bluuebunny/crossref_metadata_2025_split huggingface dataset:
Calcium and the α‐action of catecholamines on guinea‐pig taenia caeci
Authors: Hertog Adriaan Den 
Published: December 2014

1. The involvement of calcium in the α‐action of adrenaline on guinea‐pig taenia caeci was studied by measuring the changes in membrane potential and muscle contraction, using the sucrose‐gap method, and by determining the 42K efflux, in the presence of a β‐blocker (propranolol, 1·8 × 10−6
m).2. In the presence of extracellular calcium, the hyperpolarization caused by adrenaline (3 × 10−6
m) was sustained during the period of its application (5 min), both in active preparations (at 36 °C) and in quiescent muscle (22 °C). In the absence of calcium, adrenaline caused a transient hyperpolarization which was smaller at 36 °C than at 22 °C and passed off within 5 min, while adrenaline was present.3. Both the sustained and the transient hyperpolarization were associated with an increase in 42K efflux which had a similar time course. 42K flux measurements were made in depolarized tissue (52·8 m
m‐potassium), in which the effect was consistent and more pronounced than in polarized muscle (2·8 m
m‐potassium).4. The transient hyperpolarization which is resistant to calcium removal and EGTA (0·1‐2·0 m
m) could be evoked only once but, following a short exposure to calcium (2·5 m
m) for 20 sec and readmission of calcium‐free medium, it was restored.5. The sustained and the transient hyperpolarization and the increase in 42K efflux were abolished by the α‐antagonist phentolamine (10−5
m); their amplitude was dependent on the adrenaline concentration in the range 10−7 to 3 × 10−6
m, and both responses persisted in the absence of sodium or chloride.6. The hyperpolarization and the increase in 42K efflux were greater at higher external calcium concentrations (0·3‐2·5 m
m).7. Cobalt (0·6 m
m), D600 (2·5 × 10−5
m) and the bee toxin apamin (10−7
m) reduced the α‐response.8. In the presence of apamin, in calcium‐containing solution, the sustained hyperpolarization caused by adrenaline was preceded by, or converted to, depolarization, spike discharge and contraction.9. The depolarizing effect of adrenaline in the presence of apamin persisted in sodium‐free or chloride‐free medium, but was blocked in the absence of calcium and diminished by cobalt and D600.10. It is concluded that the α‐response of guinea‐pig taenia caeci consists of two components, both involving calcium. First, the activation of α‐receptors increases calcium entry, which leads to the opening of potassium channels, a sustained hyperpolarization and inhibition of muscle activity. Secondly, in the absence of external calcium, a transient hyperpolarization is revealed, presumably due to the release of bound calcium from a limited cellular store which can be replenished by addition of external calcium, and this leads to an increase in potassium permeability.
The renin—angiotensin system in drinking and cardiovascular responses to isoprenaline in the rat
Authors: Evered M. D. , Robinson M. M. 
Published: December 2014

1. We investigated the role of the renin—angiotensin system in isoprenaline‐induced drinking in the rat. Captopril, an inhibitor of angiotensin‐converting enzyme, was used to block the synthesis of angiotensin II either in the circulation alone or in the brain as well.2. Subcutaneous injections of isoprenaline (0·1 mg/kg) alone caused nine rats to drink 8·4 ± 0·9 ml water in 3 h.3. Pre‐treatment with doses of captopril (0·1‐1·0 mg/kg,
s.c.), which inhibit conversion of angiotensin I to II in the circulation but not in the brain, dose‐dependently enhanced the drinking response to isoprenaline. Captopril alone did not cause drinking.4. Higher doses of captopril (5·0‐100 mg/kg,
s.c.), which inhibit conversion of angiotensin I to II in the brain as well as in the blood, caused dose‐dependent inhibition of drinking elicited by isoprenaline.5. The highest dose of captopril tested (100 mg/kg,
s.c.) completely blocked the drinking response to isoprenaline (0·1 or 0·33 mg/kg,
s.c.) for at least 45 min. This inhibition was not caused by general debility of the rats; animals deprived of water (12 h) and treated with both captopril and isoprenaline drank as much as water‐deprived controls.6. We found no evidence that blocking the renin—angiotensin system inhibits drinking because it exacerbates isoprenaline‐induced hypotension. After injection of isoprenaline the mean arterial pressure of nephrectomized rats or rats pre‐treated with the high dose (100 mg/kg,
s.c.) of captopril (which blocked drinking) was only slightly lower (5‐10 mmHg) than that of rats pre‐treated with the low dose (0·5 mg/kg,
s.c.) of captopril (which enhanced drinking).7. Water deprivation, which caused rats treated with isoprenaline and captopril to drink, did not increase arterial pressure. Pitressin increased the arterial pressure of rats treated with isoprenaline and captopril but did not cause drinking.We conclude that the renin—angiotensin system has a direct and essential role in the drinking response to isoprenaline.
Prostaglandins alter the relationship between gastric hydrogen ion concentration and flow: evidence for stimulation of non‐parietal secretion in the cat
Authors: Gascoigne A. D. , Hirst B. H. 
Published: December 2014

1. The effect of
i.v. administration of prostaglandin (PG) E2 (10‐40 μg kg−1 h−1), 16,16‐dimethyl PGE2 (0·1‐0·5 μg kg−1 h−1), PGE1 (16‐20 μg kg−1 h−1), PGA1 (5‐11 μg kg−1 h−1) and PGF2α (40 μg kg−1 h−1) on the relationship between [H+] and flow of gastric juice during stimulation of gastric secretion by pentagastrin was investigated in conscious cats prepared with cannulated gastric fistulae.2. A‐ and E‐type prostaglandins significantly reduced pentagastrin‐stimulated acid output. This inhibition was associated with a reduction of the [H+] of the gastric juice such that the [H+] observed at any flow rate tended to be lower than the normal range observed with pentagastrin alone. With the highest doses of these prostaglandins the mean [H+] values were well below the normal range with pentagastrin alone.3. At the dose tested, PGF2α had little effect on acid output, and did not alter the relationship between [H+] and gastric flow.4. There is a linear relationship between acid output and gastric flow and this relationship is similar during stimulation of gastric secretion by pentagastrin, histamine or insulin. Gastric acid inhibitory doses of cimetidine, atropine and somatostatin did not alter this relationship. In contrast the A‐ and E‐type prostaglandins displaced this relationship to the right of the normal line observed with the acid stimulants alone. A‐ and E‐type prostaglandins reduced the slope of the line relating acid output and gastric flow from ∼ 150‐170 μequiv/ml−1 to ∼ 100‐120 μequiv ml−1, this being taken as evidence of dilution of the parietal H+ secretion with a non‐parietal secretion.5. The volume of non‐parietal gastric secretion was calculated as the gastric flow at zero acid output by extrapolation of linear plots of acid output versus gastric flow. Unstimulated gastric flow measured directly was 0·75 ml 15 min−1. The calculated non‐parietal flow was in the range 0·52‐0·90 ml 15 min−1 during stimulation of gastric secretion with pentagastrin, histamine and insulin, and inhibition of pentagastrin‐stimulated acid secretion with cimetidine, atropine and somatostatin. PGE2 (1·51 ml 15 min−1) and 16,16‐dimethyl PGE2 (1·20 ml 15 min−1) nearly doubled the calculated non‐parietal flow.6. These data demonstrate that gastric acid inhibitory doses of A‐ and E‐type prostaglandins can reduce the [H+] in the bulk fluid of the gastric lumen during stimulation of acid secretion. The data provide evidence that these prostaglandins stimulate a non‐parietal component of gastric secretion. This might be gastric bicarbonate and mucus secretion.
The influence of innervation on differentiating tonic and twitch muscle fibres of the chicken
Authors: Gordon Tessa , Vrbová Gerta , Wilcock G. 
Published: December 2014

1. The anterior (ALD) and posterior (PLD) latissimus dorsi muscles of adult chickens were denervated by section of their motor nerves. Four weeks later the contractile and membrane properties of these muscles were studied in vitro at room temperature.2. Although the time course of the PLD muscle twitch was slightly prolonged, the qualitative difference in contractile characteristics of the slow ALD and the fast PLD muscles was maintained after denervation.3. The difference in the passive membrane characteristics of the ALD and PLD muscle fibres was not lost after denervation, although the membrane resistance (Rm) and space constant (λ) of the denervated muscles fell. The membrane resistance, space (λ) and time (τm) constants of the ALD muscle remained significantly greater than for the PLD muscle fibres. The absolute values of τm in both muscles increased, implying that in the case of the ALD the membrane capacitance (Cm) was increased above normal after denervation. This is discussed in terms of the ultrastructural changes in this muscle after denervation.4. The ALD muscle was cut into small pieces and replaced in the bed of the PLD muscle, which in turn was minced and placed into the bed of the ALD muscle. These muscles regenerated and became reinnervated by the PLD and ALD nerves respectively. They aligned themselves in the muscle bed and adopted the former shape of the muscle that they replaced. The passive cable properties of the regenerated ALD muscle fibres innervated by the PLD nerve resembled the control PLD fibres and the regenerated PLD fibres reinnervated by the ALD nerve resembled those of the control ALD. Regenerated ALD and PLD reinnervated by their own nerves had contractile and membrane properties similar to those of control muscles.5. The results show that the fundamental differences, between slow and fast muscles once established, persist even when they are deprived of their innervation. The properties of developing muscle fibres however are determined by the motor nerves even in the adult animal.
β‐receptor numbers and thermodynamics in denervation supersensitivity
Authors: Bannister R. , Boylston A. W. , Davies I. B. , Mathias C. J. , Sever P. S. , Sudera D. 
Published: December 2014

1. Denervation supersensitivity to adrenergic agonists occurs after degeneration of the sympathetic nervous system in the disease called multiple system atrophy (MSA) or the Shy Drager Syndrome.2. Supersensitivity to the chronotropic effect of
i.v. isoprenaline on the heart was demonstrated in eight subjects with sympathetic nervous system degeneration and MSA.3. There was an increased number of β‐receptors present in MSA as measured by [H3]dihydroalprenolol ([H3]DHA) binding to β‐receptors on lymphocytes isolated from venous blood taken from the MSA subjects compared with [H3]DHA binding to lymphocytes from seven normal subjects. There was no difference in the affinity of lymphocyte β‐receptors for [H3]DHA in MSA.4. [H3]DHA binding to lymphocytes from MSA subjects was decreased at lower temperatures but was unaffected by lower temperatures in lymphocytes from normal subjects.5. Equilibrium constants for [H3]DHA binding to normal and MSA lymphocytes were similar, indicating that the affinity of the β‐receptors was similar in both groups. The equilibrium constants were little affected by cooling from 37 to 4 °C suggesting that the heat of reaction (enthalpy) for [H3]DHA binding was low. The Gibbs free energy change on binding was negative and similar in quantity for both normal and MSA lymphocytes. There was a similar, large, increase in entropy on binding of [H3]DHA to both normal and MSA lymphocytes, showing that the binding reaction was entropy driven.6. If lymphocyte β‐receptors reflect the status of cardiac β‐receptors, increased numbers of cardiac β‐receptors may contribute to the denervation supersensitivity to isoprenaline in MSA with sympathetic degeneration.
Extracellular potassium accumulation in the frog spinal cord induced by stimulation of the skin and ventrolateral columns
Authors: Czéh G. , Kr̆íz̆ N. , Syková Eva 
Published: December 2014

1. Changes in extracellular K+ concentration (Δ[K]e), dorsal root potentials (DRPs) and single unit activity were studied in the frog spinal cord in response to stimulation of the skin of the hindlimb by touch, pressure, hot water (heat), single electrical pulses and to stimulation of the ventrolateral columns (LC).2. Single electrical pulses, various types of adequate stimulation applied to the skin of the hind limb for 1‐2 s as well as single volleys of LC led to a Δ[K]e of up to 0.2 mmol.l−1. Stimuli which evoked larger Δ[K]e also produced larger DRPs in the same frog preparation.3. The briefest heat stimuli, which lasted about 1‐2 s, led to more prolonged activity in dorsal horn interneurones than did a single volley or a single tactile stimulus and the Δ[K]e were longer and larger and had a slower rise time.4. The ‘slow’ second component of dorsal root depolarization (presumably mediated by K+) was observed after electrical and heat stimulation of the skin on the hind limb corresponding to the time course of Δ[K]e.5. The maximum Δ[K]e induced by nociceptive stimulation occurred in the grey matter of the dorsal horn at a depth of 300‐600 μm from the dorsal surface. The maximum response to single stimuli applied to the skin occurred at a depth of 400‐800 μm, while that evoked by LC stimulation in the ventral horn at a depth of 1000‐1400 μm.6. Repetitive and more prolonged nociceptive stimulation (5‐20 s) produced a Δ[K]e of up to 1 mmol.l−1. The Δ[K]e in response to repetitive tactile stimulation does not exceed 0.2 mmol.l−1. Repetitive stimulation (100 Hz) of LC fibres led to an increase in [K]e of up to 9‐10 mmol.l−1 in the ventral horn; this level was similar to that achieved in the intermediate region by electrical repetitive stimulation of the skin (100 Hz). Tetanic stimulation of the ventral root led to a Δ[K]e of only about 0.05 mmol.l−1 at a depth of 500‐700 μm and no measurable Δ[K]e within the ventral horn.7. Spontaneous Δ[K]e associated with spontaneous DRPs and VRPs were observed during the decay phase of Δ[K]e at various intervals from several seconds to one minute after nociceptive or electrical stimulation of the skin, suggesting the occurrence of a longlasting increase in excitability.8. The depolarization of dorsal root fibres evoked by nociceptive stimulation, tetanic stimulation of the LC and single or tetanic stimulation of the skin was followed by a dorsal root hyperpolarization. Its size, as well as that of Δ[K]e, was dependent on the frequency and duration of stimulation and its time course correlated with the dissipation of Δ[K]e when stimulation was discontinued.9. It is suggested that the extracellular K+ accumulation could, under physiological conditions, contribute to the modulation of spinal cord transmission, acting both pre‐and post‐synaptically. Low levels of increased [K]e were associated with facilitation of impulse transmission while higher increases could result in its inhibition.
Orthodromic production of non‐cholinergic slow depolarizing response in the superior cervical ganglion of the rabbit
Authors: Ashe J. H. , Libet B. 
Published: December 2014

1. A late slow depolarization in the rabbit superior cervical ganglion, recorded extracellularly as ‘late late negative’ (l.l.n.) response, can be elicited by suitably repetitive stimulation of cervical sympathetic nerve. The l.l.n. response is not blocked by strong nicotinic, muscarinic or adrenergic antagonists; it appears with latencies in seconds, rise times in minutes, durations of up to 20 min or more, and extracellular amplitudes that can exceed 1 mV when recorded in an air‐gap chamber.2. The l.l.n. component is a graded post‐synaptic response that decreases with a length constant similar to those of the known p.s.p.s (fast e.p.s.p., slow i.p.s.p., and slow e.p.s.p.). This and its other characteristics indicate that the l.l.n. response is neuronally generated and represents a non‐cholinergic late slow depolarization. The term ‘slow slow e.p.s.p.’ is suggested for this response, to replace both ‘slow depolarization’ and ‘late slow e.p.s.p.’.3. The amplitudes, evaluated relative to the compound action potentials, and the durations of l.l.n. responses recorded from intact neurones of rabbit superior cervical ganglion were considerably greater and more consistently producible than the non‐cholinergic slow depolarizations recorded by others from impaled neurones of guinea‐pig inferior mesenteric ganglion.4. The l.l.n. response does not exhibit the special sensitivity to sodium azide previously found for the muscarinic ‘late negative’ or slow e.p.s.p. response.5. The total number of orthodromic volleys is the chief determinant of the amplitude and duration of the l.l.n. response. Increases in pulse frequency, with no change in pulse number, exert only a minor influence on amplitude and duration of the l.l.n. response but can markedly decrease latency and rise time.6. Even very low pulse frequencies (e.g. 1/sec) are almost as effective as higher frequencies if a sufficiently large number of stimulus pulses is applied.7. The features of orthodromic production of the l.l.n., slow slow e.p.s.p. response, as well as the amplitudes and durations of this depolarization, indicate that this non‐cholinergic post‐synaptic response could, like the muscarinic slow e.p.s.p., play a significant role in mediating physiological activities of sympathetic ganglia.
Do identical activity patterns in fast and slow motor axons exert the same influence on the twitch time of cat skeletal muscle?
Authors: Goldring J. M. , Kuno M. , Núñez R. , Weakly J. N. 
Published: December 2014

1. The fast‐twitch flexor digitorum (the lateral head; equivalent to the flexor hallucis longus) and slow‐twitch soleus muscles of the cat were denervated, and the two nerves immediately reunited to one or the other muscle. Contraction times of the dually reinnervated muscle were examined 9 weeks post‐operatively in response to separate stimulation of its own and the foreign nerve. Over a 5 week period before the terminal experiment, a variety of artificial activity patterns was imposed on the two nerves.2. Following the dual‐union operation, the flexor digitorum muscle was preferentially reinnervated by its own nerve. In contrast, the soleus muscle showed no evidence of preferential reinnervation.3. When neural activity was not artificially modified, the dually reinnervated flexor digitorum or soleus muscle showed faster contractions in response to stimulation of the flexor digitorum nerve than to stimulation of the soleus nerve.4. Following a 5 week period in which neural activity was virtually eliminated by cord transection or in which the two nerves were stimulated at the same frequency, the contraction times of the dually reinnervated soleus muscle were the same in response to stimulation of either nerve.5. In contrast, under the experimental conditions described above (cord transection or nerve stimulation), the dually reinnervated flexor digitorum muscle showed a significantly faster contraction in response to stimulation of its own nerve than to stimulation of the soleus nerve.6. It is concluded that, when neural activity is absent or identical in pattern, motoneurones normally innervating the fast‐ or slow‐twitch muscles exert the same influence on contraction times of the soleus muscle.7. The dependence of contraction times of the dually reinnervated flexor digitorum muscle upon the type of the innervating motoneurone may be explained either by selective reinnervation of a particular group of muscle fibres or by different trophic substances emanating from the motoneurones.
The summation of left and right lung volume information in the control of breathing in dogs
Authors: Cross Brenda A. , Guz A. , Jones P. W. 
Published: December 2014

1. Reflex respiratory responses to unilateral and bilateral changes of lung volume have been studied in anaesthetized paralysed, open‐chest dogs.2. The two lungs were separately ventilated by two phrenic‐driven respirators via a specially designed double‐lumen tube. Respiratory motor output was measured from the phrenic motoneurone activity recorded from the C5 root. Expiratory lung volumes were set by the use of expiratory threshold loads (e.t.l.s).3. The reflex changes of expiratory time (te) were used to study the summation of left and right expiratory lung volume information. Changes in the peak amplitude of the phrenic ‘integral’ (Phr) and inspiratory time (ti) were used to assess summation of left and right tidal volume information.4. Summation in the reflex responses to bilateral lung volume changes was estimated by comparing the measured responses to these manoeuvres with the sum of the component unilaterally evoked responses. If simple addition were present, response (measured)/response (predicted) would equal 1.0 Mutual facilitation would give a value higher than this; mutual inhibition, a lower value.5. The responses of te to changes of e.t.l. on the right side were always greater than for changes confined to the left, and in each animal the response of te to bilateral changes of e.t.l. were greater than for either of the unilaterally evoked responses. In six out of eight animals this was shown to be due to simple addition of the responses evoked from the two lungs individually. In the remaining two animals, slight mutual inhibition was seen.6. The tidal volume VT was changed in one or both lungs. During the bilateral VT changes, the volumes were changed simultaneously, either in the same direction (‘same’ VT changes) or in one direction in one lung and in the opposite direction in the other (‘opposite’ VT changes).7. In the bilateral ‘same’ VT changes, mutual facilitation was seen in the response of Phr; Phr (measured)/Phr (predicted) = 1.60 ± 0.42 (
s.d.), n = 8. There was only slight facilitation in the response of ti; ti (measured)/ti (predicted) = 1.18 ± 0.17, n = 8.8. With the bilateral ‘opposite’ VT changes, responses of ti and Phr were markedly and significantly reduced compared to those for the bilateral ‘same’ VT changes. During these manoeuvres significant mutual inhibition was seen in the response of ti, and the predicted responses of Phr in general could not be correlated with the measured response.9. The responses of the phrenic ‘integrals’ were the same in both right and left phrenic nerves.10. Unilateral vagotomy abolished both the responses of Phr and ti to ipsilateral VT changes in the range ± 100% of control VT, and also the response of te to ipsilateral expiratory volume changes.