochrome and melanin, and its significance, is still unknown. 

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