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O ?-adrenoceptors

Noradrenaline and adrenaline increase blood pressure, although in various organs the perfusion can actually be reduced. Since adrenaline, in contrast to noradrenaline, stimulates a-and jSi-adrenoceptors and the jSi-subtype as well, its vascular effects are more complex than those of noradrenaline. In many vessel beds like the splanchnic area and the skin the O -adrenoceptor-mediated vasoconstriction is dominant. However, in others, like the active skeletal muscles, the jS2-adrenoceptor-mediated vasodilatation increases the blood flow. In the lower concentration range adrenaline induce an increase in blood pressure without elevated diastolic values. Catecholamines reduce the permeability of the vascular endothelium which might be of some importance for their antiallergic properties. [Pg.302]

The hydroxyl groups of the phenyl ring are a prerequisite for the activation of all adrenoceptors, if both are absent the molecule has only an indirect sympathomimetic effect (see Fig. 5). Indirect sympathomimetics only have a -, a2 and -adrenoceptor activity since they act via an increase of the noradrenaline concentration in the synaptic cleft. If the methyl-group at the N-position of adrenaline is substituted by a longer or more bulky moiety the molecule gains affinity for the and loses affinity for O -adrenoceptors. An isopropyl moiety is already the optimum for the affinity towards 0-adrenoceptors (isoprenaline), larger substituents enhance only the binding to the 2-subtype (for example fenoterol). [Pg.304]

O -Adrenoceptor antagonists (o -blockers) are competitive inhibitors at the level of Q -adrenoceptors. These receptors are found in many organs and tissues, but their predominant functional importance is to mediate the vasoconstrictor effects of endogenous catecholamines (noradrenaline, adrenaline) released from the sympathetic nerve endings. Conversely, Q -adrenoceptor antagonism by means of an a-blocker will inhibit this constrictor activity and hence cause vasodilatation. This vasodilator effect occurs in both resistance vessels (arterioles) and capacitance vessels (veins), since a-adrenoceptors are present in both types of vascular structures. Accordingly, both cardiac afterload and preload will be lowered, in particular when elevated. [Pg.323]

O -Adrenoceptor antagonists may be used as antihypertensives and occasionally in the treatment of... [Pg.323]

Phentolamine and phenoxybenzamine are older O -adrenoceptor antagonists, which may be used occasionally in course of the surgical removal of phaeochromocytoma, with the aim to suppress the vasoconstrictor effects of noradrenaline/adrenaline released from the tumor as a result of surgical manipulation. [Pg.324]

In the treatment of hypertension a selective O -adrenoceptor agent is preferable to the older, non-selective (ai - - a2)-blockers. Doxazosin is preferable to prazosin, because it has a slower onset and longer duration of action. It therefore causes less or no reflex tachycardia and orthostatic hypotension. [Pg.324]

Dopamine stimulates dopaminergic (DAi), and O -adrenoceptors. Accordingly, it is an inotropic agent that may also stimulate the kidney function. In higher doses, dopamine may cause vasoconstriction as a result of i-adrenoceptor stimulation. Dobutamine and dopamine may be combined, although this combination is hardly rational. [Pg.338]

Dobutamine is a directly acting synthetic catecholamine with predominant effects at pi receptors. It has weak 32 and a effects. It is a racemic mixture and both stereoisomers are p-adrenoceptor agonists. The (+) isomer is approximately ten times more potent as a p-receptor agonist than the (-) isomer, which is mainly responsible for the o-adrenoceptor activity. Unlike dopamine, dobutamine does not act by releasing noradrenaline or via dopaminergic receptors. [Pg.154]

Tizanidine o -Adrenoceptor agonist in the spinal cord Presynaptic and postsynaptic inhibition of reflex motor output Spasm due to multiple sclerosis, stroke, amyotrophic lateral sclerosis Renal and hepatic elimination t duration, 3-6 h Toxicities Weakness, sedation hypotension... [Pg.595]

But a high incidence of side-effects means they are used far less often. See o-adrenoceptor antagonists. [Pg.36]

Clonidine [ban, inn, usan] (clonidine hydrochloride [inn. usan] Catapres Dixarit ) is an imidazoline derivative, a (selective a2-subtype) o-adrenoceptor agonist. It can be used (orally or transdermally) as an antihypertensive (probably acting within the CNS). It has formerly been used in ANTIMIGRAINE prophylaxis, clonidine hydrochloride clonidine. [Pg.80]

R13615) is a synthetic steroid, a PROGESTOGEN, and has been used in HRT. It has also been used in anticancer treatment of prostate and breast cancer, medroglutaric acid meglutol. medroxalol [ban, inn, usan] (medroxalol hydrochloride [usan]) is a combined O-adrenoceptor ANTAGONIST and P-adrenoceptor ANTAGONIST. It can be used therapeutically as an ANTIHYPERTENSIVE. [Pg.173]

OCtOdrine [inn, usan] is a vasoconstrictor that formerly was used in the treatment of hypotensive states, octopamine [inn] (norsynephrlne noroxedrine) is a phenylethylamine alkaloid from Capsicum frutescens, Citrus spp., Cyperus spp. (Solanaceae, Rutaceae, Cyperaceae). It occurs in many animal tissues found in high concentrations in the posterior salivary gland of Octopus vulgaris. It serves as an invertebrate neurotransmitter. It is predominantly an O-ADRENOCEPTOR AGONIST, and has been used as a hypertensive to treat hypotensive states. [Pg.206]

TRIM (1-(2-trifluoromethylphenyl)imidazole) is a nitric OXIDE SYNTHASE INHIBITOR active on neuronal sites, and is used as a pharmacological tool, trimazosin (ban, inn] (trimazosin hydrochloride (usan]) contains a piperazinyl quinazolinyl nucleus and is similar to prazosin. It is an (tti-subtype) O-ADRENOCEPTOR antagonist with structure and actions. It is an ANTIHYPERTENSIVE, and can be used in combination with other drugs in heart FAaURE TREATMENT. [Pg.281]

FIGURE 4.13 Effect of the allosteric modulator 5-(N-ethyl-N-isopropyl)-amyloride (EPA) on the kinetics dissociation of [3H] yohimbine from o -adrenoceptors. (A) Receptor occupancy of [3H] yohimbine with time in the absence (filled circles) and presence (open circles) of EPA 0.03 mM, 0.1 mM (filled triangles), 0.3 mM (open squares), 1 mM (filled squares), and 3 mM (open triangles). (B) Regression of observed rate constant for offset of concentration of [3H] yohimbine in the presence of various concentrations of EPA on concentrations of EPA (abscissae in mM on a logarithmic scale). Data redrawn from [13]. [Pg.69]

However, another dimension may have been added with reports that in animals SCCBs also interact with peripheral o -adrenoceptors involving Ca2+. Thus the normal vasoconstrictive effects of agonist ligand interactions with the peripheral a2-adrenoceptors may be obtained. It should be remembered that endogenous NE is a nonselective a-agonist. Therefore, when SCCBs are also circulating (presumably at therapeutically effective levels) a2-stimulation by NE is blocked a,-stimulation is not. Thus vascular tone and peripheral resistance are reduced—and blood pressure with it. [Pg.450]


See other pages where O ?-adrenoceptors is mentioned: [Pg.192]    [Pg.268]    [Pg.6]    [Pg.7]    [Pg.7]    [Pg.8]    [Pg.15]    [Pg.31]    [Pg.46]    [Pg.47]    [Pg.55]    [Pg.82]    [Pg.137]    [Pg.164]    [Pg.178]    [Pg.183]    [Pg.219]    [Pg.219]    [Pg.223]    [Pg.230]    [Pg.248]    [Pg.257]    [Pg.266]    [Pg.269]   
See also in sourсe #XX -- [ Pg.289 ]




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