bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mediation by 5‐hydroxytryptamine of the femoral vasoconstriction induced by acid challenge of the rat gastric mucosa
Authors: Wachter Christof H. , Heinemann Ákos , Donnerer Josef , Pabst Maria A. , Holzer Peter 
Published: September 2004

Gastric mucosal barrier disruption in the presence of luminal acid causes femoral vasoconstriction via a pathway that appears to be stimulated by messengers generated in the injured gastric mucosa. This study was undertaken to analyse the gastric factors that are responsible for the femoral vasoconstrictor response.
Gastric mucosal barrier disruption in the presence of luminal acid was induced by perfusing the stomach of urethane‐anaesthetized rats with ethanol (15 %) in 0.01‐0.15 M HCl. Blood flow in the left gastric and right femoral artery was estimated by the ultrasonic transit time shift technique.
Gastric perfusion of ethanol in HCl caused loss of H+ ions from the gastric lumen, decreased the HCO3− concentration in hepatic portal vein blood, induced macroscopic histological damage to the gastric mucosa, dilated the left gastric artery and constricted the femoral artery. These responses were related to the HCl concentration in the ethanol‐containing perfusion medium.
The femoral vasoconstriction was also seen when, instead of ethanol, taurocholate (20 mM) was used to disrupt the gastric mucosal barrier in the presence of 0.15 M HCl.
The femoral vasoconstriction evoked by gastric perfusion of ethanol in HCl was left unaltered by pharmacological blockade of gastrin and histamine receptors. In contrast, the 5‐hydroxytryptamine 5‐HT1/2 receptor antagonist methiothepin, but not the 5‐HT2A receptor antagonist ketanserin or the 5‐HT3 receptor antagonist granisetron, inhibited the ability of both 5‐hydroxytryptamine and gastric acid back‐diffusion to constrict the femoral artery.
Gastric acid back‐diffusion caused release of 5‐hydroxytryptamine into the gastric lumen, which was related to the HCl concentration in the ethanol‐containing perfusion medium.
These data show that femoral vasoconstriction evoked by gastric mucosal barrier disruption depends on back‐diffusion of acid into the mucosa. The acid‐induced damage results in release of 5‐hydroxytryptamine from the gastric mucosa, and the pathway leading to constriction of the femoral artery involves 5‐hydroxytryptamine acting via 5‐HT1/2 receptors as a messenger molecule.
Absence of early resetting of coronary baroreceptors in anaesthetized dogs
Authors: McMahon Nicholas C. , Drinkhill Mark J. , Hainsworth Roger 
Published: September 2004

Both carotid and aortic arch baroreceptors have been shown to reset after as little as 20 min exposure to a different conditioning pressure; the mid‐point of the stimulus‐response curve is displaced towards the conditioning pressure.
Coronary baroreceptors operate over much lower pressures and induce slower reflex vasoconstriction than the other baroreceptors and this investigation was designed to determine whether their resetting characteristics are also different.
In chloralose anaesthetized dogs, a perfusion circuit allowed independent control of pressures distending carotid, aortic and coronary baroreceptors. Stimulus‐response curves were obtained for carotid and coronary baroreceptors after maintaining the distending pressure at 60 or 180 mmHg for 20 min.
Neither the magnitude of the responses nor the baroreceptor pressure corresponding to 50 % of the response (BP50) of the coronary curves was changed by the conditioning regime. In contrast, conditioning carotid baroreceptors with the same regime produced significant shifts in the BP50 towards the conditioning pressure.
No changes were obtained after conditioning the coronary baroreceptors at 60 or 120 mmHg for 40 min.
These results confirm early resetting of carotid baroreceptors but show that coronary baroreceptors do not reset over a period of at least 40 min.
Premature bifurcation of the apical dendritic trunk of vibrissa‐responding pyramidal neurones of X‐irradiated rat neocortex
Authors: Ito Muneyuki , Kato Miyuki , Kawabata Masao 
Published: September 2004

Electrophysiological and morphological experiments were performed on the pyramidal neurones of the somatosensory neocortex of the adult rat that had been exposed in utero to 200 rad of X‐irradiation. Under urethane anaesthesia, evoked gross potentials, extracellular and intracellular neuronal responses, and laminar field potentials were recorded. The evoked epicortical potential to deflection of a single whisker was a long‐lasting positive wave which contrasted with a biphasic positive‐negative complex in unirradiated controls. Neurones were initially tested during extracellular recording for responses to whisker deflections. This was followed by intracellular injection with horseradish peroxidase (HRP), and the HRP‐stained neuronal elements were visualized using diaminobenzidine as a chromagen.
Fifty neurones were recorded and stained through the soma. The mean response latency was 15.1 ms. Of these, thirty‐six showed premature bifurcation of the apical dendrite. The angle of bifurcation of the apical dendrite was measured in the coronal plane and was found to be a function of the depth at which the soma was located and the distance between the soma and bifurcation point. It was suggested that the apical dendrites of these neurones underwent premature bifurcation due to an imbalance between the growth of neurones and skull.
Fifteen neurones were recorded and stained through the presumed apical dendritic shaft. The mean response latency was 19.5 ms. The electrode track left in the histological specimen pointed to the stained apical dendrite. Dendritic elements distal to the entry point were preferentially filled with HRP. In no cases were somata stained. There was, in turn, no evidence of recording from dendritic elements distal to the bifurcation since no electrode track was found to point to these elements. That dendritic spike responses may not travel beyond the bifurcation was further substantiated by laminar analysis of field potentials.
Role of endogenous endothelin in the regulation of basal coronary tone in the rat
Authors: Goodwin Andrew T. , Amrani Mohamed , Gray Caroline C. , Jayakumar Jay , Yacoub Magdi H. 
Published: September 2004

Coronary vascular tone is a vital factor that regulates the delivery of oxygen to cardiac muscle. We tested the hypothesis that basal coronary tone may depend on the release of an endogenous vasoconstrictor peptide, endothelin (ET).
Using an isolated, Krebs solution‐perfused rat heart we measured the changes in coronary flow following the administration over a 30 min period of the ET antagonists Ro61‐0612 (mixed ETA/ETB), PD155080 (ETA) and BQ788 (ETB).
In a second series of experiments, hearts were randomly assigned to perfusion with plain Krebs solution, or with Krebs solution to which L‐NAME and/or indomethacin had been added. The effect on coronary flow following the addition of Ro61‐0612 was then measured.
Perfusion with Ro61‐0612 (10−4 M) alone increased coronary flow by 57.8 %vs. control (P= 0.00001). PD155080 (10−4 M) increased coronary flow by 28.9 % (P= 0.009), whereas BQ788 had no effect on coronary flow.
In the second series of experiments, Ro61‐0612 increased coronary flow by 6.6 ± 0.8 ml min−1 in hearts perfused with plain Krebs solution, by 3.8 ± 0.8 ml min−1 in hearts to which both L‐NAME and indomethacin had been added, by 3.3 ± 0.7 ml min−1 in hearts to which L‐NAME had been added, and by 6.9 ± 0.5 ml min−1 in hearts to which indomethacin had been added to the Krebs buffer.
In hearts perfused with Krebs solution alone, nitric oxide (NO) release into the coronary sinus increased from 219.8 to 544.9 pmol min−1 g−1 following the addition of Ro61‐0612 (P= 0.06). There was no detectable release of NO from hearts perfused with L‐NAME alone or in combination with indomethacin either before or after the addition of Ro61‐0612.
We conclude that endogenous ET plays a role in coronary tone mediated via ETA receptors. This vasodilatation is partially due to an increase in endogenous NO release. However, a significant vasodilatation is still seen following the inhibition of NO synthesis. We propose that basal coronary tone depends on a balance between the endogenous release of vasodilators such as NO and vasoconstrictors such as ET.
Activation of α‐ and β‐adrenoceptors by sympathetic nerve stimulation in the large intestine of the rat
Authors: Luckensmeyer Greta B. , Keast Janet R. 
Published: September 2004

The effects of sympathetic nerve stimulation on the motility of the circular and longitudinal muscle of the large intestine were investigated in vitro, and the involvement of various adrenoceptor subtypes determined. A comparison between the sympathetic supply arising from the prevertebral and pelvic ganglia was also made.
In the longitudinal muscle of the distal colon, sympathetic nerve stimulation caused responses which were contractile (0.1–2 Hz), biphasic (5–10 Hz) or purely inhibitory (20–30 Hz). All contractile responses were removed with phentolamine (3 μM), whereas the inhibitory responses were significantly diminished by propranolol (0.1 μM) and completely abolished by alprenolol (3 μM) or nadolol (300 μM).
In the longitudinal muscle of the proximal colon, the effects of sympathetic nerve stimulation were predominantly inhibitory. Some of this inhibition was removed by propranolol (0.1 μM), but was largely unaffected by alprenolol (3 μM). The remainder of the inhibitory response was probably non‐noradrenergic as it was not removed by a combination of phentolamine (3 μM) and alprenolol (3 μM).
In the circular muscle of both the proximal and distal colon, sympathetic stimulation caused a strong contractile response which was completely removed by phentolamine (3 μM) to reveal an inhibitory response. This inhibitory response was unchanged by propranolol (0.1 μM) but was removed by alprenolol (3 μM), following which a weak non‐noradrenergic contractile response was unmasked.
Stimulation of the hypogastric nerve to activate pelvic sympathetic pathways had no effect on the motility of the longitudinal muscle, but caused a contractile response in the circular muscle which was completely removed by phentolamine (3 μM).
We conclude that sympathetic nerves innervate adrenoceptors of different types in the various muscle layers and regions of the colon. They innervate a mixture of α‐, and β3‐adrenoceptors in the longitudinal muscle of the proximal colon, α‐, classical β‐ and β3‐adrenoceptors in the distal colon, and primarily α‐adrenoceptors with a few β3‐adrenoceptors in the circular muscle. In addition, the pelvic sympathetic innervation of the rectum differs from the prevertebral supply by innervating only excitatory α‐adrenoceptors.
Extrinsic neural control of nitric oxide synthase expression in the myenteric plexus of rat jejunum
Authors: Nakao Koji , Takahashi Toku , Utsunomiya Joji , Owyang Chung 
Published: September 2004

The role of extrinsic innervation in the expression of nitric oxide synthase (NOS) in the myenteric plexus remains unknown. In this study, we investigated the effect of extrinsic denervation on NOS expression in rat jejunum.
N
G‐nitro‐L‐arginine methyl ester (L‐NAME)‐sensitive non‐adrenergic, non‐cholinergic (NANC) relaxations induced by transmural nerve stimulation were significantly increased in muscle strips obtained from rats treated with splanchnic ganglionectomy or 6‐hydroxy‐dopamine (6‐OH‐dopamine). Truncal vagotomy or treatment of the coeliac ganglia with capsaicin did not significantly affect NANC relaxations.
The number of NOS‐immunopositive cells in the myenteric plexus was significantly increased in tissues obtained from rats treated with splanchnic ganglionectomy or 6‐OH‐dopamine.
Western blot analysis and Northern blot analysis showed a significant increase in the density of the immunoreactive NOS band and the NOS mRNA band, respectively, of the tissues obtained from rats treated with splanchnic ganglionectomy or 6‐OH‐dopamine.
Truncal vagotomy or treatment of the coeliac ganglia with capsaicin did not significantly affect the density of NOS band or NOS mRNA band.
It is concluded that neuronal NOS expression in the myenteric plexus is independent of vagus nerve and is negatively regulated by the splanchnic nerves in the rat small intestine.
Transepithelial electrochemical gradients in the proximal convoluted tubule during potassium depletion in the rat
Authors: Shirley D. G. , Walter S. J. , Folkerd E. J. , Unwin R. J. , Bailey M. A. 
Published: September 2004

In order to examine the electrochemical gradient for potassium reabsorption across the S2 segment of the proximal convoluted tubule, transepithelial potential differences and transepithelial potassium concentrations were measured in anaesthetized potassium‐replete and potassium‐depleted rats.
Potassium‐depleted rats were markedly hypokalaemic (plasma potassium, 1.4 ± 0.1 vs. 4.1 ± 0.1 mmol l−1 in potassium‐replete rats) and had a significantly reduced muscle potassium content. In confirmation of previous reports, glomerular filtration rate was slightly reduced, while fractional reabsorption in the proximal convoluted tubule was enhanced.
In potassium‐replete animals, the transepithelial potential difference (PD) at the late proximal convoluted tubule was +2.1 ± 0.3 mV (lumen positive) and the tubular fluid to plasma ultrafiltrate concentration ratio for potassium (TFK/UFK) at the same site was 1.03 ± 0.01. In potassium‐depleted rats, there was a striking reversal of the transepithelial PD (to −4.0 ± 0.4 mV), while the TFK/UFK was increased to 1.19 ± 0.03.
The data from both potassium‐replete and potassium‐depleted animals are consistent with accumulating evidence that potassium reabsorption in the proximal convoluted tubule is passive in nature and depends partly on diffusion down an electrochemical gradient.
Effect of transverse‐tubular chloride conductance on excitability in skinned skeletal muscle fibres of rat and toad
Authors: Coonan J. R. , Lamb G. D. 
Published: September 2004

The influence of the transverse‐tubular (T‐) system Cl− conductance on membrane excitability in skeletal muscle fibres of toad and rat was examined because of conflicting conclusions of previous studies on Cl− conductance. A mechanically skinned fibre preparation was used that permitted investigation of Ca2+ release via the normal T‐system voltage‐sensor mechanism after complete removal of the surface membrane, which thereby allowed estimation of the T‐system potential from force measurements.
When a skinned fibre was bathed in a high‐[K+] solution, the sealed T‐system became polarized and could be rapidly depolarized by replacing the K+ with Na+, thereby eliciting Ca2+ release from the sarcoplasmic reticulum. In rat skinned fibres, addition of 20 mM Cl− to the ‘myoplasm’ (i.e. bathing solution) partially depolarized the T‐system, inducing Ca2+ release and subsequent voltage‐sensor inactivation. These effects were completely abolished with 100 μM of the Cl− channel blocker 9‐anthracene carboxylic acid (9‐AC). Voltage‐sensor inactivation increased in a graded manner over the range 3‐20 mM myoplasmic Cl−.
In toad fibres, voltage‐sensor inactivation was only detectable at > 10 mM myoplasmic Cl−, and 20 mM Cl− was only able to depolarize the T‐system sufficiently to trigger Ca2+ release if the myoplasmic [K+] was reduced by 50 %. In toad fibres, 100 μM 9‐AC caused little if any block of the T‐system Cl− conductance.
It was also found that when skinned fibres were obtained from muscles that had been bathed in a zero Cl− extracellular solution, the initial Na+ substitutions were more effective at depolarizing the T‐system. This is consistent with Cl− trapped in the sealed T‐system exerting a polarizing effect on T‐system potential.
These results unequivocally demonstrate that there is a large 9‐AC‐sensitive Cl− conductance in the T‐system of rat fibres, and a smaller, though still appreciable, Cl− conductance in the T‐system of toad fibres, which is relatively insensitive to 9‐AC. The results are important for understanding the basis of the Cl− channel aberration in myotonia.
Carbachol‐induced oscillations in membrane potential and [Ca2+]i in guinea‐pig ileal smooth muscle cells
Authors: Kohda M. , Komori S. , Unno T. , Ohashi H. 
Published: September 2004

Cytosolic free Ca2+ concentration ([Ca2+]i) and membrane potential were simultaneously recorded from single smooth muscle cells of guinea‐pig ileum, using a combination of nystatin‐perforated patch clamp and fura‐2 fluorimetry techniques.
Carbachol (CCh, 2 μM) produced oscillatory changes in [Ca2+]i and membrane potential which coincided well in time with each other, and peaks of membrane potential oscillations reached a saturated level of around −7 mV. Thapsigargin (1 μM) abolished these effects of 2 μM CCh. La3+ (3 μM) immediately prevented the discharge of spike potentials, but allowed both on‐going oscillatory responses to persist for a while.
CCh (0.25‐0.75 μM) caused membrane potential and [Ca2+]i to oscillate in some 20 % of cells studied. Every membrane potential oscillation was preceded by the discharge of single or multiple spike potentials. The effects of CCh were readily abolished by La3+ (3 μM).
In cells exhibiting no oscillatory response to 0.25‐0.75 μM CCh, an electrically evoked action potential usually generated changes in [Ca2+]i and membrane potential similar to those following spontaneously evoked action potentials, and sometimes it did so only after [Ca2+]i or InsP3 had been slightly elevated by repeatedly evoking action potentials or by increasing CCh concentration in the bath medium.
The results suggest that in ileal smooth muscle cells, the oscillations of [Ca2+]i and membrane potential arising from muscarinic stimulation result from release of Ca2+ from internal stores and that there is a Ca2+‐induced potentiation of coincidently elicited cation channel openings. Under weak muscarinic stimulation, Ca2+ entry upon action potential discharge can trigger such a release of stored Ca2+, resulting in synchronous generation of a large rise in [Ca2+]i and a slow, large membrane depolarization.
Central role of heterocellular gap junctional communication in endothelium‐dependent relaxations of rabbit arteries
Authors: Chaytor A. T. , Evans W. H. , Griffith T. M. 
Published: September 2004

The contribution of gap junctions to endothelium‐dependent relaxation was investigated in isolated rabbit conduit artery preparations pre‐constricted by 10 μM phenylephrine (PhE).
Acetylcholine (ACh) relaxed the thoracic aorta by ≈60 % and the superior mesenteric artery (SMA) by ≈90 %. A peptide possessing sequence homology with extracellular loop 2 of connexin 43 (Gap 27, 300 μM) inhibited relaxation by ≈40 % in both artery types. Gap 27 also attenuated the endothelium‐dependent component of the relaxation induced by ATP in thoracic aorta but did not modify force development in response to PhE.
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G‐nitro‐L‐arginine methyl ester (L‐NAME, 300 μM), an inhibitor of NO synthase, attenuated ACh‐induced relaxation by ≈90 % in the aorta but only by ≈40 % in SMA (P < 0.05). Residual L‐NAME‐insensitive relaxations were almost abolished by 300 μM Gap 27 in aorta and inhibited in a concentration‐dependent fashion in SMA (≈50 % at 100 μM and ≈80 % at 10 mM). Gap 27 similarly attenuated the endothelium‐dependent component of L‐NAME‐insensitive relaxations to ATP in aorta.
Responses to cyclopiazonic acid, which stimulates endothelium‐dependent relaxation through a receptor‐independent mechanism, were also attenuated by Gap 27, whereas this peptide exerted no effect on the NO‐mediated relaxation induced by sodium nitroprusside in preparations denuded of endothelium.
ACh‐induced relaxation of ‘sandwich’ mounts of aorta or SMA were unaffected by Gap 27 but completely abolished by L‐NAME.
We conclude that direct heterocellular communication between the endothelium and smooth muscle contributes to endothelium‐dependent relaxations evoked by both receptor‐dependent and ‐independent mechanisms. The inhibitory effects of Gap 27 peptide do not involve homocellular communication within the vessel wall or modulation of NO release or action.
The hypoxic response of neurones within the in vitro mammalian respiratory network
Authors: Ramirez J. M. , Quellmalz U. J. A. , Wilken B. , Richter D. W. 
Published: September 2004

The transverse brainstem slice preparation containing the pre‐Bötzinger complex (PBC) was used in mice to study developmental changes of the response of the in vitro respiratory network to hypoxia. This preparation generates at different postnatal stages (postnatal days (P) 0‐22) spontaneous rhythmic activity in hypoglossal (XII) rootlets that occur in synchrony with periodic bursts of neurones in the PBC.
In slices from P0‐4 mice, hypoxia did not significantly affect the amplitude of rhythmic synaptic drive potentials in four of five inspiratory neurones. Hypoxia reduced, but did not suppress, the amplitude of synaptic drive potentials in only one inspiratory neurone. Spike discharge and phasic ‘inspiratory’ hyperpolarizations of six expiratory neurones were suppressed during hypoxia revealing a phasic ‘inspiratory’ depolarization.
The coupling between rhythmic activity in PBC neurones and XII bursts occurred under control conditions in preparations from P0‐4 mice in a 1:1 manner (n= 11) and from mice older than P5 in a 3:1 manner (n= 9). During hypoxia, PBC and XII activity were linked in a 1:1 manner in all slices.
In six of fourteen inspiratory PBC neurones, the amplitude of synaptic drive potentials of slices from mice older than P8 was increased during the period of augmentation, reduced during the period of depression and suppressed during a hypoxic response which we refer to as central apnoea. Augmentation led to a weak‐to‐moderate membrane depolarization which on average was 4.8 ± 3.7 mV. This depolarization was followed by a hyperpolarization of 6.2 ± 4.1 mV only in four inspiratory neurones. In the majority of neurones (n= 9), however, membrane depolarization remained stable and was not followed by hyperpolarization. In expiratory neurones (n= 12) from this age group hypoxia suppressed phasic hyperpolarizations that occurred in synchrony with XII bursts. As similarly seen in inspiratory neurones, membrane potentials were depolarized by 5.1 ± 4.1 mV during the period of hypoxic augmentation.
The hypoxic response of respiratory neurones within the pre‐Bötzinger complex resembles the response of neurones that were previously described under in vivo conditions. Thus we conclude that the ‘transverse rhythmic slice’ is a good model for studying the hypoxic response of the respiratory network under in vitro conditions.