Alpha-2 adrenergic agonists

Svensson, T. H., Bunney, B. S., and Aghajanian, G. K. (1975) Inhibition of both noradrenergic and serotonergic neurons in brain by the alpha-adrenergic agonist, clonidine. Brain Res., 92 291— 306. 

Primarily an alpha-adrenergic agonist, indora-mine in a dose of 50 mg/d has also antihistamine and antidopamine properties. 

Mechanism of Action An ocular alpha-adrenergic agent that is a relatively selective alphaj receptor agonist. Therapeutic Effect Reduces intraocular pressure. 

Mechanism of Action An alpha-adrenergic agonist that stimulates alphaj-adrenergic receptors. Inhibits sympatheticcardioaccelerat or and vasoconstrictor center to heart, kidneys, peripheral vasculature. Therapeutic Effect Decreases systolic, diastolic blood pressure (BP). Chronic use decreases peripheral vascular resistance. Pharmacohinetics Well absorbed from gastrointestinal (GI) tract. Widely distributed. Protein binding 90%. Metabolized in liver. Excreted in urine and feces. Not removed by hemodialysis. Half-life 6 hr. 

Mechanism of Action An alpha-adrenergic receptor agonist that causes vasoconstriction, reflex bradycardia, inhibits GI smooth muscle and vascular smooth muscle supplying skeletal muscle and increases heart rate and force of heart muscle contraction. Therapeutic Effect Increases both systolic and diastolic pressure. 

Clonidine reduces opiate withdrawal symptoms because it acts on the noradrenergic system, and some opiate withdrawal symptoms are due to noradrenergic overactivity. Specifically, it is an alpha-adrenergic agonist which acts preferentially on presynaptic alpha-2 neurons to inhibit noradrenergic transmission, with the action in the locus... 

Mechanism of Action Fomis an active metabolite, desglymidodrine, an alpha, adrenergic-agonist. Activation of the arteriolar and venous vasculature, producing and increase in vascular tone and elevation of blood pressure. 

Ghosh S, Sinhababu S P, Sukul N C. 1997. Suppression of alpha adrenergic agonist-induced catalepsy in mice by potentized Agaricus muscarius. BrHomJ 86 139-141. 

The primary side effects associated with alpha-1-specific agonists are caused by excessive stimulation of alpha-adrenergic responses. Some of the more frequent side effects include increased blood pressure, headache, and an abnormally slow heart rate (because of reflex bradycardia). Some patients also report chest pain, difficulty breathing, and feelings of nervousness. These side effects are quite variable and are usually dose-related (i.e., they occur more frequently at higher doses). 

Rm did not correlate with the intrinsic activity of agonists for their ability to attenuate adenylate cyclase stimulation (36).In that system, only the ratio of K./K appeared to correlate with the intrinsic activity ofLthe alpha-adrenergic agonists. Here, in anterior pituitary membranes constant proportions of both receptor states were evidenced but ratios of 30-200 were found for K./Km for a series of dopaminergic agonists despite the fact that these agonists all appear to display full intrinsic activity in their ability to inhibit prolactin secretion from pituitary cells. 

As with most DA, agonists, the majority of DA2 agonists are active on other receptors. In particular, many ergot derivatives exhibit alpha-adrenergic and serotonin activity (26). 

In contrast, Bach et al (27) reported that the pyrazole derivative (LY 141865) is devoid of alpha and serotonin agonist and antagonist effects. Preliminary studies in our laboratories demonstrated that LY 141865 is a potent DA2 agonist without alpha-adrenergic or DAj activity. 

The purpose of this model is to produce a setting in which proarrhythmic drugs may exacerbate the occurrence of a torsade-like ventricular tachycardia. This is achieved using anesthetized rabbits receiving an intravenous infusion of the alpha-adrenergic agonist methoxamine as described by Carlsson et al. (1990). 

These are used in treatment of migraine and in obstetrics (to control late uterine bleeding - postpartum haemorrhage). Their predominant action involves vasoconstriction (partial agonist effects at alpha-adrenergic receptors and 5-HT receptor-mediated effects). They are metabolized mainly via CYP3A4. 

Haws CM, Heinricher MM, Fields HE (1990) Alpha-adrenergic receptor agonists, but not antagonists, alter the tail-flick latency when microinjected into the rostral ventromedial medulla of the lightly anesthetized rat. Brain Res 533 192-195 Hayes RL, Mao J, Price DD, Germane A, D Avella D, Fieri M, Mayer DJ (1992) Pretreatment with gangUosides reduces abnormal nociceptive responses associated with a rodent peripheral neuropathy. Pain 48 391-396... 

Gharagozloo NZ, Relf SJ, Brubaker RF. Aqueous flow is reduced by the alpha-adrenergic agonist apraclonidine hydrochloride (ALO 2145). Ophthalmology 1988 95 1217-1220. 

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