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PubMed1992

Blockade by antiarrhythmic drugs of glibenclamide-sensitive K+ channels in Xenopus oocytes.

1. The outward K+ current induced by KRN2391 (K+ channel opener) in Xenopus oocytes is blocked by glibenclamide. We have investigated the effects of various classes (I-IV) of antiarrhythmic drugs on this KRN2391-induced response. 2. All class I antiarrhythmic drugs (Na+ channel blockers) tested concentration-dependently suppressed KRN2391-induced responses with the rank order of potency (IC50 in microM), disopyramide (17.8) > aprindine (29.5) > propafenone (63.1) > ajmaline (145) > quinidine (151). Flecainide, SUN1165, lignocaine, mexiletine and procainamide were much less potent (IC50, 450- > 1000 microM) than quinidine. 3. The class II antiarrhythmic drugs (beta-blockers), timolol, (-)- and (+/-)- propranolol, and (+)- propranolol (a non-beta-blocker) inhibited KRN2391-induced K+ currents in a concentration-dependent manner with values for IC50 (microM) of 79, 131, 151 and 129, respectively, whilst butoxamine, oxprenolol, alprenolol, pindolol, nadolol, metoprolol and acebutolol were either weak (IC50, 300 microM-600 microM) or virtually inactive (IC50, > 1000 microM). 4. The class III antiarrhythmic drugs, amiodarone and (+)-sotalol scarcely affected KRN2391 responses. 5. All class IV drugs (Ca2+ antagonists) tested suppressed KRN2391-induced responses in a concentration-dependent manner with an IC50 of 6.3 microM for bepridil, 38 microM for prenylamine, 85 microM for verapamil and 135 microM for diltiazem. 6. In conclusion, antiarrhythmic drugs of classes I, II and IV potently blocked glibenclamide-sensitive K+ channels in Xenopus oocytes.

Adrenergic beta-Antagonists↗

PubMed1994

Blood pressure reflexes following activation of capsaicin-sensitive afferent neurones in the biliopancreatic duct of rats.

1. Inflammatory diseases of the pancreas or diseases which cause obstruction within the biliary or within the biliary or pancreatic duct system are associated with severe pain. Although neuropeptides such as substance P are present in the biliary tree, only few capsaicin-sensitive, substance P-positive nerve fibres have been found in the ducts. In order to obtain functional evidence whether capsaicin-sensitive afferent neurones transmit nociceptive information arising from the biliopancreatic duct, blood pressure reflexes following electrical stimulation of the duct or increases in intraductal pressure were determined in barbiturate-anaesthetized rats. 2. Electrical stimulation of neurones in the biliopancreatic duct was carried out at 30 V, 3 ms, 50 Hz for 20s. In untreated animals the electrical stimulation resulted in rises in blood pressure by up to 25 mmHg, but in about a quarter of all animals tested this response was absent. Following the administration of phentolamine (7 mumol kg-1, i.p.) the blood pressure responses were changed to pronounced and reproducible depressor reflexes of -5 to -30 mmHg. Retrograde injections into the biliopancreatic duct of 300 microliters of a 154 mM sodium chloride solution produced increases in intraductal pressure of approximately 10 mmHg. This elicited shortlasting falls in blood pressure of 3-15 mmHg. Phentolamine significantly augmented the fall in blood pressure to 8-30 mmHg. 3. The depressor reflexes observed in both models after the administration of phentolamine were abolished by morphine (1 mumol kg-1, i.v.). The inhibition by morphine was reversed by naloxone (3 mumol kg-1, i.v.). Naloxone given before morphine did not affect the depressor reflex but prevented the inhibitory action of subsequently injected morphine.4. Acute s.c. injection of capsaicin (30 mg kg-1) abolished the depressor reflexes in response to both types of nociceptive stimulation in phentolamine-treated rats. The initial pressor effects of electrical stimulation were only partly inhibited by capsaicin whereas the basal depressor reflexes in response to elevation of intraductal pressure were abolished. In rats which had received capsaicin on the day before the experiment or had been treated with capsaicin as neonates, only minor rises in blood pressure were induced by electrical stimulation at the beginning of the experiment and no changes in blood pressure occurred after the administration of phentolamine. After adult or neonatal pretreatment with capsaicin the depressor reflexes in response to increased intraductal pressure were only small and were unchanged by phentolamine.5. The depressor reflexes following either electrical stimulation or increases in intraductal pressure were abolished by the unselective Beta-blocker, (-)-propranolol (3 micromol kg-1, i.p.), and greatly reduced by the Beta 1-blocker, metoprolol (6 micromol kg- 1, i.p.). The Beta2-preferring adrenoceptor antagonist, butoxamine(3 micromol kg-1, i.p.), had no effect on the depressor responses. The reflex falls in blood pressure were also abolished by hexamethonium (10 micromol kg-1, i.p.) but not by atropine (3 micromol kg-1, i.p.).6. Both models of stimulation of nociceptive afferents caused identical patterns of blood pressure responses following adrenalectomy or chemical sympathectomy. In adrenalectomized rats, the initial responses consisted of depressor reflexes which were not augmented but significantly reduced by phentolamine and further inhibited by metoprolol. In rats that had been pretreated with 6-hydroxydopamine(total dose 0.6 mmol kg-1) to accomplish chemical sympathectomy, nociceptive stimulation caused rises in blood pressure. Phentolamine treatment abolished these pressor effects but revealed only minor, if any, depressor responses that were unaffected by metoprolol.7. In summary, the hypotensive effects in both models constitute nociceptive reflexes since they are abolished by morphine and restored by naloxone. The afferent part of the reflex is mediated by nerve fibres sensitive to capsaicin. Both experimental procedures seem to elicit two, presumably separate, reflex mechanisms. Firstly, catecholamines released from the adrenal medulla elevate blood pressure or limit hypotensive responses via activation of vascular alpha receptors. Secondly, the reflex inhibition of the sympathetic nerve activity in the heart and the vasculature causes the nociceptive depressor reflexes.

Adrenalectomy↗

PubMed1980

The blood-brain barrier in adrenaline-induced hypertension. Circadian variations and modification by beta-adrenoreceptor antagonists.

Rats were subjected to adrenaline-induced acute hypertension during either the day or night. Albumin leakage into the brain was studied with Evans blue and 125I labeled serum albumin. The leakage was significantly lower during the night than during the day (P less than 0.001). d,1-propranolol had a protective effect (P less than 0.001) during the day and a slight reduction of the radioactivity (P less than 0.05 in some parts of the brain) was obtained by metoprolol (10 mg/kg) but not by butoxamine (10 mg/kg). None of the drugs reduced the tracer leakage during the night. The results suggest that the degree of alertness is of importance for the function of the blood-brain barrier in acute hypertension. However, the present experimental situation does not allow a separation of the effect of alertness per se and dark/light cycles. The changed vulnerability during the night could be related to enhanced neuronal activity, altered beta-adrenoreceptor sensitivity or to hormonal factors.

Adrenergic beta-Agonists↗

PubMed1986

Growth of rat salivary glands after terbutaline or dobutamine.

Six days after commencement of a regimen of twice daily administration of 25, 50, or 75 mg/kg body wt doses of the beta 1 adrenergic agonist, dobutamine, or the beta 2 adrenergic agonist, terbutaline, submandibular and parotid glands of rats were enlarged in size. The beta 1 receptor was responsible for mediation of these changes with both agonists, since the effects of either agonist were prevented when a 10 mg/kg dose of the beta 1 antagonist, atenolol, was injected 20 min prior to the agonists but were not prevented when the beta 2 antagonist butoxamine, was given prior to each agonist. The increase in gland size caused by dobutamine was more marked than that induced by terbutaline; total amount of DNA of the parotid gland was also higher with dobutamine than with terbutaline. The response of the parotid gland to each dose of either agonist was greater than that of the submandibular gland, suggesting that the parotid gland has more beta receptors than does submandibular gland. The data also show that the increase in cell size precedes an increase in cell number. The increase in cell size depends on activation of fewer receptors than are required for the increase in DNA, since at the same dose of dobutamine, e.g., increase in cell size but not cell number was observed; moreover, the same dosage effected an increase in DNA of parotid but not submandibular gland. The data thus show that enlargement of both glands, as well as increase in size and number of their acinar cells, is dependent on activation of beta 1 adrenoceptors only.

Animals↗

PubMed1999

beta-Adrenergic receptor subtypes in melanophores of the marine gobies Tridentiger trigonocephalus and Chasmichthys gulosus.

The subtype of beta-adrenergic receptors in melanophores of the marine gobies Tridentiger trigonocephalus and Chasmichthys gulosus was studied. Pigment of denervated melanophores in isolated, split caudal fins was preliminarily aggregated by incubating the specimens in a physiological saline containing 10 microM phentolamine and 30-100 microM verapamil or 2-10 nM melatonin, and the responses of the melanophores to a beta-adrenergic agonist added to the incubating medium were recorded photoelectrically. The beta-adrenergic agonists noradrenaline, adrenaline, isoproterenol, salbutamol and, dobutamine were all effective in evoking a dispersion of melanophore pigment in the presence of phentolamine and verapamil or melatonin. The pigment-dispersing effect of noradrenaline (beta 1-selective agonist) was inhibited by metoprolol (beta 1-selective antagonist), propranolol,- and butoxamine. Whereas, the effect of salbutamol (beta 2-selective agonist) was hardly inhibited by metoprolol, though it was considerably inhibited by propranolol and ICI-118551. It was estimated that beta 1- and beta 2-adrenergic receptors coexist at ratios of 8.6:91.4, in the melanophore of Tridentiger trigonocephalus, and 25:75, in the melanophore of Chasmichthys gulosus, through the analyses of Hofstee plots of the effects of the beta-adrenergic drugs. It was suggested that the relation between the pigment-dispersing effect of a beta-adrenergic agonist on the melanophores and the concentration of the drug follows mass action kinetics, when the effect is mainly caused by the activation of beta 2-adrenergic receptors of the melanophores. However, when it is mainly caused by the activation of beta 1-adrenergic receptors of the melanophores, the relation does not follow mass action kinetics.

Adrenergic alpha-Agonists↗

PubMed1981

The action of beta-adrenoceptor agonists on acid secretion by the rat isolated stomach.

1. The action of beta-adrenoceptor agonists on acid secretion by an immature rat isolated stomach preparation has been studied. 2. Isoprenaline, salbutamol, salmefamol, adrenaline and noradrenaline all stimulated acid output over a concentration range of 2 X 10(-7) M--10(-5) M. 3. These responses were antagonized by propranolol (2 X 10(-5) M), pindolol and timolol (10(-6) M). 4. The antagonism of isoprenaline and salmefamol by propranolol was consistent with competitive inhibition. 5. Selective beta-adrenoceptor antagonists (practolol, atenolol, butoxamine and ICI 118 551) caused significant inhibition of noradrenaline-stimulated secretion but not of that due to the other agonists. 6. An adult rat isolated mucosa preparation responded to adrenaline in a similar manner to the immature stomach preparation. 7. Acid secretion stimulated by beta-adrenoceptor agonists was not antagonized by atropine (10(-5) M), metiamide (10(-4) M) or prostaglandin E2 (10(-5) M). The concentrations of these three antagonists caused marked inhibition of the responses to submaximal concentrations of bethanechol, histamine and pentagastrin respectively. 8. The results are discussed in relation to the possible mechanisms of action of beta-adrenoceptor stimulation of acid secretion: it is concluded that the response is probably mediated by beta-receptors on the parietal cell.

Adrenergic Agonists↗

PubMed2004

The effect of dehydroepiandrosterone on regional blood flow in prepubertal anaesthetized pigs.

Dehydroepiandrosterone has been implicated in vascular disease and its associated insulin resistance and hypertension, though little is known about its vascular effects. We have recently shown in prepubertal anaesthetized pigs that intravenous infusion of dehydroepiandrosterone caused coronary vasoconstriction through the inhibition of a vasodilatory beta-adrenergic receptor-mediated effect related to the release of nitric oxide. The present study was designed to investigate the effect of dehydroepiandrosterone on mesenteric, renal and iliac vascular beds. In prepubertal pigs of both sexes anaesthetized with sodium pentobarbitone, changes in superior mesenteric, left renal and left external iliac blood flow caused by intravenous infusion of dehydroepiandrosterone were assessed using electromagnetic flowmeters. Changes in heart rate and arterial blood pressure were prevented by atrial pacing and by connecting the arterial system to a pressurized reservoir containing Ringer solution. In 22 pigs, infusion of 1 mg h(-1) of dehydroepiandrosterone decreased mesenteric, renal and iliac blood flow. In a further 10 pigs, dose-response curves were obtained by graded increases in the infused dose of hormone between 0.03 and 4 mg h(-1). The mechanisms of the above response were studied in the 22 pigs by repeating the experiment after haemodynamic variables had returned to the control values observed before infusion. Blockade of alpha-adrenoceptors with intravenous phentolamine (five pigs) did not affect the dehydroepiandrosterone-induced mesenteric, renal and iliac vasoconstriction. This response was abolished by blockade of beta(2)-adrenoceptors with intravenous butoxamine (five pigs) and by blockade of mesenteric, renal and iliac nitric oxide synthase with intra-arterial administration of N(omega)-nitro-L-arginine methyl ester (seven pigs), even after reversing the increase in local vascular resistance caused by the two blocking agents with intravenous infusion of papaverine. In five pigs, the increase in measured blood flow caused by intravenous infusion of isoproterenol (isoprenaline) was significantly reduced by infusion of dehydroepiandrosterone. The present study showed that intravenous infusion of dehydroepiandrosterone primarily caused mesenteric, renal and iliac vasoconstriction. The mechanisms of this response were shown to be due to the inhibition of a vasodilatory beta(2)-adrenergic receptor-mediated effect, which possibly involved the release of nitric oxide.

Adrenergic alpha-Antagonists↗

PubMed2005

Beta1 adrenergic receptor-mediated enhancement of hippocampal CA3 network activity.

Norepinephrine is an endogenous neurotransmitter distributed throughout the mammalian brain. In higher cortical structures such as the hippocampus, norepinephrine, via beta adrenergic receptor (AR) activation, has been shown to reinforce the cognitive processes of attention and memory. In this study, we investigated the effect of beta1AR activation on hippocampal cornu ammonis 3 (CA3) network activity. AR expression was first determined using immunocytochemistry with antibodies against beta1ARs, which were found to be exceptionally dense in hippocampal CA3 pyramidal neurons. CA3 network activity was then examined in vitro using field potential recordings in rat brain slices. The selective betaAR agonist isoproterenol caused an enhancement of hippocampal CA3 network activity, as measured by an increase in frequency of spontaneous burst discharges recorded in the CA3 region. In the presence of alphaAR blockade, concentration-response curves for isoproterenol, norepinephrine, and epinephrine suggested that a beta1AR was involved in this response, and the rank order of potency was isoproterenol > norepinephrine = epinephrine. Finally, equilibrium dissociation constants (pK(b)) of subtype-selective betaAR antagonists were functionally determined to characterize the AR subtype modulating hippocampal CA3 activity. The selective beta1AR antagonists atenolol and metoprolol blocked isoproterenol-induced enhancement, with apparent K(b) values of 85 +/- 36 and 3.9 +/- 1.7 nM, respectively. In contrast, the selective beta2AR antagonists ICI-118,551 and butoxamine inhibited isoproterenol-mediated enhancement with apparent low affinities (K(b) of 222 +/- 61 and 9268 +/- 512 nM, respectively). Together, this pharmacological profile of subtype-selective betaAR antagonists indicates that in this model, beta1AR activation is responsible for the enhanced hippocampal CA3 network activity initiated by isoproterenol.

Adrenergic beta-1 Receptor Agonists↗

PubMed2000

The direct effects of catecholamines on hepatic glucose production occur via alpha(1)- and beta(2)-receptors in the dog.

The role of alpha- and beta-adrenergic receptor subtypes in mediating the actions of catecholamines on hepatic glucose production (HGP) was determined in sixteen 18-h-fasted conscious dogs maintained on a pancreatic clamp with basal insulin and glucagon. The experiment consisted of a 100-min equilibration, a 40-min basal, and two 90-min test periods in groups 1 and 2, plus a 60-min third test period in groups 3 and 4. In group 1 [alpha-blockade with norepinephrine (alpha-blo+NE)], phentolamine (2 microg x kg(-1) x min(-1)) was infused portally during both test periods, and NE (50 ng x kg(-1) x min(-1)) was infused portally at the start of test period 2. In group 2, beta-blockade with epinephrine (beta-blo+EPI), propranolol (1 microg x kg(-1) x min(-1)) was infused portally during both test periods, and EPI (8 ng x kg(-1) x min(-1)) was infused portally during test period 2. In group 3 (alpha(1)-blo+NE), prazosin (4 microg x kg(-1) x min(-1)) was infused portally during all test periods, and NE (50 and 100 ng x kg(-1) x min(-1)) was infused portally during test periods 2 and 3, respectively. In group 4 (beta(2)-blo+EPI), butoxamine (40 microg x kg(-1) x min(-1)) was infused portally during all test periods, and EPI (8 and 40 ng x kg(-1) x min(-1)) was infused portally during test periods 2 and 3, respectively. In the presence of alpha- or alpha(1)-adrenergic blockade, a selective rise in hepatic sinusoidal NE failed to increase net hepatic glucose output (NHGO). In a previous study, the same rate of portal NE infusion had increased NHGO by 1.6 +/- 0.3 mg x kg(-1) x min(-1). In the presence of beta- or beta(2)-adrenergic blockade, the selective rise in hepatic sinusoidal EPI caused by EPI infusion at 8 ng x kg(-1) x min(-1) also failed to increase NHGO. In a previous study, the same rate of EPI infusion had increased NHGO by 1.6 +/- 0.4 mg x kg(-1) x min(-1). In conclusion, in the conscious dog, the direct effects of NE and EPI on HGP are predominantly mediated through alpha(1)- and beta(2)-adrenergic receptors, respectively.

3-Hydroxybutyric Acid↗

PubMed1993

Effect of norepinephrine on rat basilar artery in vivo.

In anesthetized rats, we used a cranial window to examine effects of topical norepinephrine on diameter of the basilar artery in vivo. Topical application of norepinephrine increased the diameter of the basilar artery. NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase, inhibited vasodilatation to acetylcholine but did not attenuate dilator responses to norepinephrine. Indomethacin also did not attenuate vasodilatation in response to norepinephrine. Dilatation of the basilar artery to norepinephrine was inhibited by propranolol and the beta 1-antagonist atenolol but not by the beta 2-antagonist butoxamine. Thus dilatation of the basilar artery in response to norepinephrine is produced by activation of beta 1-receptors and is not mediated by endothelium-derived relaxing factor or prostanoids. Glibenclamide, a selective inhibitor of ATP-sensitive K+ channels, partially inhibited vasodilatation in response to norepinephrine. Forskolin, a direct activator of adenylate cyclase, also increased the diameter of the basilar artery, and glibenclamide attenuated the dilatation. Thus dilatation of rat basilar artery in response to norepinephrine is mediated, in part, by activation of ATP-sensitive K+ channels, and activation of these K+ channels may be achieved by an adenosine 3',5'-cyclic monophosphate-dependent mechanism.

Animals↗

PubMed1993

Dietary calcium modulates blood pressure through alpha 1-adrenergic receptors.

To investigate the role of adrenergic receptor activity in dietary calcium-induced alterations in blood pressure, weanling spontaneously hypertensive rats (SHR) were placed on either high-calcium (2.0%) or low-calcium (0.1%) diets for 1-2 wk. Baseline blood pressure was higher and pressor responses to exogenous norepinephrine (NE) were greater in the SHR on low-calcium diets than high-calcium diets. There was no difference between diet groups in circulating NE or in the pressor response to angiotensin II. The difference in basal blood pressure was eliminated by the alpha 1-adrenergic receptor blockers phentolamine and prazosin but was not altered by alpha 2-, beta 1-, or beta 2-adrenergic receptor blockade (idazoxan, metoprolol, and butoxamine, respectively). Furthermore, hypotension produced by either calcitonin gene-related peptide, captopril, or nitroprusside failed to eliminate the diet-induced difference in blood pressure. The results suggest the possibility that diet-induced differences in alpha 1-adrenergic activity may be responsible, in part, for variations in blood pressure on different calcium diets.

Adrenergic Agonists↗

PubMed2000

Suppression of NK cell activity and of resistance to metastasis by stress: a role for adrenal catecholamines and beta-adrenoceptors.

Although acute stress has been reported to suppress natural killer cell activity (NKA) and host resistance to metastasis, it is unclear whether the sympathetic nervous system (SNS) has a role in these effects. The current study in Fischer 344 rats assessed the involvement of adrenal catecholamines and beta(1)- and beta(2)-adrenoceptors in mediating these deleterious effects of swim stress. In addition to assessing the number and activity of NK cells following swim stress, we used a tumor model based on the MADB106 mammary adenocarcinoma line: this syngeneic tumor metastasizes only to the lungs, and its lung tumor retention (LTR) and metastatic colonization are highly sensitive to NKA. The findings indicate that stress increased both LTR, assessed 24 h after inoculation, and the number of lung metastases, counted 3 weeks later. These effects were attenuated or completely abolished by the ganglionic blocker chlorisondamine (3 mg/kg i.p.), by adrenal demedullation, by a selective beta-adrenergic antagonist (nadolol, 0.4 mg/kg), and additively by a selective beta(1)- (atenolol, 1-6 mg/kg) and a selective beta(2)-antagonist (either butoxamine 4-32 mg/kg or ICI-118,551 0.3-8 mg/kg). Stress also suppressed NKA, and adrenal demedullation prevented this suppression. Administration of adrenaline (0.1-1 mg/kg) or of a beta-adrenergic agonist (metaproterenol, 0.8 mg/kg), in physiologically relevant doses, suppressed NKA in a dose-dependent manner, and increased LTR to levels characteristic of swim stress. Taken together, these findings suggest that acute stress, by releasing catecholamines from the adrenal glands and activating beta(1)- and beta(2)-adrenoceptors, suppresses NKA and consequently compromises resistance to NK-sensitive metastasis.

Adrenal Medulla↗

PubMed2001

Effect of SR59230A on atypical beta-adrenoceptor mediating relaxation in the Guinea Pig gastric fundus.

The purpose of the present study was to clarify whether atypical beta-adrenoceptors which presented in the guinea pig gastric fundus are beta(3)-adrenoceptors or putative beta(4)-adrenoceptors. In the presence of both the selective beta(1)-adrenoceptor antagonist atenolol (10(-4) mol/l) and the selective beta(2)-adrenoceptor antagonist butoxamine (10(-4) mol/l), the selective beta(3)-adrenoceptor antagonist SR59230A caused a concentration-dependent rightward shift of the concentration-response curve to catecholamines (isoprenaline, noradrenaline and adrenaline) and beta(3)-adrenoceptor agonists (BRL37344 and CGP12177A) in the guinea pig gastric fundus. Schild plot analyses of SR59230A against these agonists gave pA(2) values of 7.35 +/- 0.03 (isoprenaline), 7.26 +/- 0.04 (noradrenaline), 7.26 +/- 0.05 (adrenaline), 7.79 +/- 0.03 (BRL37344) and 6.74 +/- 0.03 (CGP12177A), respectively, and all Schild slopes were not significantly different from unity. These results suggest that atypical beta-adrenoceptors mediating relaxant responses of these agonists in the guinea pig gastric fundus are beta(3)-adrenoceptors rather than putative beta(4)-adrenoceptors.

Adrenergic beta-3 Receptor Antagonists↗

PubMedDate not supplied

Adrenoceptor-mediated regulation of the contractility in horse penile resistance arteries.

The receptors mediating the contractions to both exogenously applied noradrenaline and electrical field stimulation (EFS) were characterized in horse isolated penile resistance arteries. The alpha 1-adrenoceptor-selective antagonist, prazosin, caused competitive rightward shifts of the contractile concentration-response curves (CRC) to phenylephrine. The alpha 2-antagonist, rauwolscine, also displaced to the right the CRC to the alpha 2-adrenoceptor-selective agonist, BHT 920. EFS (0.3 ms, 20-second trains) caused tetrodotoxin-sensitive frequency-dependent contractions which were enhanced in the presence of NG-nitro-L-arginine (L-NOARG, 3 x 10(-5) M), but not affected by mechanical endothelial cell removal. In experiments performed in the presence of L-NOARG, prazosin inhibited contractions to EFS, while rauwolscine inconsistently enhanced the contractile responses. Exogenously added noradrenaline induced contractions which were not changed in endothelium-denuded arteries, but significantly increased in the presence of L-NOARG. Prazosin inhibited the noradrenaline-induced contractions, while rauwolscine did not change the response to noradrenaline either alone or in the presence of prazosin. In the presence of phentolamine (10(-5) M), isoprenaline, adrenaline and the beta 2-adrenoceptor agonist, salbutamol, concentration-dependently relaxed penile resistance arteries, while the relaxations to noradrenaline and dobutamine, which activate beta 1-adrenoceptors, were negligible. Isoprenaline-induced relaxations were not changed in the presence of the beta 1-antagonist, atenolol (10(-7)-10(-6) M), but competitively inhibited by the beta 2-adrenoceptor antagonist, butoxamine (10(-6)-10(-5) M). The present results indicate that stimulation of adrenergic nerves in horse penile resistance arteries releases noradrenaline, which induces vasoconstriction through a predominant activation of alpha 1-adrenoceptors, while postjunctional alpha 2-adrenoceptors apparently play a minor role. Functional beta 2-adrenoceptors are also present in these arteries.

Animals↗

PubMed1986

Beta adrenergic control of extrarenal potassium disposal. A beta-2 mediated phenomenon.

Beta adrenergic control of extrarenal potassium disposal was evaluated by examining the effects of physiologic doses of beta adrenergic agonists and antagonists on potassium tolerance in acutely nephrectomized rats. Following an acute intravenous potassium load (0.17 mEq/100 g over 60 min), the plasma potassium concentration rose significantly less in animals concomitantly treated with epinephrine at a dose that raises plasma epinephrine concentration to levels found during surgical stress (maximum plasma K 2.2 vs. 2.9 mEq/1 in controls receiving KCl alone; p less than 0.005). Similar results were observed with the selective beta-2 agonists salbutamol and terbutaline. Conversely, the rise in plasma potassium concentration was significantly greater in rats treated with low-dose propranolol (beta-1 + beta-2 blockade) and with butoxamine (beta-2 blockade) compared to control animals. In contrast, the selective beta-1 blocking agent metoprolol had no effect on potassium tolerance. Alterations in potassium tolerance following the administration of various beta adrenergic agonists and antagonists could not be explained by changes in plasma insulin, renin, or glucose concentration or by differences in the acid-base or hemodynamic status of the animals. The data suggest that beta adrenergic control of extrarenal potassium disposal occurs with physiologic stimulation or blockade of the beta-2 receptor site.

Acid-Base Equilibrium↗

PubMed1980

Central beta-adrenergic effects on the control of ventilation in cats.

beta-Adrenergic mimetics and blockers, as well as a local anesthetic (xylocaine) were infused into the vertebral artery of paralyzed and artificially ventilated cats. The effects of the drugs on the central control of ventilation was assessed by measuring the changes in phrenic nerve activity. beta-Mimetics [isoprenaline (1 and 2), metroprolol (1), oxprenolol (1 and 2)] decreased the phrenic nerve activity. beta 2-Mimetics (Salbutamol) and blockers (Butoxamine, H 35/35) had no clear effects. The mode of action of the beta-blockers is most probably not by their local anesthetic properties. It is concluded that beta-adrenergic mechanisms in the brain stem stimulate the ventilatory control system. The receptors are most probably beta 1-receptors.

Adrenergic beta-Agonists↗

PubMed1991

Beta-2-adrenoceptor agonists up-regulate the in vitro Fc epsilon receptor II/CD23 expression on, and release from, the promonocytic cell line U937 and human blood monocytes.

The possible regulatory role of beta 2-adrenoceptor agonists in the modulation of CD23 on the human promonocytic cell line U937 and on human monocytes was investigated. Incubation for 48 h in the presence of interleukin-4 (IL-4; 30 U/ml) induced optimal expression and release of CD23 on both U937 cells and human monocytes. When a beta 2-adrenoceptor agonist, either salbutamol or fenoterol, was added to U937 cells or monocytes both the IL-4-induced CD23 expression and release were markedly up-regulated. This effect was dose-dependent, starting at 10 nM and reaching a maximum at 1 microM final concentration of either salbutamol or fenoterol. The potentiating effect of salbutamol and fenoterol on CD23 expression and release was not observed when a beta-adrenoceptor antagonist, either D,L-propranolol (1 microM) or butoxamine (1 microM), was added to the incubation medium. The alpha-adrenoceptor agonist norepinephrine (1 microM) was ineffective in enhancing the IL-4-induced expression and release of CD23 from U937 cells or human monocytes, demonstrating the specificity of the beta 2-adrenoceptor-mediated effect. In the absence of IL-4, a moderate but significant increase in the CD23 expression on U937 cells and human monocytes by these drugs was observed, as compared to the basal values. These results indicate that, besides their bronchodilator effect, beta 2-adrenoceptor agonists may regulate IgE-dependent processes.

Adrenergic beta-Agonists↗

PubMed1992

Role of the autonomic nervous system in catheter-induced urethral inflammation.

We have studied role of the autonomic nervous system on experimentally induced urethral inflammation in the rat. Urethral inflammation was produced by inserting latex strips into the urethra. The effects of different experimental procedures were assessed by using a 4-grade inflammation scale based on histological findings. Rats pretreated with the nonspecific catecholamine depletors reserpine or quanethidine had a significantly less severe urethral inflammation than vehicle-treated controls. The severity of urethral inflammation was increased in spontaneous hypertensive rats, which have an increased sympathetic tone as compared to the normotensive rats. Propranolol, a nonselective beta-adrenergic receptor antagonist reduced and butoxamine, a beta 2-antagonist, significantly reduced the urethral inflammation. Neither phenoxybenzamine (nonselective) nor prazosin (alpha 1) or yohimbine (alpha 2), alpha-adrenergic receptor antagonists, affected the degree of urethral inflammation. These data taken together indicate that the autonomic innervation of the urethral mucosa is critically involved in the inflammatory reaction and that the use of beta 2-antagonist may be a treatment alternative in the future for the treatment of catheter-induced inflammation.

Animals↗