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Results for “Adrenergic alpha-Agonists”

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At least 19 recordsLinked to original sources
PubMed1976

Effects of metabolic and pharmacologic interventions on myocardial infarct size following coronary occlusion.

A number of hemodynamic, pharmacologic and metabolic interventions were found to change the extent of acute ischemic injury of the myocardium and subsequent necrosis following experimental coronary artery occlusion. Reduction in myocardial damage occurred by decreasing myocardial oxygen demands (beta-adrenergic blocking agents, intra-aortic balloon counterpulsation, external counterpulsation, nitroglycerin, decreasing afterload in hypertensive patients, inhibition of lipolysis, and digitalis in the failing heart); by increasing myocardial oxygen supply either directly (coronary artery reperfusion or elevating arterial pO2), or through collateral vessels (elevation of coronary perfusion pressure by alpha-adrenergic agonists, intra-aortic balloon counterpulsation); or by increasing plasma osmolality (mannitol, hypertonic glucose); presumably by augmenting anaerobic metabolism (glucose-insulin-potassium, hypertonic glucose); by enhancing transport to the ischemic zone of substrates utilized in energy production (hyaluronidase); by protecting against autolytic and heterolytic damage (hydrocortisone, cobra venom factor, aprotinin). Augmentation of myocardial ischemic damage occurred as a consequence of increasing myocardial oxygen requirements (isoproterenol, glucagon, ouabain, bretylium tosylate, tachycardia); by decreasing myocardial oxygen supply either directly (hypoxia, anemia) or through reduction of collateral flow (hemorrhagic hypotension, minoxidil) or by decreasing substrate availability glycemia). Pilot studies have been carried out in patients with hyaluronidase, nitroglycerin, intra-aortic balloon counterpulsation, beta-blocking agents and Arfonad and have shown that these interventions may also reduce myocardial damage, suggesting that the concept of reduction in infarct size following coronary occlusion is applicable clinically.

Acute Disease↗
PubMed1975

Mechanism of action of pentagastrin and acetylcholine on the longitudinal muscle of the canine antrum.

1. Electrical and mechanical activities of the longtitudinal muscle of the dog antrum were recorded with the double sucrose-gap technique. 2. The muscle exhibited spontaneous action potentials which consisted of a spike-like potential which, after a brief and partial repolarization, was followed by a negative-going, plateau-type potential. In 97% of the preparations, no tension changes were produced by spontaneous action potentials. 3. Tetrodotoxin, atropine, alpha- and beta-adrenoceptor antagonists, and H1 and H2 receptor blocking agents had no effect on the action potential. It was concluded that the action potential was myogenic in origin. 4. The mean frequency of the action potential at 37+/- 0.5 degrees C was 1.0/min+/-0.06 (s.e. of mean, n=92) and the mean duration 7.1+/-0.2 sec (s.e. of mean, n=11). 5. Steady depolarizing current increased whereas hyperpolarizing current decreased the frequency of the action potential. 6. Length-tension relations were studied. In twelve strips, the average resting, passive, tension at LO was 570 mg. The active force of isometric contraction produced by acetylcholine increased with strip length up to a maximum, then decreased wtih further increased in length. There were no mechanical responses to pentagastrin. 7. Pentagastrin had two sites of action. On smooth muscle, it increased the frequency of the action potential in a dose dependent fashion. Threshold concentraions ranged from 2X10-14 to 10-11M. The ED50 was 2X10-10M. The maximum response, 5.4/min, was reached at 10-8M. Pentagastrin also released acetylcholine from intramural cholinergic nerves. 8. Pentagastrin reduced the amplitude and duration of the action potential.

Acetylcholine↗
PubMed1975

Comparison of beta-adrenoceptor blocking properties of sotalol, oxprenolol, propranolol and pindolol on rabbit intestinal smooth muscle.

Adrenergic agonists produced a characteristic and definite decrease in the amplitude of spontaneous contractions and tone of the isolated rabbit jejunum. Effect of phenylephrine was abolished either by phenoxybenzamine or phentolamine. Relaxation induced by epinephrine and by norepinephrine was inhibited after combined treatment with phentolamine and propranolol. Phentolamine alone diminished the response to epinephrine and to norepinephrine, but the diminution for epinephrine was greater, indicating that epinephrine has a greater affinity for alpha- than for beta-receptors in the rabbit jejunum. Stimulation of the beta-receptors by isoproterenol was inhibited by propranolol, oxprenolol, sotalol and pindolol, but the block was incomplete. The activity of these four beta-blockers in preventing the inhibitory response to isoproterenol was as follows: inidolol greater than or equal to oxprenolol greater than propranolol greater than sotalol. This demonstrates the fact that not all beta-adrenergic blocking agents possess an identical pharmacologic spectrum of activity. Also it can be suggested that the beta-receptors of jejunum differ in specificity from those of other organs.

Adrenergic alpha-Agonists↗
PubMed1979

Direct binding studies of adrenergic receptors: biochemical, physiologic, and clinical implications.

Recently developed radioligand binding techniques permit direct investigation of the alpha- and beta-adrenergic receptors for catecholamines in a wide variety of tissues. These techniques allow the receptors to be quantitated, characterized, and studied under varying conditions of physiologic and pathophysiologic interest. They are providing fresh insights into the mechanisms by which endogenous catecholamines and other hormones regulate the properties of the adrenergic receptors and, in turn, control tissue sensitivity to catecholamine action.

Adrenergic alpha-Agonists↗
PubMed1975

The clinical use of dopamine in the treatment of shock.

Dopamine is a direct-acting catecholamine with a short half-life that has many advantages in treating visceral hypoperfusion states such as shock and refractory heart failure. Unlike other inotropic drugs, dopamine directly dilates the mesenteric, renal, and cerebral vessels and redirects blood flow to essential viscera. This dopaminergic effect is prominent with doses of 100-700 mug/min in adults and is attenuated by phenothiazines and haloperidol. At doses of 700-1400 mug/min, dopamine also has a significant beta-adrenergic, inotropic effect, increasing myocardial contractility. The inotropic effect is equivalent to that of isoproterenol, epinephrine, and norepinephrine, but tachycardia, tachyarrhythmias, and angina may be less frequent with dopamine. In doses greater than 1400 mug/min, dopamine is a vasoconstrictor with pressor effects usually equivalent to that of norepinephrine. Dopamine dilates pupils, does not dilate bronchi, and does not shunt blood from viscera to skeletal muscles as does isoproterenol. Because dopamine increases myocardial contractility, selectively redistributes perfusion to essential viscera and allows a pharmacologic titration of effect, it is a logical first-choice catecholamine for treatment of shock and refractory heart failure.

Adrenergic alpha-Agonists↗
PubMed1975

On the mechanism of the relaxing adrenaline effect on cat jejunum.

The effect of propranolol, phentolamine, papaverine, theophyline and Ca++, administered in different combinations of their threshold doses, on the relaxing effect of adrenaline was studied on an isolated segment of proximal jejunum of male cats. It was established that phentolamine weakened the relaxing effect of adrenaline, while propranolol had no effect on it. Papaverine potentiated the relaxinf effects of adrenaline both when administered alone and in combination with propranolol or with phentolamine. Theophylline weakened the relaxing effect of adfrenaline and of the combination phentolamine-adrenaline. Ca++ increased the smooth-muscle tone. The interpretation of the results obtained leads to the fundamental conclusions that the relaxing effect of adrenaline on cat jejunum is more alpha- than beta-adrenergically determined and that the system of the cyclic AMP participates in its realization. At the smae time, however, the possibility of participation of other mechanisms is not excluded. The smooth-muscle effect of papaverine and theophylline is not determined only by their inhibitory effect on phosphodiesterase.

Adrenergic alpha-Agonists↗
PubMed1975

Metabolic inhibition and adrenoceptor interconversion.

The adrenergic receptor responses of isolated strips of iris dilator muscle from rabbits were studied. An alpha agonist, norepinephrine and a beta agonist, isoprenaline, were used to assess adrenergic sensitivity before and after pretreatment of tissues with metabolic inhibitors at 22, 29 and 37 degrees C. The metabolic inhibitors used were iodoacetic acid and dinitrophenol. Temperature change altered adrenoceptor sensitivity in the same manner before and after metabolic inhibition. Iodoacetic acid (10.4 mug/ml) pretreatment increased both alpha and beta responses. Dinitrophenol (1.8 mug/ml) pretreatment increased alpha and decreased beta responsiveness. The results obtained indicate that some metabolic process altered by dinitrophenol may be involved in this adrenoceptor interconversion seen when temperature is changed. This supports the theory that local environment determines the drug sensitivity (alpha or beta) of a single adrenergic receptor.

Adrenergic alpha-Agonists↗
PubMed1975

N-Isopropyl derivatives of dopamine and 5,6-dihydroxy-2-aminotetralin.

Secondary and tertiary amino homologs of the title compounds have been prepared, bearing an N-isopropyl group. In peripheral evaluation, certain members of the series exhibited beta-adrenergic agonist effects of lower activity than isoproterenol. N-Methyl-N-isopropyl-5,6-dihydroxytetralin exhibited marked properties consistent with its being an alpha agonist, and it is concluded that introduction of considerable bulk about the nitrogen of a catecholamine does not a priori destroy alpha-agonist effects. The compounds qualitatively paralleled the effects of dopamine in assays based upon direct intrastriatal administration in rats, although they were less potent than dopamine.

2-Naphthylamine↗
PubMed1975

Relative pre- and postsynaptic potencies of alpha-adrenoceptor agonists in the rabbit pulmonary artery.

The rabbit pulmonary artery contains postsynaptic alpha-adrenoceptors which meidate smooth muscle contraction; its noradrenergic nerves contain presynaptic alpha-adrenoceptors which mediate inhibition of the release of the transmitter evoked by nerve impulses. Dose-response curves for the pre- and postsynaptic effects of eight alpha-receptor agonists were determined on superfused strips of the artery in the presence of cocaine, corticosterone and propranolo. 1. According to the concentrations which caused 20% of the maximal contraction (EC20 post), the postsynaptic rank order of potency was: adrenaline greater than noradrenaline greater than oxymetazoline greater than naphazoline greater than phenylephrine greater than tramazoline greater than alpha-methylnoradrenaline greater than methoxamine. The pA2 values of phentolamine againstoxymethazoline, phenylephrine, alpha-methylnoradrenaline and methoxamine were 7.43, 7.48, 7.59 and 7.69, respectively. 2. For the investigation of presynaptic effects, the arteries were preincubated with 3H-noradrenaline. All agonists inhibited the overflow of tritium evoked by transmural sympathetic nerve stimulation. According to the concentrations which reduced the stimulation-induced overflow by 20% (EC20 pre), the rank order of potency was: adrenaline greater than oxymetazoline greater than tramazoline greater than alpha-methylnoradrenaline greater than noradrenaline greater than naphazoline greater than phenylephrine greater than methoxamine. 10(-5) M phentolamine shifted the presynaptic dose-response curves for moradrenaline and oxymethazoline to the right. 3. The ratio EC20 pre/EC20 post was calculated for each agonist as an index of its relative post- and presynaptic potency. According to the ratios, the agonists were arbitrarily classified into three groups. Group 1 (ratio about 30: preferentially postsynaptic agonists) comprised methoxamine and phenylephrine; group 2 (ratio near 1; similar pre- and postsynaptic potencies) comprised noradrenaline, adrenaline and naphazoline; group 3 (ratio below 0.2; preferentially presynaptic agonists) comprised oxymetazoline, alpha-methylnoradrenaline and tramazoline (as well as clonidine). 4. Preferentially presynaptic and preferentially postsynaptic agonists had opposite effects on the basoconstrictor response to nerve stimulation. Methoxamine and phenylephrine either did not change or enhanced, but never reduced, the response. In contrast, oxymetazoline, alpha-methylnoradrenaline and tramazoline at low concentrations selectively inhibited the response to stimulation at low frequency (0.25-2Hz). 5. It is concluded that alpha-adrenoceptor agonists vary widely in their relative pre- and postsynaptic potencies, possibly because of structural differences between pre- and postsynaptic alpha-receptors. Pre- and postsynaptic components contribute to their overll postsynaptic effec in actively transmitting synapses. The preferential activation of presynaptic alpha-receptors results in alpha-adrenergic inhibition of synaptic transmission.

Adrenergic alpha-Agonists↗
PubMed1975

Investigation into some imidazoline compounds, with respect to peripheral alpha-adrenoceptor stimulation and depression of cardiovascular centers.

Peripheral alpha-adrenoceptor stimulation was tested by means of hypertensive effects of the drugs following i.v. injection in spinal rats. Naphazoline (NP), oxymetazoline (OM), St 91-2-(2,6-diethylphenylimino)-2-imidazolidine--and St 1697--2-(2-ethyl, 6-methylphenylimino)-2-imidazolidine--were 3 to 5 times more potent in tthis respect thatn clonidine (CLON) whereas St 363--2-(2,4-dichlorophenylimino)-2-imidazolidine--and xylazine (XY) exerted only approx. 1/20 the effect of that of clonidine. Sympathoinhibitory activity after i.v. injection was tested by the bradycardiac effect in vagotomized rats; St 1697, St 363 and XY were active, approx. 1/10-1/30 of CLON, whereas NP, OM and St 91 were inactive. However, following intracisternal (i.ci.) injection of cardiovascular depression, typical for clonidine: (1) in dogs with blocked beta-adrenoceptors, the drugs facilitated the vagally meditated cardiodepressor reflex in response to baroreceptor stimulation by i.v. injection of angiotensin; (2) in dogs treated with atropine and in (3) vagotomized cats (only NP, OM and St 363) a long lasting decrease in heart rate was observed. Some of the experiments were complicated by increases in blood pressure, due to the "leakage" of small amounts of the highly vasopressor active drugs, from the cisternal spaces into the peripheral circulation. The majority of results indicated, that the central cardiovascular depressor effects of the tested drugs depend on their alpha-adrenoreceptor stimulating potency and on their ability to penetrate from cerebrospinal fluid or from the blood to cardiovascular centers. Relationships between the ability for penetration and the lipoid affinity are discussed.

Adrenergic alpha-Agonists↗
PubMed1976

Importance of the aromatic ring in adrenergic amines. 2. Synthesis and adrenergic activity of some nonaromatic six- and eight-membered ring analogs of beta-phenylethanolamine.

The synthesis of beta-phenylethanolamine analogs in which the phenyl ring is replaced by cyclohexyl, cyclohexen-4-yl, cyclooctyl, cyclooctenyl, cycloocta-1,3-dien-2-yl, cycloocta-1,5-dienyl, and cyclooctatetraenyl was accompanied by conversion of the corresponding aldehydes to the cyanohydrins followed by reduction with lithium aluminum hydride. A preparatively useful synthesis of 1-formylcyclooctatetraene is described utilizing the photocycloaddition of methyl propiolate to benzene followed by reduction to the alcohol and oxidation with MnO2. All compounds, as their hydrochloride salts, exhibited indirect adrenergic activity on the rat vas deferens. On the reserpinized rat vas deferens all compounds potentiated the effects of exogenous norepinephrine. The results are in agreement with the conclusion that the more saturated the ring moiety, the greater the affinity for the amine uptake site of the vas deferens and suggest that there is no important interaction between the drug and this uptake site that involves pi-complex formation.

Adrenergic alpha-Agonists↗