Innervation adrenergic

Isoproterenol is given sublingually or by iv. It is metabolized by monoamine oxidase and catechol-0-methyltransferase in brain, Hver, and other adrenergically innervated organs. The pharmacological effects of isoproterenol are transient because of rapid inactivation and elimination. About 60% is excreted unchanged. Adverse effects using isoproterenol therapy include nervousness, hypotension, weakness, dizziness, headache, and tachycardia (86). 

The initial component of the PTX-induced contraction is selectively inhibited by ouabain, whereas the second component is rather potentiated by it (77). A similar inhibitory effect of ouabain on the contractile response to PTX is observed in the umbilical artery, which is devoid of adrenergic innervation 18). 

Cathinone and norpseudoephedrine have antagonist effects at the neuromuscular junction (Guantai et al. 1987). This is likely a direct blocking effect, independent of cholinergic and adrenergic innervation. However, motor effects are not reported at doses commonly used. 

This group consists of j3-adrenergic receptor blockers, the antiarrhythmic activity of which is associated with inhibition of adrenergic innervation action of the circulatory adrenaline on the heart. Because all 8-adrenoblockers reduce stimulatory sympathetic nerve impulses of catecholamines on the heart, reduce transmembrane sodium ion transport, and reduce the speed of conduction of excitation, sinoatrial node and contractibility of the myocardium is reduced, and automatism of sinus nodes is suppressed and atrial and ventricular tachyarrhythmia is inhibited. 

This can be accomplished either by reducing the load on the heart, or by lowering systemic venous and arterial pressure (nitrates and nitrites), or by partial suppression of adrenergic innervation of the heart (j3-adrenoreceptors), or by suppressing calcium ion transport in myocardial cells since the contraction of smooth muscles vessels is controlled by the concentration of calcinm ions in the cytoplasm (Ca channel blockers). The resulting effect of the aforementioned drngs is that they reduce the need for oxygen in the heart. 

These drugs are best avoided in patients with cerebrovascular, cardiovascular and hepatic disorders. Some sympathomimetic effects may occur, mainly mild tremor and occasionally cardiac arrhythmias. Apparent anticholinergic effects may also occur but these are the result of sympathetic potentiation in tissues with dual cholinergic/adrenergic innervation, e.g. pupil. Sympatholytic effects can also occur, principally postural hypotension, because of synthesis of relatively inactive false transmitters, e.g. octopamine, in nerve terminals following inhibition of MAO and activation of alternative metabolic pathways. 

Distribution of receptors Adrenergically innervated organs and tissues tend to have a predominance of one type of receptor. For example, tissues such as the vasculature to skeletal muscle have both a and p2 receptors, but the p2 receptors predominate. Other tissues may have one type of receptor exclusively, with practically no significant numbers of other types of adrenergic receptors. For example, the heart contains predominantly Pi receptors. 

Topical instillation of a 1% solution in eyes with normal adrenergic innervation causes mydriasis and also some vasoconstriction. However, hydroxyamphetamine is used only as a mydriatic agent. After topical application onset occurs within 15 minutes, maximum dilation occurs within 60 minutes, and the duration of mydriasis is approximately 6 hours. The U.S. Food and Drug Administration has labeled this drug as a Pregnancy Category C. 

The ocular effects of cocaine include anesthesia (see Chapter 6), mydriasis, and vasoconstriction. The mydriatic effect of cocaine depends on the presence of a functioning adrenergic innervation. After topical appUcation to the eye, the pupil begins to dilate within 15 to 20 minutes. The maximum effect, which is typically less than 2 mm of dilation, occurs within 40 to 60 minutes, and the pupil may remain dilated for 6 or more hours. The mydriasis is accompanied by vasoconstriction that causes blanching of the conjunctiva. Cocaine is also readily absorbed through the mucous membranes into the systemic circulation. 

A review of adrenergic innervation of the manunalian oviduct includes a summary of drugs that modify the sympathetic nervous system and affect ovum transport and fertility.125 plants are a relatively untapped potential source of new antifertility agents.126... 

Pinealoma. The circadian rhythms of the pineal gland and their ancient beginnings, and their oncologic connotations, are present in the pinealoma. This neuroendocrine organ receives its adrenergic innervations from the hypothalamic suprachiasmatic... 

F]Fluorometaraminol Demetallation Cardiac adrenergic innervation Matsson et al. (1999)... 

The coronary vessels are innervated by both the parasympathetic and sympathetic divisions of the autonomic nervous system, as demonstrated by light microscope (Woollard, 1926) and electron microscope (Lever etal, 1965 Malor et ai, 1973). Cholinergic innervation has been demonstrated with the acetylcholinesterase-staining technique (Denn and Stone, 1976 Gerova et ai, 1979) and adrenergic innervation has been shown with flourescent histochemical methods (Denn and Stone 1976 Dolezel et ai, 1978, Nielsen and Owman, 1968). 

One or more triggering factors, such as stress, certain foods, trauma, or hormone changes, usually initiate the onset of the migraine leading to vasoconstriction and subsequent vasodilatation of the adrenergically innervated blood vessels at the base of the brain and in the meninges. 

Donald J. Comparative study of the adrenergic innervation of the teleost gill. J Morphol 1987 193 63-73. 

L-amino acid decarboxylase . However, the enzyme has been studied only in a few tissues in which it occurs in great abundance (kidney, adrenal medulla) and it is not clear whether in fact a single enzyme is common to all tissues with decarboxylase activity. In common with other amino-acid decarboxylases, DOPA decarboxylase requires pyridoxal phosphate as a cofaaor. The enzyme is present in relatively high activity in the adrenal medulla and in adrenergically innervated tissues (Van about 1000 times that of tyrosine hydroxylase). 

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