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At least 721 records · Page 40Linked to original sources
PubMed1984

Regional myocardial tissue blood flow during beta-adrenergic blockade in cat hearts with acute ischaemia.

Selective beta 1- or beta 2-adrenergic blockade was achieved by practolol or IPS 339, respectively, in cats with acute ligation of a coronary artery. During blockade, heart rate was kept constant by atrial pacing and blood pressure reduction was prevented by aortic clamping. Regional myocardial blood flow was measured by the distribution of 15 micron labelled microspheres. Practolol slightly reduced epicardial blood flow in ischaemic myocardium, while blood flow in border and normally perfused myocardium remained unchanged. Following IPS 339, myocardial tissue flow increased in normally perfused myocardium, on average by 37% in the endocardium and 30% in the epicardium. No changes occurred in the other regions. The flow changes brought about by IPS 339 were unrelated to haemodynamic changes, and the coronary vascular resistance was reduced. These results are indicative of coronary vasodilation related to beta 2-adrenergic receptor blockade and was confined to well-oxygenated areas surrounding the acutely ischaemic zone.

Adrenergic beta-Antagonists↗
PubMed1973

Assessment of selective beta-adrenoceptor blockade in man.

1. Selective antagonism of the cardiac beta(1)-adrenoceptors has been studied in normal human volunteers.2. Practolol and UK 6558 produced greater antagonism of the chronotropic and inotropic responses to i.v. isoprenaline than of the vasodilator response to either i.v. or intra-arterial isoprenaline. A third drug, M&B 17,803A, produced non-selective beta-adrenoceptor blockade in 2 of 3 subjects studied.3. Practolol, UK 6558 and M&B 17,803A, produced an attenuation of the responses to Valsalva's manoeuvre.4. A substantial reduction in blood pressure was seen in 3 of 4 normotensive subjects given UK 6558.

Adrenergic beta-Antagonists↗
PubMed1974

Blockade of peripheral vascular responses to isoprenaline by three beta-adrenoceptor antagonists in the anaesthetized dog.

1 A dog's hind limb was vascularly isolated by strong nylon snares and its sympathetic nerve supply interrupted. Blood was perfused at constant flow into the femoral artery and drained from the femoral vein. In some dogs the cardiac nerves were cut.2 Isoprenaline infused intravenously caused an increase in heart rate and a decrease in arterial resistance.3 Practolol (2 mg/kg) effectively blocked heart rate responses to isoprenaline infused at up to 10 mug/min but was relatively ineffective in blocking arterial responses. ICI 66082 (2 mg/kg) reduced vasomotor responses and propranolol (0.5 mg/kg) abolished vasomotor responses.4 Small cumulative doses of beta-adrenoceptor antagonists were given to some dogs. Practolol blocked heart rate responses in lower doses than were required to block vasomotor responses. Propranolol preferentially blocked vasomotor responses and ICI 66082 was intermediate between the other two in its effects.

Acetamides↗
PubMed1974

Beta-adrenoceptor blocking agents and responses to adrenaline and 5-hydroxytryptamine in rat isolated stomach and uterus.

1 Four beta-adrenoceptor blocking agents, (+/-)- and (+)-propranolol, practolol and oxprenolol, were found to antagonize, apparently competitively, the responses of both the rat isolated stomach and uterus to 5-hydroxytryptamine (5-HT).2 The pA(2) values for each of these agents as antagonists of the contractile action of 5-HT on the rat stomach were found to be: (+/-)-propranolol, 6.08; (+)-propranolol, 4.94; practolol, 3.43; and oxprenolol, 5.99. These values were very similar to the corresponding figures for antagonism of 5-HT-induced contractions of the uterus.3 pA(2) values for antagonism of adrenaline-induced relaxations by the four blocking agents on the rat stomach and uterus did not differ from the values for 5-HT blockade.4 To antagonize contractile responses to acetylcholine of the rat stomach it was necessary to give 100 times more (+/-)-propranolol than was needed to antagonize responses to 5-HT.

Adrenergic beta-Antagonists↗
PubMed1977

The beta-adrenoceptor of the human lymphocyte and human lung parenchyma.

1 The response of the beta-adrenoceptors of human lymphocytes to selective agonists and antagonists has been studied quantitatively by measuring changes in cyclic adenosine-3',5'-monophosphate (cyclic AMP) levels. 2 The receptor was activated by isoprenaline and by salbutamol, and blocked by propranolol but not by practolol. A similar pattern of response was obtained with fragments of human lung tissue. 3 The mean value for pA2 for propranolol was 8.34 and for practolol was 3.95. 4 These findings indicate that the lymphocyte beta-adrenoceptor is a beta2-receptor and support the solidity of using lymphocytes to study beta-adrenoceptor function in bronchial asthma. It may also be of use in the evaluation of selective beta2-blocking drugs in man.

Albuterol↗
PubMed1977

Profile of beta-adrenoceptors in femoral, superior mesenteric and renal vascular beds of dogs.

1. The homogeneity of beta-adrenoceptors in femoral, superior mesenteric and renal vascular beds was investigated by the use of the regional perfusion technique in dogs. 2. Isoprenaline and salbutamol produced dose-related increases in femoral and superior mesenteric blood flow. The dose-response curves for the two agonists were parallel, but salbutamol was approximately 1/15 as potent as isoprenaline on a weight basis. 3. Isoprenaline and salbutamol increased renal blood flow in a dose-related manner. However, salbutamol was approximately 1/240 as potent as isoprenaline on a weight basis, and the slope of the dose-response curve for salbutamol was less steep than that for isoprenaline. 4. The dose-response curves to isoprenaline for increase in femoral and superior mesenteric blood flow were shifted to the right by intravenous pindolol but not by intravenous or intra-arterial practolol. 5. The dose-response curves to isoprenaline for increase in renal blood flow were shifted to the right more markedly by intravenous pindolol than by intravenous or intra-arterial practolol. 6. The results indicate that beta-adrenoceptors of the renal vascular bed consist of beta1-type and beta2-type whereas the femoral and superior mesenteric vascular beds contain only beta2-adrenoceptors.

Albuterol↗
PubMed1979

The subdivision of beta-adrenoceptors in the cardiovascular system of the rat.

1 The antagonism by the beta-adrenoceptor blocking drugs, propranolol (non-selective) and practolol (beta-selective), of the cardiovascular actions of isoprenaline has been investigated in the rat. 2 All doses of practolol (0.1, 1 and 3 mg/kg) blocked the cardio-accelerator action of isoprenaline but only the largest dose blocked the vasodilator effect. 3 All doses of propranolol (0.01, 0.03 and 0.1 mg/kg) blocked the vasodilator effect of isoprenaline but only the largest dose diminished the tachycardia. 4 It is concluded that in the rat, as in other species, beta-adrenoceptors may be subdivided into beta 1 (cardiac) and beta 2 (peripheral vascular) types.

Animals↗
PubMed1979

Beta-adrenoceptors in the pregnant and non-pregnant myometrium of the goat and cow.

The muscle relaxing effect of beta-adrenoceptor agonists was examined without and with the presence of beta-adrenoceptor antagonists in strips from the pregnant and non-pregnant myometrium of the goat and from the pregnant myometrium of the cow. Isoprenaline, salbutamol and ritodrine caused a dose-dependent reduction of the spontaneous contractions of the pregnant myometrium and a dose-related and parallel shift to the right of the isoprenaline dose-response curve was obtained with butoxamine but not with practolol. Isoprenaline but neither salbutamol nor ritodrine caused a dose-related reduction of the spontaneous contractions in the non-pregnant myometrium and a dose-related and parallel shift to the right of the dose-response curve of isoprenaline was brought about with propranolol but not with either butoxamine or practolol. The muscle relaxing effect of ritodrine on the pregnant myometrium of the goat and cow shown in vitro was also demonstrated in vivo in the same species within eight hours of delivery. It is concluded that the beta-adrenoceptors in the pregnant myometrium of the goat and cow belong to the beta2-group whereas those in the non-pregnant myometrium cannot be classified as either beta1- or beta2-adrenoceptors.

Albuterol↗
PubMed1981

beta 1-Adrenoceptors mediating relaxation of the guinea-pig trachea: experiments with prenalterol, a beta 1-selective adrenoceptor agonist.

In the presence of 17 beta-oestradiol, prenalterol, a beta-selective adrenoceptor agonist, caused a dose-dependent relaxation of the isolated, pilocarpine-contracted guinea-pig trachea. This effect was blocked by the antagonists propranolol (non-selective) and practolol (beta 1-selective) but not by IPS 339 [(t-butylamino-3-ol-2-propyl)oximino-9-fluorene HCl] (beta 2-selective). The relaxing effect of terbutaline, a beta 2-selective adrenoceptor agonist, was more efficiently blocked by IPS 339 than by practolol. These data support the hypothesis that the guinea-pig trachea contains both beta 1- and beta 2-adrenoceptors mediating relaxation and that the beta 1-adrenoceptors are selectively stimulated by prenalterol. The efficacy of prenalterol was less than that of terbutaline, thus confirming its partial agonistic activity. In the absence of 17 beta-oestradiol, the ability of prenalterol to relax the pilocarpine-contracted trachea was lost. It is suggested that 17 beta-oestradiol may act as a functional antagonist to pilocarpine as it caused a partial relaxation itself.

Adrenergic beta-Agonists↗
PubMed1977

Beta-adrenergic receptor blocking drugs: tear lysozyme and immunological screening for adverse reaction.

Patients who had received long-term therapy with practolol and other beta-adrenergic receptor blocking drugs were examined ophthalmologically. Tear lysozyme concentration and serum autoantibodies (antinuclear antibodies, DNA-binding antibodies and intercellular cement substance antibodies) were measured. It was found that beta-adrenergic receptor blocking drugs may have a pharmacological effect on the lachrymal glands, but this was not associated with dry eyes or adverse reaction. Practolol was found to be capable of reducing tear lysozyme concentrations to very low levels, and this was initially associated with high titres of ICC antibody. No other drug tested produced these effects.

Adrenergic beta-Antagonists↗
PubMed1983

Analysis of cardiac adrenergic mechanisms in hypoxic lambs.

Adrenergically mediated inotropic and chronotropic responses to hypoxemia were studied in 12 neonatal lambs ranging from 1 to 10 days of age. Six lambs were adrenalectomized (Adnx) and six were sham operated. Inotropic changes were assessed from measurements of left ventricular dP/dtmax under controlled hemodynamic conditions. Atropine (1 mg) was given and hypoxia produced by adding N2 to the respirator. In the sham-operated lambs, dP/dtmax increased as a function of the level of hypoxemia. With a mean arterial O2 partial pressure (PaO2) of 21.7 +/- 2.0 Torr, dP/dtmax averaged 17 X 10(2) mmHg/s above control values. Adnx did not reduce resting dP/dtmax, but comparable levels of hypoxemia elicited a much smaller increase (5 X 10(2) mmHg/s) in this group (P less than 0.02). In the sham-operated lambs, ganglionic blockade with tetraethylammonium chloride (TEAC, 100 mg) reduced the hypoxic response to similar values (6.5 X 10(2) mmHg/s). These residual inotropic responses were completely abolished by beta-adrenergic blockade with practolol (4 mg/kg). Chronotropic changes were identical in both groups (18.7 beats/min) and abolished by TEAC alone. It is concluded that the major fraction of adrenergic inotropic stimulation during hypoxemia is derived from the adrenal glands and that autonomic neural function is essential to the release process. Heart rate responses are independent of adrenal integrity. A residual source of inotropic stimulation, blocked by practolol, is derived from unidentified sources.

Adrenalectomy↗
PubMed1979

Antagonism by some beta-adrenoceptor-blocking agents to cholinergic stimulation of skeletal muscle in vitro.

Antiacetylcholine activity some beta-adrenoceptor-blocking drugs was investigated using isolated guinea pig cremaster muscle and frog fectus abdominis muscle. On the cremaster muscle, the antagonism to acetylcholine was non competitive in K0 1313, (+/-)-INPEA and (--)-INPEA, competitive in (+)-INPEA and functional in practolol; All three INPEA isomers, practolol and propranolol behaved as noncompetitive antagonists of acetylcholine on frog rectus muscle. Caffeine-induced contractions of this muscle were partially inhibited by propranolol but not by the other drugs. It is suggested that the beta-adrenoceptor-blocking drugs produce their antiacetylcholine action by interaction with sites on the muscle which are different from the cholinceptor, and which vary between compounds and species.

Acetylcholine↗
PubMed1985

Direct analysis of beta-adrenergic receptor subtypes on intact adult ventricular myocytes of the rat.

beta 1- and beta 2-Adrenergic receptors co-exist in the adult rat ventricle. We have employed radioligand binding and cell purification techniques to determine the cellular origin of these receptors. The beta-adrenergic antagonist ligand (+/-)-[125I] iodocyanopindolol binds to 2 X 10(5) receptors per purified adult rat cardiomyocyte, with a dissociation constant of 70 pM. The subtype-selective antagonists betaxolol (beta 1), practolol (beta 1), and zinterol (beta 2) compete for [125I]iodocyanopindolol-binding sites on intact myocytes in monophasic manners with dissociation constants of 46, 845, and 923 nM, respectively. [125I]iodocyanopindolol binding to membranes prepared from nonmyocyte elements of rat ventricle occurs with a dissociation constant of 43 pM and a capacity of 88 fmol/mg membrane protein. Computer analysis of competition of [125I]iodocyanopindolol binding by betaxolol, practolol, and zinterol in nonmyocyte membranes demonstrates biphasic curves that comprise binding to both beta 1- and beta 2-receptors. These data demonstrate that purified adult ventricular myocytes possess only beta 1-receptors, and that the beta 2-receptors found in rat ventricle are located on nonmyocyte cell types.

Adrenergic beta-Agonists↗
PubMed1973

Effects of splenectomy and beta-adrenoceptor blockade on cardiac output response to acute hypoxemia.

Acute hypoxemia produced by the inhalation of 8% and 5% oxygen increased cardiac output in intact anesthetized dogs by 38% and 62%, respectively. Although practolol, a cardioselective beta-adrenergic blocking agent, reduced the increase in cardiac output in dogs subjected to severe hypoxemia (5% O(2) breathing) from 62% to 43%, it only slightly reduced the cardiac output rise in dogs subjected to moderate hypoxemia (8% O(2) breathing). Splenectomy, on the other hand, abolished the increase in cardiac output produced by moderate hypoxemia except for a small initial rise, but it reduced the increase in cardiac output during severe hypoxemia only to 37%. The entire increase, except for a small initial rise, disappeared only when splenectomized dogs were pretreated with practolol. Sham operation did not affect the cardiac output response to hypoxemia. It is concluded that an intact spleen is required for a significant portion of the increased cardiac output that occurs during both moderate and severe hypoxemia and that catecholamines do not participate in the regulation of cardiac output unless severe hypoxemia occurs.

Adrenergic beta-Antagonists↗
PubMed1974

Autonomic mechanisms in hemodynamic responses to isometric exercise.

Selective autonomic blockade with intravenous propranolol, practolol, atropine, and combined atropine-propranolol was utilized to elucidate the role of the autonomic nervous system in the hemodynamic responses in young adult male volunteers to handgrip sustained at 30% of maximal voluntary contraction for 3 min. The initial 30 s of the tachycardia response was found to be mediated by withdrawal of vagal dominance, as evidenced by blockade of this response by prior atropinization. The mid and late portion of the heart rate response curve was demonstrated to be sympathetic in origin, since it was unaffected by atropine, but was suppressed by combined atropine-propranolol blockade. Sympathetic stimulation appears to be a secondary mechanism for increasing the heart rate, however, as it becomes operative only after the first mechanism of vagal withdrawal has been utilized. This was confirmed by the finding that beta adrenergic receptor blockade alone had little effect on the heart rate response curve. The pressor response to handgrip was accompanied by increased cardiac output and no change in calculated systemic vascular resistance. After propranolol, handgrip resulted in increased peripheral resistance and an equivalent rise in arterial pressure, but no increase in cardiac output. It was concluded that the increase in resistance was the result of sympathetically induced vasoconstriction. This response was shown to be independent of peripheral beta adrenergic receptor blockade by the use of practolol, a cardio-selective beta adrenergic receptor-blocking drug which caused identical hemodynamic responses to those observed after propranolol. Left ventricular ejection time (corrected for heart rate) was prolonged by handgrip. The increased afterload imposed on the left ventricle by sustained handgrip may explain the prolongation of ejection time index. Preejection period was prolonged by SHG after propranolol and shortened after atropine. In addition to confirming the previously defined role of the parasympathetic nervous system, this study delineates the role of the sympathetic nervous system in the heart rate and pressor responses to sustained handgrip.

Adult↗
PubMed1979

Beta-adrenergic potentiation of the increased in vitro accumulation of cycloleucine by rat thymocytes induced by triiodothyronine.

We have previously demonstrated that 3,5,3'-triiodothyronine (T(3)), whether administered in vivo or added to suspending media in vitro, promptly stimulates the in vitro accumulation of the nonmetabolized amino acids, alpha-aminoisobutyric acid, and cycloleucine (CLE) by thymocytes isolated from weanling rats. In these studies, we have examined the in vitro interaction between catecholamines and T(3) with respect to this effect. The previously reported enhancement of CLE accumulation in thymocytes by T(3) in vitro (1 muM) was confirmed. When added alone in concentrations ranging between 10 nM and 0.1 mM, the adrenergic agonists, epinephrine and norepinephrine, had no effect on CLE accumulation. At a concentration of 1 muM, isoproterenol, terbutaline, and phenylephrine were also without effect. However, the effect of T(3) was clearly potentiated by the concomitant addition of epinephrine, norepinephrine, and possibly isoproterenol, whereas terbutaline and phenylephrine were without effect. Neither basal nor T(3)-enhanced CLE accumulation was affected by the addition alone of the adrenergic blocking agents, propranolol (0.1 mM), phentolamine (10 muM), or practolol (0.1 mM). Nevertheless, the beta(1)- and beta(2)-antagonist, propranol, and the beta(1)-antagonist, practolol, blocked the increment in CLE accumulation produced by epinephrine; the alpha-antagonist, phentolamine, was without effect. The enhancement of CLE accumulation that occurred in the presence of T(3), with or without epinephrine, was seen to be a result of an inhibition of CLE efflux, because T(3) alone inhibited CLE efflux, and this effect was increased when epinephrine was also present. On the other hand, neither T(3) alone nor T(3) plus epinephrine appreciably altered the rate of inward transport of CLE. As judged from studies of the ability of thymocytes to exclude trypan blue, neither T(3) alone nor T(3) plus epinephrine either enhanced or impaired viability of cells during 3-h periods of incubation. Cell water content, measured with [(3)H]urea, was unaffected by T(3), either alone or in the presence of epinephrine. In confirmation of previous results, the stimulatory effect of T(3) on CLE accumulation was unaffected by concentrations of puromycin sufficient to inhibit protein synthesis by at least 95%, and the potentiating action of epinephrine on the response to T(3) was similarly unaffected. From these findings, it is concluded that the effect of T(3) to increase CLE accumulation by thymocytes in vitro, though itself independent of adrenergic mediation, is potentiated by beta(1)-adrenergic stimulation. This interaction appears distinctly different from other thyroid hormone-catecholamine interactions, in which thyroid hormones enhance physiological responses to catecholamines. Its mechanism remains unclear, but the properties of the T(3) effect, and possibly the interaction itself, suggest that T(3) enhances CLE accumulation by an action at the level of the cell membrane.

Adrenergic beta-Agonists↗
PubMed1978

Evidence for activation by beta2-adrenergic receptors of adenosine 3',5'-monophosphate formation in Ehrlich ascites tumor cells.

The existence of aminergic receptors in mouse Ehrlich ascites tumor cells was studied. L-Isoproterenol in vitro stimulated the formation of cAMP in isolated Ehrlich ascites tumor cells. Stimulation by isoproterenol of cAMP formation was not significantly inhibited by practolol, a beta1-adrenoceptor antagonist-Salbutamol, a beta2-adrenoceptor agonist, markedly stimulated the formation of cAMP in Ehrlich ascites tumor cells at concentrations from 10(-8)-10(-3) M. After the addition of salbutamol, cAMP levels reached a maximum in 10 min and declined to about 2-fold of the basal level to 30 min. The stimulation by salbutamol of cAMP formation was markedly inhibited by butoxamine, a beta2-adrenoceptor antagonist, but not by practolol. Furthermore, the effect of a maximal dose of salbutamol was additive to that of prostaglandin E2. Histamine and 4-methylhistamine, a histamine H2 receptor agonist, had no significant effects. Therefore, it is suggested that a beta2-adrenergic receptor exists in the membranes of Ehrlich ascites tumor cells in terms of the adenylate cyclase-cAMP system.

Albuterol↗
PubMed1975

Coronary vasodilatation and adrenergic receptors in the dog heart and coronary.

The question of whether the coronary blood vessels contain an intrinsic adrenergic mechanism for vasodilatation of physiological significance has been examined in the canine heart-lung preparation with a donor by studying the response of the coronary vessels to epinephrine, norepinephrine, isoproterenol and salbutamol in combination with practolol. To differentiate the vasodilatation mediated through adrenoceptors in the coronary vessels from that resulting from an increase in the myocardial O2 consumption, a special method of analysis was developed based on the linear relation between the coronary flow and the myocardial O2 consumption. It was found that all four compounds produced an increase in the coronary flow attributable to an increased myocardial O2 consumption. Epinephrine and norepinephrine produced a decrease in the coronary flow after practolol which completely abolished the increase in the myocardial O2 consumption as well as the positive inotropic and chronotropic effects produced by these compounds, while isoproterenol and salbutamol produced an increase. These results indicate that adrenergic beta-receptor exists in the coronary subserving a vasodilatation. However, the vasodilatation through this mechanism is of minor importance under physiological conditions and becomes completely masked in the presence of an overwhelmingly strong vasodilatation consequent to an increase in the myocardial O2 consumption.

Albuterol↗