bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of N6, 2‘‐0‐dibutyryladenosine 3’,5‘‐cyclic monophosphate, adenosine, and of oxotremorine and 3‐isobutyl‐1‐methylxanthine on the electrically evoked [3H] acetylcholine secretion in the guinea‐pig ileum myenteric plexus
Authors: ALBERTS P. 
Published: December 2008

The guinea‐pig ileum longitudinal muscle‐myenteric plexus preparation, pre‐incubated with [3H]choline, was mounted in an organ bath and superfused with Tyrode's solution. [3H]Acetylcholine secretion was evoked by 150 electrical shocks at 0.5 Hz.>N6,2′‐0‐Dibutyryladenosine 3′,5′‐cyclic monophosphate (dibutyryl cyclic AMP) enhanced the [3H]acetylcholine secretion in the presence of eserine and the adenosine receptor antagonist 8‐phenyltheophylline (10 μmol 1‐1). Conversely, in the absence of 8‐phenyltheophylline the [3H]acetylcholine secretion was reduced by dibutyryl cyclic AMP. In the absence and presence of 8‐phenyltheophylline(apparent KD= 12 μ.mol 1‐1), adenosine reduced the [3H]acetylcholine secretion to 33% of control (IC50= 8, μmol l‐1) and to 48% of control (IC50= 14 μmol l‐1) respectively. Neither butyrate, dibutyryl cyclic GMP nor guanosine altered the [3H]acetylcholine secretion.Interaction experiments with 3‐isobutyl‐1‐methylxanthine and oxotremorine were done in the absence of eserine, i.e. when oxotremorine is effective. Oxotremorine depressed the fractional secretion of [3H]acetylcholine with a ‘maximal inhibition’ of 13% of control (IC50= 10 nmol l‐1). In the presence of 3‐isobutyl‐1‐methylxanthine (5 mmol l‐1) oxotremorine depressed the secretion to 2% of control with an apparent IC50) value of 0.9 μmol l‐13‐Isobutyl‐I‐methylxanthine (0.01–4 mmol l‐1) enhanced the fractional secretion of [3H]acetylcholine with a ‘maximal enhancement’ value of 232% of control (EC50= 0.19 mmol l‐1). The presence of oxotremorine (30 nmol l‐1) counteracted, and higher concentrations reversed, the enhancement caused by 3–isobutyl‐I‐methylxanthine.The results are consistent with the suggestion that the presynaptic muscarinic acetylcholine receptor‐mediated control of the secretion of [3H]acetylcholine in the guinea‐pig ileum myenteric plexus may be mediated both by cyclic AMP and calcium ions.
Capsaicin and histamine antagonist‐sensitive mechanisms in the immediate allergic reaction of pig airways
Authors: ALVING K. , MATRAN R. , LACROIX J. S. , LUNDBERG J. M. 
Published: December 2008

The airway vascular and bronchial responses were studied in pigs sensitized with Ascaris suum. Ascaris, histamine (H) and capsaicin aerosol all induced a clear‐cut increase in blood flow in the nasal, laryngeal and bronchial circulation with a decrease in vascular resistance of 20–40%. When delivered to the lung both ascaris and histamine, but not capsaicin, caused pulmonary airflow obstruction with increase in resistance and a fall in dynamic compliance of 40–70%. After pretreatment of pigs with a combination of the H1‐ and H2 ‐receptor antagonists terfenadine and cimetidine, the vascular and bronchial responses were strongly reduced to both histamine (by > 77%) and ascaris (by > 58%), but not to capsaicin aerosol. The bronchoconstriction to histamine was found to be mediated by H1‐receptors only, while both H1‐ and H2‐antagonists were necessary to block the vasodilatory response, with H2‐receptors being more important in the bronchial circulation and H1‐receptors being more important in the laryngeal and nasal circulation. Furthermore, when pigs were pretreated with capsaicin systemically 2 days before the experiment, the vasodilatation was decreased upon capsaicin (by 80%), ascaris (by > 40%) and histamine (by > 50%) aerosol challenge. When histamine was administered intravenously the desensitizing effect of capsaicin pretreatment was much less pronounced. The effect of capsaicin desensi‐tization on the pulmonary obstruction upon ascaris and histamine challenge was limited to a 60% reduction of the fall in dynamic compliance and a delayed peak in resistance upon ascaris challenge.We conclude that histamine is one of the main vasodilatory mediators released upon allergen challenge at three different levels of the pig airways. A considerable part of the histamine effect is indirect and probably due to activation of capsaicin‐sensitive sensory nerves.
Transmitter characteristics of small mesenteric arteries from the rat
Authors: SJÖBLOM‐WIDFELDT N. , GUSTAFSSON H. , NILSSON H. 
Published: December 2008

We have studied the neurogenic response of small mesenteric arteries from the rat to evaluate the involvement of possible co‐transmitters under various modes of stimulation.Segments of small branches of the mesenteric artery were mounted in a myograph and the intramural nerves were activated with transmural electrical stimulation.A single stimulation of the nerves caused a contraction that was reduced by only 20% in the presence of adrenergic blocking agents (prazosin or phenoxybenzamine), whereas the steady‐state response to continuous nerve stimulation of high frequency was reduced by 90–95 %. In contrast, all responses to applied noradrenaline in doses up to at least 1 mM were eliminated by phenoxybenzamine treatment. The stable ATP analogue, α,β‐methylene ATP, reduced the response to a single nerve stimulation by 70%, but reduced the contraction caused by continuous high‐frequency nerve stimulation by only 10%. None of these agents affected the response to applied neuropeptide Y (NPY). The response of relaxed vessels to nerve stimulation was totally blocked by the combination of an adrenoceptor‐blocking agent and α,β‐methylene ATP, although even in this situation a further neurogenic response could be revealed in vessels precontracted with vasopressin.Responses to either single stimuli or brief burst stimulations were potentiated after high‐frequency stimulation. Both the adrenergic and non‐adrenergic components were enhanced to roughly the same extent. Also the potentiated response was eliminated by the combined application of prazosin and α,β‐methylene ATP.The non‐adrenergic transmitter in the sympathetic nerves of small arteries thus appears to be the dominant transmitter during low‐frequency nerve stimulation, causing rapid but phasic activation. Noradrenaline is the most important transmitter for higher frequencies, exerting slower but sustained contractions. The post‐stimulatory potentiation affects both the adrenergic and the non‐adrenergic part of the neurogenic response.
Sympathetic transmission in small mesenteric arteries from the rat: influence of impulse pattern
Authors: SJÖBLOM‐WIDFELDT N. , NILSSON H. 
Published: December 2008

We have previously studied the transmitters involved in, and the calcium dependency of, the neurogenic response to continuous, regular nerve stimulation in small mesenteric arteries from the rat. We have now studied responses to irregular nerve stimulation in these respects.Small mesenteric arteries from rat were mounted into a myograph and the intramural sympathetic nerves were activated by field stimulation. Irregular nerve stimulation was patterned after recorded activity in human cutaneous nerves.The response to irregular stimulation was reduced by only approximately 50% in the presence of the α1‐adrenoceptor antagonist prazosin. In particular, responses to low‐frequency stimulation were resistant to prazosin.When the extracellular calcium concentration was reduced from 2.5 to 1.0 mM, approximately 50% of the response to irregular nerve stimulation remained. Responses to low‐frequency stimulation were particularly reduced.Thus in these arteries the neurogenic response is caused by noradrenaline and a, perhaps purinergic, co‐transmitter. The co‐transmitter is important for the response to low‐frequency stimulation and for the initial part of the contraction caused by high‐frequency stimulation. Reducing the calcium concentration affects more strongly the response to low‐frequency nerve stimulation.
On the role of vasoactive intestinal polypeptide and tachykinins in the secretory reflex elicited by chemical peritonitis in the cat small intestine
Authors: BRUNSSON I. , FAHRENKRUG J. , JODAL M. , SJÖQVIST A. , THEODORSSON E. , LUNDGREN O. 
Published: December 2008

Peritonitis induced by serosal application of 0.1 M hydrochloric acid causes net fluid secretion via the enteric nervous system. The aim of the present study was to investigate present study was to investigate the roles of vasoactive intestinal peptide (VIP) and tachykinins in this reflex(es). The release of tachykinins (substance P [SP], neurokinin A [NKA], neuropeptide K [NPK]) and VIP into the mesenteric circulation, net fluid transport, intestinal blood flow and sometimes motility were recorded simultaneously in extrinsically denervated jejunal segments of the catin vivo. The release of both VIP and NKA was increased upon application of HCI to the cat jejunal serosa. Tetrodotoxin, hexamethonium and methionine enkephalin inhibited both the induced VIP release and the secretory response. The increased release of NKA was unaffected by hexamethonium.We propose that the intramural secretory reflex evoked by acid application of the serosa consists of an ‘afferent’ tachykinin neuron, a cholinergic interneuron and an ‘efferent’ VIPergic neuron innervating the secretory enterocytes.
The role of protein kinase C in histamine secretion from mast cells
Authors: CHAKRAVARTY N. 
Published: December 2008

Receptor activation on the cell surface is coupled through a guanine nucleotide regulatory protein to polyphosphoinositide phosphodiesterase. The activation of this enzyme catalyses the hydrolysis of phosphatidylinositol biphosphate. One of the products of this hydrolysis is diacylglycerol, which activates protein kinase C. It can also be activated by tumour‐promoting phorbol esters. The synthetic diacylglycerol, 1‐oleoyl‐2‐acetyl‐rac‐glycerol (OAG) and the phorbal ester 12‐O‐tetradecanoylphorbol 13‐acetate (TPA) have been used to stimulate protein kinase C in a pure population of rat peritoneal mast cells. Both of them caused histamine release, but the rate of release with TPA or OAG alone was slow. The release was inhibited by blocking the oxidative energy metabolism with antimycin A, and was associated with progressive exocytosis, showing that it is a secretory process. Studies on the interaction between the stimulation of protein kinase C by OAG/TPA and the secretagogues showed a dual effect, both potentiation and inhibition. Antigen (in sensitized cells) and compound 48/80 showed this pattern of response. With the calcium ionophore, A23187, potentiation was the dominant effect, although some inhibition could be shown with TPA. This is possibly related to the large calcium influx which causes translocation of protein kinase C to the membranes and enhances its activity. The potentiation suggests that protein kinase C is involved in the secretion process by the secretagogues, while the inhibition reflects a regulatory function, which is apparently exerted through an inhibition of phosphatidylinositol breakdown.Calcium uptake was enhanced by both TPA and OAG. Protein kinase C may thus contribute to the replenishment of the intracellular calcium stores after the secretory response.
Vascular adrenergic responses in morphine‐dependent rats
Authors: GUSTAFSSON H. , DELLE M. , NILSSON H. 
Published: December 2008

The circulatory effects of morphine abstinence have recently been found to involve decreased renal sympathetic nerve activity and increased mean arterial pressure, induced by vasoconstriction. A direct influence of morphine withdrawal on the peripheral vasculature could possibly contribute to the increased resistance. Therefore, contractile responses to transmural nerve stimulation and to applied noradrenaline of peripheral arteries from morphine‐dependent and untreated rats were examinedin vitrounder paired conditions.No increase in contractile response was observed after chronic morphine treatment, either on nerve stimulation or on applied noradrenaline. Instead the smooth muscle sensitivity to adrenergic stimulation was reduced. Consequently, the present study does not support a peripheral adrenergic origin of the vasoconstriction during naloxone‐precipitated morphine abstinence.
Diet‐induced changes in subcutaneous adipose tissue blood flow in man: effect of β‐adrenoceptor inhibition
Authors: SIMONSEN L. , BÜLOW J. , ASTRUP A. , MADSEN J. , CHRISTENSEN N. J. 
Published: December 2008

The effect of a carbohydrate‐rich meal on subcutaneous adipose tissue blood flow was studied with and without continuous i. v. infusion of propranolol in healthy volunteers.The subcutaneous adipose tissue blood flow was measured with the133Xe washout method in three different locations: the forearm, the thigh and the abdomen. The subjects were given a meal consisting of white bread, jam, honey and apple juice (about 2300 kJ). The meal induced a twofold increase in blood flow in the examined tissues. Propranolol abolished the flow increase in the thigh and the abdomen and reduced it in the forearm. This indicates that the mechanism for the flow increase is elicited by a stimulation of vascular β‐adrenoceptors in the subcutaneous adipose tissue, since the β‐adrenoceptor inhibition did not affect the overall metabolic and hormonal responses to the meal.
Resumption of rat oocyte meiosis is paralleled by a decrease in guanosine 3‘,5’‐cyclic monophosphate (cGMP) and is inhibited by microinjection of cGMP
Authors: TÖRNELL J. , BILLIG H. , HILLENSJÖ T. 
Published: December 2008

The aim of the present study was to measure the level of cyclic GMP (cGMP) compared with the level of cyclic AMP (cAMP) in rat oocytes during resumption of meiosis I (oocyte maturation) and to microinject these cyclic nucleotides into the oocyte to study their effects on oocyte maturation. Immature oocytes were obtamed from prepubertal rats primed with pregnant mare's serum gonadotropin. Oocytes were isolated and short‐term cultured under conditions enabling spontaneous maturation. The levels of cGMP and cAMP decreased in the oocyte during spontaneous maturation (from 0.41 to 0.25 and from 0.64 to 0.42 fmol per oocyte respectively). The decrease was observed during the first hour of culture, and no further decline was seen after 2 h. Microinjection of cGMP or cAMP into isolated immature oocytes delayed the spontaneous maturation, cGMP being slightly more effective than cAMP, whereas 2‐deoxy‐cAMP (which does not stimulate protein kinase A) did not.These results demonstrate for the first time that the level of cGMP decreases in the oocyte parallel to spontaneous meiosis, as already shown for cAMP. This suggests that cGMP, as well as cAMP, may be of importance for regulating this process. This assumption is further supported by data demonstrating a delay in the maturation of oocytes injected with cGMP.
Lactate and potassium fluxes from human skeletal muscle during and after intense, dynamic, knee extensor exercise
Authors: JUEL C. , BANGSBO J. , GRAHAM T. , SALTIN B. 
Published: December 2008

This study examines lactate and K+ fluxes from muscle to blood during and after intense exercise. Ten men performed exhaustive dynamic exercise (mean load 65 W, mean duration 3.18 min) with the knee extensors of one leg. The mean lactate efflux was 15.5 (range 8.9–24.0) mmol min‐1 at exhaustion, and it was linearly related to the lactate gradient. A linear relationship was also obtained if the H+ gradient was taken into account. Muscle pH decreased from 7.14 at rest to 6.71 (range 6.50–6.87) at exhaustion. At rest and during late recovery blood lactate was distributed across the erythrocyte membrane according to the membrane potential (intra‐/extracellular ratio of 0.5), but during rapid lactate release this ratio decreased to 0.2. In‐vitro experiments demonstrated a time constant of 1.2 min for lactate efflux from the erythrocytes.Approximately 70% of the K+ ions released from the muscle to the blood accumulated in the plasma; the rest were taken up by other tissues. However, erythrocytes were not involved as a dilution space. The small change in erythrocyte K+ concentration was due to cellular volume changes. During recovery the kinetics of K+ reuptake by the muscle were described by a very fast (< 1 min) and a slow component (> 1 min): the magnitude of the former was equivalent to what had accumulated in the plasma. Individuals displayed a wide range of intramuscular lactate concentrations and pH values at exhaustion. Further, the pH changes were not as extreme as previously reported, suggesting that pH may not be the only factor involved in the fatigue process. A possible role for the potassium shifts as a limiting factor for muscle function is discussed.
The effect of a meal on cardiac output in man at rest and during moderate exercise
Authors: WAALER B. A. , ERIKSEN M. , JANBU T. 
Published: December 2008

Cardiac output at rest increased by 11–63 % in a group of healthy individuals after the consumption of a medium‐sized, mixed meal. The maximum post‐prandial levels of cardiac output were reached from 10 to 30 min after termination of the meal. Cardiac output values at rest fluctuate around a mean level, and this fluctuation was considerably more marked after a meal, when changes in cardiac output from one 15–s period to another could be of the order of 1–1.5 1 min‐l.Recording of flow in the superior mesenteric artery before and also after a meal was successful in two subjects in whom anatomical conditions were favourable. Flow in the artery was approximately doubled from the fasting to the post‐prandial situation, an augmentation that accounted for about 50% of the concomitant increase in cardiac output.The increases in cardiac output caused by 2–min bouts of standardized, moderate and rhythmic exercise were consistently larger in the post‐prandial than in the fasting situation. It thus appears that any tendency for redistribution of blood flow, for example from the gastrointestinal tract to the working muscles, during moderately intense exercise is less marked after a meal than before.
Effect of 12‐O‐tetradecanoyl phorbol 13‐acetate on solute transport and production of cAMP in isolated frog skin
Authors: ANDERSEN H. , BJERREGAARD H. , NIELSEN R. 
Published: December 2008

In the present study we have examined the action of the phorbol diester tetradecanoyl phorbol acetate, an activator of protein kinase C, on the transepithelial transport of sodium, chloride and water and the production of cAMP in the isolated frog skin epithelium (Rana esculenta).Addition of tetradecanoyl phorbol acetate to the mucosal solution resulted initially in an increase in the short‐circuit current, which was followed by a progressive decrease. If the short‐circuit current was first activated by addition of the antidiuretic hormone, arginine vasotocin, then the addition of tetradecanoyl phorbol acetate resulted only in a pronounced inhibition. The changes in the short‐circuit current were the result of changes in the active influx of Na+.The effect of tetradecanoyl phorbol acetate on the intracellular potential measured under short‐circuited conditions (Vscc) was time‐dependent. Just after addition of tetradecanoyl phorbol acetate to the mucosal solution. Vscc depolarized; this was followed by a slight hyperpolarization, after which Vscc continued to decline.The inhibition of the Na+ transport by tetradecanoyl phorbol acetate was associated with a decline in the response to the antidiuretic hormone (arginine vasotocin), but the ability of arginine vasotocin to increase the cellular level of cAMP and to stimulate the osmotic water flow was not affected by the presence of tetradecanoyl phorbol acetate.In skin halves in which the short‐circuit current was stimulated with arginine vasotocin, addition of tetradecanoyl phorbol acetate resulted in a dose‐dependent inhibition of the short‐circuit current, but only minor changes in Vscc were observed.The results presented suggest that the addition of tetradecanoyl phorbol acetate to the isolated frog skin first increases and then decreases the arginine vasotocin‐sensitive sodium permeability of the apical membrane. This might be due to a stimulating effect of tetradecanoyl phorbol acetate on both the activation and deactivation (turnover) of the sodium channels.
Adenosine A1‐receptor‐mediated inhibition of evoked acetylcholine release in the rat hippocampus does not depend on protein kinase C
Authors: FREDHOLM B. B. 
Published: December 2008

The possible involvement of protein kinase C and/or a lipoxygenase product in the mechanism by which adenosine inhibits release of [3H]acetylcholine evoked by electrical pulses from [3H]choline‐labelled hippocampal slices was examined. For comparison, the muscarinic autoreceptors were examined using carbachol. The order of potency of adenosine analogues (CHA = R‐PIA > NECA± CGS 21680, CV 1808) indicates that the adenosine receptor responsible is of the A1subtype. Adenosine (10 μM) and R‐PIA (0.1 μm) were virtually equiactive as inhibitors and were antagonized to an equal extent by 8–CPT with a potency (IC50approximately 25 nm) which is also compatible with A1‐receptor mediation. The effects of carbachol and of R‐PIA were not antagonized by the lipoxygenase inhibitor NDGA (10 or 50 μm). Stimulation of protein kinase C by the phorbol ester 4β‐phorbol 12, 13–dibutyrate caused a concentration‐dependent increase in stimulation‐evoked3H overflow, but did not antagonize the presynaptic inhibitory effect of R‐PIA or carbachol (0.01–1 μm). Staurosporine (0.1 μm), which inhibited the stimulating effect of phorbol dibutyrate, did not alter the effects of carbachol or R‐PIA. The presynaptic effects of phorbol dibutyrate, R‐PIA and adenosine were reduced by pretreatment withN‐ethylmaleimide (100, μ M for 10 min), which inactivates G‐proteins. The evoked transmitter release was unaffected by nifedipine (1 μ M) in the presence and in the absence of phorbol dibutyrate.These results indicate that adenosine, by acting at presynaptic A,‐receptors, reduces transmitter release by a mechanism that involves neither an NDGA‐sensitive lipoxygenase nor protein kinase C. The results also indicate that the enhancement of transmitter release by phorbol esters is due to protein kinase C activation and that a G‐protein may be involved in the effect but a dihydropyridine‐sensitive L‐type Ca2+channel probably is not.
The effects of μ, δ‐ and ±‐opioid receptor antagonists on the pain threshold increase following muscle stimulation in the rat
Authors: HOFFMANN P. , CARLSSON S. , THORÉN P. 
Published: December 2008

In a previous study, prolonged low‐frequency muscle stimulation, inducing dynamic contractions in the hind leg of unanaesthetized rats, was shown to give rise to a hypoalgesia. The increase in pain threshold, measured as squeak threshold to noxious electric pulses, lasted 3 h.In the present study, the involvement of the endogenous opioid system in the post‐stimulatory analgesia was investigated using selective opioid receptor antagonists. The post‐stimulatory analgesia was completely reversed back to prestimulatory control levels by naloxone, 1 mg kg‐1. ICI 154, 129 and MR 2266 BS, selective δ‐ and ±‐receptor antagonists respectively, did not significantly influence the post‐stimulatory analgesia, although ICI 154, 129 had a minor pain threshold‐lowering effect. Rats pretreated with β‐funaltrexamine, a μ‐preceptor antagonist, did not exhibit any post‐stimulatory analgesia.These results suggest that opioid systems are involved in the increase in pain threshold after muscle stimulation and that the analgesic response is both elicited and maintained by the μ‐preceptor.