Predominantly beta-adrenergic control of equine sweating

1984 ◽  
Vol 246 (3) ◽  
pp. R349-R353 ◽  
Author(s):  
J. Bijman ◽  
P. M. Quinton
Keyword(s):  
Sweat Glands ◽  
Maximal Response ◽  
Exocrine Glands ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Sweat Secretion ◽  
Adrenergic Antagonist ◽  
Adrenergic Control

Single equine sweat glands were found to secrete for more than 1 h in vitro in response to pharmacologic secretagogues. The adrenergic agonists epinephrine and norepinephrine evoked maximal sweat rates of 2.0 nl X gland-1 X min-1. However, the concentration of norepinephrine (10(-5) M) required to evoke the maximal response was 10 times higher than that for epinephrine. Maximal sweat rates also were stimulated with the beta 2-adrenergic agonist terbutaline. This stimulation was blocked by the beta-adrenergic antagonist propranolol. Moderate sweating responses were also obtained with the alpha-adrenergic agonists phenylephrine and methoxamine, but these responses also were blocked by propranolol. Neither the muscarinic blocker atropine nor the alpha-adrenergic antagonist phentolamine inhibited any of the pharmacologically induced sweat responses. Unlike most other mammalian exocrine glands, cholinergic agonists were ineffective in stimulating sweat secretion. Therefore equine sweat glands apparently are under predominantly beta-adrenergic control.

Influence of calcium and cyclic nucleotides on beta-adrenergic sweat secretion in equine sweat glands

1984 ◽  
Vol 247 (1) ◽  
pp. C10-C13 ◽  
Author(s):  
J. Bijman ◽  
P. M. Quinton
Keyword(s):  
Cyclic Nucleotides ◽  
Ethylenediaminetetraacetic Acid ◽  
Sweat Rate ◽  
Sweat Glands ◽  
Ionophore A23187 ◽  
Beta Adrenergic ◽  
Cyclic Monophosphate ◽  
Sweat Secretion ◽  
Adrenergic Antagonist

The effects of Ca2+, the cyclic nucleotides adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP), and other parameters of sweat secretion from single equine sweat glands were examined in vitro. Extracellular Ca2+, the Ca2+ ionophore A23187, and the Ca2+ channel antagonist verapamil were all without effect on sweat secretion. Prolonged rinsing of the glands in Ca2+-free Ringer solution with 5 mM ethylenediaminetetraacetic acid decreased the secretion to 30% of the control sweat rate in response to the beta-adrenergic agonist isoproterenol; the sweat response was restored upon adding Ca2+ to the Ringer. cAMP but not cGMP analogues were as effective in stimulating sweat rates as isoproterenol, which elicited maximal secretory rates in vitro. cAMP stimulation was not inhibited by the beta-adrenergic antagonist propranolol. Because the equine sweat gland is predominantly stimulated via the beta-adrenergic receptor, we conclude that cAMP is a principal intracellular messenger in coupling this type of stimulus to the fluid secretion response in this tissue.

Pharmacologic responsiveness of isolated single eccrine sweat glands

1981 ◽  
Vol 240 (1) ◽  
pp. R44-R51 ◽  
Author(s):  
K. Sato ◽  
F. Sato
Keyword(s):  
Dose Response ◽  
Dissociation Constants ◽  
Sweat Rate ◽  
Sweat Glands ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Adrenergic Agents ◽  
Eccrine Sweat Glands ◽  
Eccrine Sweat

Pharmacologic responsiveness of the eccrine sweat gland has never been studied under well-defined in vitro experimental conditions. Using isolated cannulated single monkey palm eccrine sweat glands, the dose response to both cholinergic and alpha- and beta-adrenergic agents and the effects of various antagonists on agonists were studied. The maximal sweat rate was highest after stimulation with cholinergic agonists, was lower with the beta-adrenergic agonist, and was least with the alpha-adrenergic agonist. Each secretory response was inhibited by its specific antagonist. Attempts to demonstrate the spare receptor, if any, by means of preincubation of the glands with N-(2-chlorethyl)dibenzylamine (Dibenamine) were unsuccessful. From the hyperbolic dose-response curves the values for KA and KB, dissociation constants for agonists and antagonists, respectively, were thus tentatively estimated according to Clark's classical receptor theory. Schild plots for each agonist-antagonist interaction produced straight lines with slopes of near unity, indicating the adequacy of the methodology. It was concluded that the isolated eccrine sweat glands retain their pharmacologic viability in vitro and show responsiveness to cholinergic as well as both alpha- and beta-adrenergic stimulations.

Regulation of Trypanosoma cruzi infectivity by alpha- and beta-adrenergic agonists: desensitization produced by prolonged treatments or increasing agonist concentrations

Parasitology ◽  
1990 ◽  
Vol 100 (3) ◽  
pp. 429-434 ◽  
Author(s):  
A. Ayala ◽  
F. Kierszenbaum
Keyword(s):  
Trypanosoma Cruzi ◽  
Prolonged Exposure ◽  
Inhibitory Effect ◽  
Tissue Level ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonists ◽  
Alpha Adrenergic Agonist

SUMMARYWe previously reported that blood forms of Trypanosoma cruzi express alpha- and beta-adrenergic receptors and that binding of specific agonists to these receptors modifies the infective capacity of the parasite in vitro. The present study has revealed that the inhibitory effect of the beta-adrenergic agonist L-isoproterenol and the stimulatory effect of the alpha-adrenergic agonist L-phenylephrine are not produced when the parasite is subjected to prolonged exposure to otherwise effective doses of these agonists or when supraoptimal doses of these agonists are used. We refer to these phenomena as ‘desensitization’ because of their analogy with vertebrate cells becoming desensitized by prolonged exposure to, or relatively high concentrations of, adrenergic agonists. At a constant agonist concentration, T. cruzi desensitization was time-dependent and, when the time of parasite treatment with the agonists was not changed, the higher concentrations of the agonist tested were the most effective in producing desensitization. The reduced infectivity resulting from treatment with optimal doses of L-isoproterenol was accompanied by elevated levels of cyclic adenosine mono- phosphate (cAMP) which were not detectable when L-isoproterenol concentrations producing desensitization were used. This finding implicated cAMP as a likely second signal in the inhibitory mechanisms of this agonist. No significant change in cAMP was detectable in parasites treated with L-phenylephrine, leaving open the question about how optimal doses of this alpha-adrenergic agonist enhance T. cruzi infectivity. Parasite responsiveness to alpha- and beta-adrenergic agonists as well as the desensitization effects define a system which regulates infectivity and could be modified at the host tissue level by naturally occurring agonists.

Dopaminergic suppression of pancreatic somatostatin secretion

1982 ◽  
Vol 101 (1) ◽  
pp. 56-61 ◽  
Author(s):  
Mitsuyasu Itoh ◽  
Brian L. Furman ◽  
John E. Gerich
Keyword(s):  
Pancreatic Islet ◽  
Cell Function ◽  
Potential Interaction ◽  
Beta Adrenergic ◽  
Adrenergic Antagonist ◽  
Adrenergic Mechanism ◽  
D Cell ◽  
D Cells ◽  
Dopaminergic Antagonists

Abstract. To characterize dopaminergic influences on pancreatic islet D cell function and its potential interaction with islet A and B cell function, the effect of dopamine (0.5–100 μm) on immunoreactive somatostatin (IRS), insulin (IRI), and glucagon (IRG) release from rat islets incubated in vitro was studied. Dopamine significantly suppressed the release of IRS (P< 0.001) and IRI (P < 0.001) and augmented IRG release (P < 0.001). Maximum suppression of IRS and IRI release was evident at 20 μm dopamine with half-maximal suppression occurring at 0.5–1 μm. Maximal stimulation of IRG release was observed at 100 μm dopamine with a halfmaximal response occurring at 5–10 μm. Suppression of IRS secretion by dopamine (20 μm) was completely reversed by the dopaminergic antagonists haloperidol (5 μm) and pimozide (5 μm), but was only partially reversed by the alpha adrenergic antagonist phentolamine (2 μm), and was further suppressed by the beta adrenergic antagonist propranolol (2 μm). Suppression of IRI release by dopamine was completely reversed by propranolol, but was unaffected by haloperidol, pimozide, and phentolamine. There results indicate that dopamine directly affects pancreatic islet D cell function, and that islet B and D cells appear to be more sensitive to dopamine than are A cells. Dopamine suppresses IRS secretion predominantly through activation of dopaminergic receptors, whereas it suppresses IRI release through an alpha adrenergic mechanism and stimulates IRG release through a beta adrenergic mechanism.

Effect of adrenergic agonists on big and small renin

1980 ◽  
Vol 238 (5) ◽  
pp. E416-E420
Author(s):  
H. Iwao ◽  
C. S. Lin ◽  
A. M. Michelakis
Keyword(s):  
Submaxillary Gland ◽  
Plasma Renin ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Molecular Weights ◽  
Submaxillary Glands ◽  
Beta Adrenergic Agonists ◽  
Beta Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

The effect of alpha- and beta-adrenergic agonists on renal and submaxillary renin of different molecular weights was studied using male albino mice as experimental animals. Phenylephrine or isoproterenol was administered intravenously after removal of the submaxillary glands and/or kidneys. Renin was isolated from plasma by column chromatography and then measured by a direct radioimmunoassay. Phenylephrine increased both 68,500-dalton renin (big renin) and 38,000-dalton renin (small renin) in the plasma of nephrectomized mice. Isoproterenol increased big and small renin in the plasma of mice whose submaxillary glands were removed. In both cases, the increase of small renin was significantly greater than that of big renin. The results suggest that the alpha-adrenergic agonist phenylephrine affects the submaxillary gland, leading to the increase of both big and small plasma renin. In contrast, the beta-adrenergic agonist isoproterenol affects the kidney, leading to the increase of both big and small plasma renin.

scholarly journals Autoradiographic localization of beta-adrenoreceptors in rat uterus.

1988 ◽  
Vol 36 (12) ◽  
pp. 1475-1479 ◽  
Author(s):  
M Tolszczuk ◽  
G Pelletier
Keyword(s):  
Quantitative Estimation ◽  
Cell Types ◽  
Receptor Subtypes ◽  
High Concentration ◽  
Rat Uterus ◽  
Beta Adrenergic ◽  
Adrenergic Antagonist ◽  
Beta 2 ◽  
Different Cell Types

The inhibitory effects of catecholamines on uterine smooth muscle are known to be mediated through beta-adrenergic receptors. To investigate further the distribution of these receptors in the rat uterus, we utilized in vitro autoradiography using [125I]-cyanopindolol [CYP], a specific beta-receptor ligand that has equal activity for both beta 1- and beta 2-receptor subtypes. The specificity of the labeling and the characterization of receptor subtypes in different cell types were achieved by displacement of radioligand with increasing concentrations of zinterol, a beta-adrenergic agonist with preferential affinity for the beta 2-adrenoreceptor subtype, and practolol, a beta-adrenergic antagonist that binds preferentially to the beta 1-subtype. Quantitative estimation of ligand binding was performed by densitometry. It was shown that the vast majority of beta-adrenoreceptors were of the beta 2-subtype and were found in high concentration not only in the myometrium but also in the endometrial and serosal epithelia. Specific labeling was also observed in glandular elements. These results suggest that beta-adrenoreceptors might be involved in different functions in the uterus.

The effect of feeding the beta-adrenergic agonist ractopamine on the behaviour of market-weight pigs

1992 ◽  
Vol 72 (1) ◽  
pp. 15-21 ◽  
Author(s):  
A. L. Schaefer ◽  
S. D. M. Jones ◽  
A. K. W. Tong ◽  
A. M. B. dePassille ◽  
J. Rushen ◽  
...  
Keyword(s):  
Aggressive Behaviour ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Treatment Groups ◽  
Beta Adrenergic Agonists ◽  
Key Words Pig ◽  
Ad Libitum ◽  
Beta Adrenergic Agonist ◽  
Effect Of Feeding

A total of 86 ad libitum fed Lacombe bred barrows and gilts weighing on average 90 kg were used to determine the effect of feeding ractopamine on animal behaviour. Four treatment groups consisted of a control (N = 22) and three levels of ractopamine (10 ppm (N = 15), 15 ppm (N = 24) and 20 ppm (N = 25) in the diet). The pigs received the ractopamine treatments for 5–6 wk prior to behavioural observations. There was little effect of ractopamine on behaviour. The ractopamine-fed pigs were observed to lie down in a group more frequently (P = 0.06) and to walk around their pen less frequently (P = 0.01). No abnormal, stereotyped, agonistic or aggressive behaviour was induced by the ractopamine. The data from the present study suggest that ractopamine, added to the diet of market-weight pigs at levels reported, does not cause marked changes in behaviour. Key words: Pig behaviour, beta-adrenergic agonists, ractopamine

scholarly journals The effect of β-adrenergic agonists on the membrane potential of fat-cell mitochondria in situ

1982 ◽  
Vol 206 (3) ◽  
pp. 611-618 ◽  
Author(s):  
R J Davis ◽  
B R Martin
Keyword(s):  
Membrane Potential ◽  
Fat Cells ◽  
Adrenergic Agonists ◽  
Fat Cell ◽  
Beta Adrenergic ◽  
Fatty Acid Binding ◽  
Beta Adrenergic Agonists ◽  
Adrenergic Antagonist ◽  
Beta Adrenergic Agonist

1. The accumulation of [3H]methyltriphenylphosphonium by isolated fat-cells was used to estimate the membrane potential of mitochondria in situ. 2. Adrenaline caused a large decrease in the accumulation of [3H]methyltriphenylphosphonium. Mitochondria in fat-cells incubated in the presence of adrenaline had a very low calculated membrane potential. This effect was also given by isoprenaline (a beta-adrenergic agonist) and was blocked by propranolol (a beta-adrenergic antagonist). 3. The effect of isoprenaline could be partially antagonized by the use of media with high albumin concentrations. Addition of sodium oleate to saturate the fatty acid-binding sites on the albumin reversed this antagonism. 4. It is proposed that the decrease in the calculated mitochondrial membrane potential is due to the uncoupling effect of the non-esterified fatty acids released by the stimulation of lipolysis observed in the presence of beta-adrenergic agonists.

Dietary Adrenergic Active Compounds and The Response of Broilers to Isoproterenol and Cyclic Adenosine Monophosphate in Vitro

2001 ◽  
Vol 71 (6) ◽  
pp. 352-355
Author(s):  
R. W. Rosebrough
Keyword(s):  
Broiler Chickens ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Acetate Incorporation ◽  
Beta Adrenergic ◽  
Adrenergic Agents ◽  
Beta Adrenergic Agonists ◽  
Adrenergic Antagonist ◽  
Malic Enzyme Activity

Broiler chickens, growing from 7–28 days of age, were fed diets containing 18% protein and 0, 1, 10 or 100 mg/kg yohimbine (alpha2-adrenergic antagonist) or metaproterenol (beta-adrenergic agonist) to determine the role of adrenergic agents in the regulation of feeding behavior and metabolism. Data from this experiment suggest that beta-adrenergic agonists have slight effects on feed intake, growth and more pronounced effects on metabolism in the broiler chicken. In vitro lipogenesis (IVL) was determined by incubating liver explants for 2 h at 37°C in the presence of cAMP or isoproterenol (ISO) and [2-14C]acetate and by measuring acetate incorporation into total hepatic lipid. Metaproterenol and yohimbine (100 mg/kg) depressed growth from 7 to 28 days. Both metaproterenol and yohimbine (100 mg/kg) decreased (P < 0.05) IVL compared to controls. These dietary additions also decreased (P < 0.05) hepatic malic enzyme activity without affecting the activities of either isocitrate dehydrogenase or aspartate aminotransferase.

Cyclic GMP accumulation during cholinergic stimulation of eccrine sweat glands

1984 ◽  
Vol 247 (3) ◽  
pp. C234-C239 ◽  
Author(s):  
K. Sato ◽  
F. Sato
Keyword(s):  
Time Course ◽  
Sweat Glands ◽  
Cgmp Level ◽  
Ionophore A23187 ◽  
Cholinergic Stimulation ◽  
Sweat Secretion ◽  
Transient Elevation ◽  
Eccrine Sweat Glands ◽  
Eccrine Sweat

The possibility that guanosine 3'5'-cyclic monophosphate (cGMP) may be an intracellular mediator of cholinergic stimulation [methacholine chloride (MCh)] was explored by comparing the relationship between the time course of cGMP accumulation and sweat secretion by use of isolated monkey palm eccrine sweat glands. Isolated sweat glands were incubated with MCh or other agents, and tissue levels of cGMP were determined by radioimmunoassay. In parallel experiments, sweat secretion was induced from cannulated single sweat glands in vitro. Stimulation with MCh produced a Ca-dependent transient elevation of cGMP level from 10 to 80 fmol/gland, peaking at 1-2 min but returning to the basal level by 5 min. The MCh-induced cGMP level was dose dependent and was inhibited by atropine. Ionophore A23187 (2 X 10(-4) M), however, caused persistent elevation of cGMP level for at least 20 min. Neither 10(-4) M MNNG, which elevated the cGMP level comparably with MCh stimulation, nor 8-bromo-cGMP (2 mM) induced sweat secretion. Thus although a parallelism between the cGMP level and sweating rate appears to hold for the initial stage of MCh-induced sweating, it does not hold for the steady state of sweat secretion. Data could not be interpreted to favor the notion that cGMP may be the intracellular mediator of cholinergic sweat secretion.

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