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At least 307 records · Page 17Linked to original sources
PubMed1981

Cyclic AMP accumulation in the beta adrenergic mechanism of eccrine sweat secretion.

Tissue cyclic 3'5'-AMP (cAMP) concentrations were measured after stimulation of isolated monkey palm eccrine sweat glands with various stimulants of sweat secretion. The cellular cAMP levels increased curvilinearly with time of incubation to reach a steady state after 5 min of incubation with isoproterenol. Theophylline more than doubled the isoproterenol-induced cAMP accumulation, whereas theophylline alone increased the basal cAMP level to a minor extent. Phenylephrine failed to stimulate cAMP accumulation. There was no increase in the cAMP level after stimulation with methacholine. A calcium ionophore, A23187, also failed to stimulate cAMP accumulation. Since isoproterenol, theophylline (or isobutylmethylxanthine), and dibutyryl cAMP all induced eccrine sweat secretion in isolated, cannulated sweat glands to varying degrees in vitro, cAMP is probably involved in the beta adrenergic mechanism of sweat induction. The isoproterenol-induced cAMP accumulation was not inhibited by removal of Ca2+ from the incubation medium for as long as 30 min. The striking similarity between the eccrine sweat gland and the salivary glands in the roles that Ca2+ and cAMP play in stimulus secretion coupling indicates that the eccrine sweat gland will serve as another useful model system for the study of the mechanisms of exocrine secretion.

Animals↗
PubMed1976

Alterations during postnatal period in the secretory responsiveness of the sweat glands in rats to mecholyl.

A study was made to know the alterations in the secretory responsiveness of the plantar and palmar sweat glands to local administration of mecholyl in rats during postnatal period. Nonresponsiveness of the plantar and palmar sweat glands to mecholyl was observed in 0- to 16-day-old and 0- to 10-day-old rats, respectively. After the nonresponsive period, a gradual increase in the responsiveness to mecholyl was observed in the plantar sweat glands. In the palmar sweat glands, however, a rapid increase followed by a temporary decrease and a subsequent gradual increase in the secretory responsiveness to mecholyl was found. This temporary decrease in the secretory responsiveness was observed on days soon after weaning.

Animals↗
PubMed1979

Extracellular free calcium and fluid secretion by the rabbit lacrimal gland in vivo.

A possible role of extracellular free Ca2+ in methacholine-induced fluid secretion in the in vivo rabbit lacrimal gland has been investigated. Lowering the extracellular Ca2+ concentration by either intra-arterial injection or infusion of EGTA at doses which caused no systemic effects produced a dose related and reversible inhibition of methacholine-induced secretion. The inhibitory effect of EGTA was diminished when EGTA chelated with CaCl2 in varying concentration ratios was administered. On the other hand, intra-arterial injection of CaCl2 potentiated fluid secretion stimulated by submaximal doses of methacholine. These results suggest that fluid secretion from the rabbit lacrimal gland is dependent on the extracellular free Ca2+ concentration.

Animals↗
PubMed1980

Augmented amylase release from rat parotid gland slices, in vitro.

Using a continuous amylase assay the effect of a simultaneous stimulation of adrenergic and cholinergic receptors on amylase release by perfused rat parotid slices was investigated. Superimposing adrenergic stimulation (isoprenaline) on continual submaximal cholinergic stimulation (acetyl-beta-methylcholine) resulted in an augmented amylase release compared with the sum of the two separate effects. This could also be shown with continual adrenergic stimulation with cholinergic stimulation superimposed on this. Possible explanations of this effect are discussed with particular respect to the role of Ca++.

Amylases↗
PubMed1986

Effect of methacholine on ionic permeability of basal membrane of the eccrine secretory cell.

In an attempt to clarify the possible change in ionic permeability of the basal membrane of secretory cells during methacholine (MCH) stimulation, the effect of ionic substitution on membrane potential (PD) was studied in the isolated monkey palm eccrine secretory tubule. The mean PD (Vcb) was -73 mV. Stimulation with local iontophoresis of MCH caused a biphasic change in Vcb, an initial transient depolarization of 5 to 10 mV, followed by repolarization near the resting PD. MCH-induced PD transient reversed its polarity at -43 mV (MCH-null potential). Vcb markedly depolarized by an increase in [K+]b or a decrease in [Cl-]b. Ion-dependent partial potential ratio (Ti) using the estimated change in electromotive force delta Eb yielded values of 0.72 for K+ and 0.26 for Cl-, indicating that the basal membrane is conductive predominantly to K+ and Cl-. However, delta Vcb due to K+ or Cl- replacement did not change before or during MCH stimulation. Although replacement of Na+ with Tris+ or Li+ transiently depolarized Vcb, the delta Vcb reversed to hyperpolarization during MCH stimulation, suggesting that MCH causes a small increase in Na+ conductance across the basal membrane. The implication of these data have been discussed within the conceptual framework of ionic movements in Cl- transporting epithelia.

Animals↗
PubMed1985

Characterization of the muscarinic receptor in human tracheal smooth muscle.

Muscarinic receptors in human tracheal smooth muscle were characterized by radioligand binding and functional studies. Specific [3H]-(-)-quinuclidinylbenzilate ([3H]-(-)-QNB) binding to tracheal smooth muscle membranes was reversible, stereoselective and of high affinity (Kd = 47 +/- 4 pmol/l; RT = 920 +/- 120 fmol/g tissue). Inhibition of specific [3H]-(-)-QNB binding by the M-1 selective antagonist pirenzepine was found to occur at relative high concentrations classifying the muscarinic receptor population as belonging to the M-2 subclass. Inhibition of specific [3H]-(-)-QNB binding by muscarinic agonists revealed the presence of high and low affinity sites in nearly equal proportions. 5'-Guanylylimidodiphosphate converted high affinity sites into low affinity sites although its effect was minimal. Log dose-contraction curves of methacholine had Hill coefficients of 1.10 +/- 0.04 with pD2-values of 6.75 +/- 0.02. Inhibition of specific [3H]-(-)-QNB binding by methacholine, however, was best described by a two binding site model with pKi-values considerably lower. The difference between these affinity values points to the presence of substantial receptor reserve.

Adolescent↗
PubMed1989

Different muscarine receptors mediate the prejunctional inhibition of [3H]-noradrenaline release in rat or guinea-pig iris and the contraction of the rabbit iris sphincter muscle.

To investigate the muscarine receptor type mediating inhibition of [3H]-noradrenaline release from the isolated rat and guinea-pig iris we have determined the potency of antimuscarinic drugs to antagonize the methacholine-induced inhibition of [3H]-noradrenaline overflow evoked by field stimulation (3 Hz, 2 min). The prejunctional apparent affinities were compared with those obtained for postjunctional muscarine receptors mediating the methacholine-induced contraction of the isolated rabbit iris sphincter muscle. Prejunctional apparent affinity constants of pirenzepine (6.67), himbacine (8.51), methoctramine (7.92), 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP, 8.00), hexahydro-difenidol enantiomers (6.92, (R); 5.77, (S)) in the rat iris and methoctramine (7.58) in the guinea-pig iris indicate the presence of M2 receptors. Although the postjunctional affinity constants in the rabbit iris sphincter of methoctramine (5.93), gallamine (3.92), and 4-DAMP (9.07) confirm our previous suggestions of the presence of M3-like receptors, the results obtained with the hexahydro-difenidol enantiomers do not agree with that concept. The postjunctional affinity constants of the hexahydro-difenidol enantiomers were not different from the prejunctional values (6.86, (R); 5.55, (S)), indicating a similar and low degree of stereoselectivity for these stereoisomers at both receptor sites (14 and 17, (R)/(S)-ratios, respectively). Hence, the postjunctional muscarine receptor in the rabbit iris sphincter fails to exhibit the high degree of stereoselectivity observed for hexahydro-difenidol enantiomers at M3 receptors on other smooth muscles.

Animals↗
PubMed1989

Comparison of the muscarinic receptors in the coronary artery, cerebral artery and atrium of the pig.

The affinity of various muscarinic antagonists for the muscarinic receptors mediating contraction (induced by acetyl-beta-methylcholine) of the isolated pig coronary and basilar artery was determined in order to compare the muscarinic receptor subtype involved in the contractile response of these arteries. In order to identify the muscarinic receptor subtype(s) involved, the affinity of the antagonists for the M2 receptor present in the pig atria was also investigated. The following muscarinic antagonists were used: atropine, pirenzepine, AF-DX 116 (11-2[[2-[(diethylamino)methyl]-1- piperidinyl]acetyl]-5,11-dihydro-6H- pyrido[2,3-b][1,4]benzodiazepin-6-one),4-DAMP(4-diphenylacetoxy-N- methylpiperidine methiodide), HHSiD (hexahydrosiladifenidol), methoctramine (N,N'-bis[6-[(2- methoxybenzyl)amino]hexyl]-1,8-octane-diamine tetrahydrochloride) and ipratropium. The order of affinity of the antagonists with respect to the muscarinic receptor in the coronary artery was clearly different from that for the muscarinic receptor in the basilar artery. The order of affinity established on the basilar artery closely resembled that for the M2 receptor in the atria. It is concluded that the muscarinic receptors on smooth muscle of the coronary and basilar arteries are not identical. The muscarinic receptor involved in the contraction of the basilar artery adheres to the M2 receptor subtype. A comparison of the selectivity of the antagonists suggests that the muscarinic receptor involved in the contraction of the coronary artery belongs to the M3 (like in exocrine glands) or M4 (as found in ileal smooth muscle) receptor subtype.

Animals↗
PubMed1975

Genesis of arrhythmias and mechanism of electrical defibrillation of the heart.

Atrial arrhythmias were induced in experiments on dogs by electrical stimulation or by local application of aconitine and methacholine to the atrium. The action of the defibrillator discharge on these arrhythmias was studied. The defibrillator discharge abolished the arrhythmias maintained by the circus movement of the excitation wave over the atria but did not abolish sinus tachycardia or ectopic aconitine tachysystoles. The threshold of the defibrillating effect depends on the existence of micro-or macro-reentries. Thmechanism of defibrillation consists of excitation of the atrial myocardium with a consequent decrease in the pathway for the circulation of excitation to below the critical size for maintaining the circus movement of the excitation wave. The axtion of the defibrillator does not inihibit the automatism of the nomotopic and heterotopic cardiac pacemakers.

Aconitum↗
PubMed1977

Gastric secretory and motility studies in chronic chagasic patients.

In Chagas' disease, the degeneration of the nerve cells of the intramural parasympathetic ganglia of the stomach causes a wide range of motor and secretory disturbances of the organ. To assess and to correlate the alterations of these two gastric functions, electromanometric and secretory studies were performed in 22 chagasic patients and in 12 control individuals. The gastric antrum electromanometric records were carried out in basal conditions and under the stimulation of methacholine chloride (Mecholyl). Gastric secretory studies were carried out in two sessions with a Kay's test: in the first, with the test alone; in the second, associated with bethanechol chloride (Urecholine). The chagasic patients were divided into two groups according to their gastric motor response to methacholine. It was concluded that the parasympathetic denervation in Chagas' disease changes both acid and pepsin secretions in the same direction but that as the disease worsens, the responsiveness of pepsin secretion to cholinergic action tends to disappear earlier than that of acid secretion.

Adult↗
PubMed1976

A functional description of the canine choledochoduodenal flutter valve.

Forward- and reverse-opening pressures of the choledochoduodenal junction were measured in anesthetized, vagotomized dogs. Mean reverse-opening pressures were found to be significantly greater in most cases including those following the intraductal administration of vasoactive agents which are known to significantly influence mean forward-opening pressures. The polypeptides CCK-PZ and CCK-C8 were ineffective in reducing mean forward-opening pressures regardless of the route of administration. Previously published observations have indicated that mean forward-opening pressures are also unaffected by nervous activity. It is concluded that the canine choledochoduodenal junction possesses the physical and functional properties of a passive flutter valve during duodenal relaxation.

Animals↗
PubMed1984

Factors related to gastric hypersecretion during pregnancy and lactation in rats.

We attempted to elucidate the factors involved in gastric hypersecretion of rats during pregnancy and lactation. Acid secretion in pylorus-ligated and vagally denervated fistula rats stimulated with histamine, tetragastrin, and methacholine increased from midterm pregnancy and persisted during lactation. Pepsin secretion remained unaltered during pregnancy but increased during lactation. Vagal denervation itself abolished this hypersecretion. In late pregnancy, a delayed appearance of maximal acid response to histamine was apparent, as compared to nonpregnant rats, and was abolished by aminoguanidine treatment. There was a delay in the maximal response to tetragastrin but not to methacholine. Serum histamine concentrations were 3-4 times higher in late pregnancy, as compared to nonpregnant, lactating and nonlactating rats. Gastric DNA and protein concentrations were significantly increased in lactating rats with concomitant elevation of food intake and serum gastrin levels. Those changes disappeared in nonlactating rats, and gastric secretion was much the same in the nonpregnant rats. These results indicate that acid hypersecretion during pregnancy was exclusively associated with vagal innervation plus high serum histamine levels, while acid and pepsin hypersecretion in lactating rats were associated with vagal innervation plus hyperplastic gastric mucosa and high serum gastrin levels.

Animals↗
PubMed1981

Mechanisms for the effects of acetylcholine on sodium transport in frog skin.

In frog skin (Rana temporaria) acetylcholine applied to the serosal surface produces either a sustained inhibiton or sustained stimulation of short-circuit current (SCC). The former effect is accompanied by a reduction and the latter by an increase in total tissue conductance. Both effects of acetylcholine can be accounted for, within experimental error, by changes in net sodium flux across the tissue. By use of selective agonists and antagonists it is concluded that acetylcholine interacts with muscarinic receptors in the serosal membrane. The effects of cholinoceptor agents are also seen with isolated epithelium. The stimulatory effect of acetylcholine is potentiated by theophylline and blocked by inhibitors of prostaglandin synthetase and by mepacrine. It is suggested that acetylcholine stimulates transport by liberating prostaglandins which may then activate adenylcyclase. The inhibitory effect of acetylcholine is correlated with a reduction in cyclic AMP content of the epithelium. Calcium appears to be an important determinant of the type of response seen eith acetylcholine, but the mechanism is not known.

Acetylcholine↗