bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effects of external cations and ouabain on the intracellular sodium activity of sheep heart Purkinje fibres
Authors: Ellis David 
Published: December 2014

1. The intracellular Na activity of sheep heart Purkinje fibres has been measured using recessed‐tip Na+‐sensitive glass micro‐electrodes.2. The internal Na activity was 7·2 ± 2·0 m
M (mean ±
S.D., n = 32) at the normal external Na concentration, [Na]o, in these experiments of 140 m
M (equivalent to an external Na activity of 105 m
M). The equilibrium potential for Na across the fibre membrane was therefore approximately + 70 mV.3. When the [K]o was altered the internal Na activity changed, reaching a new level within about 20 min. Increasing the [K]o from 4 to 25 m
M decreased the internal Na by approximately 30%, while decreasing the [K]o from 4 to 1 m
M increased internal Na by 20%.4. The removal of external K produced an easily reversible increase in the internal Na with an initial rate equivalent to a concentration change of 0·24 ± 0·07 m‐mole/min (mean ±
S.D., n = 8).5. Ouabain produced increases in the internal Na activity that were only very slowly reversible. The threshold concentration for producing an increase was approximately 10−7
M.6. When [Na]o was reduced the internal Na activity fell rapidly with a single exponential time course (time constant 3·3 ± 0·8 min, mean ±
S.D., n = 16) to a new, relatively stable level. The recovery of internal Na on return to the normal [Na]o did not have a simple time course. It was normally complete within 10‐30 min.7. The relationship of the stabilized level of the internal Na activity to the [Na]o was approximately linear over the range 140‐14 m
M‐[Na]o. When [Na]o was reduced from 140 to 14 m
M the internal Na activity fell by 72 ± 5% (mean ±
S.D., n = 21).8. When the [Na]o was reduced, the decrease in the internal Na activity was partially inhibited by Mn or by removal external Ca.9. When the [Ca]o was altered over the range 0·2‐16 m
M the internal Na activity was reduced by approximately 50% for a tenfold increase in the [Ca]o.10. The relationship between internal Na and contractility is discussed.
Compensatory renal hypertrophy in hypophysectomized rats
Authors: Dicker S. E. , Greenbaum A. L. , Morris Christine A. 
Published: December 2014

1. After hypophysectomy, both body and kidney weights fall, but at different rates. The rate at which the kidney decreases in weight is faster than that of the whole body.2. Seven days after unilateral nephrectomy, the dry weight of the remaining kidney of hypophysectomized rats, with the exception of rats which had been hypophysectomized for 2 days only, was always heavier than the kidney of control hypophysectomized rats of similar body weight.3. The difference between the dry weight of kidneys of unilaterally nephrectomized hypophysectomized and control hypophysectomized rats increased from 15% in early hypophysectomized (9 days) to about 35% in late hypophysectomized animals (23 days).4. The implantation of renal cortical cells from 2 day hypophysectomized rats into unilaterally nephrectomized control litter‐mates inhibited compensatory renal hypertrophy in the latter. When a similar operation was made using kidney cells from animals which had been hypophysectomized for 23 days, there was no significant inhibition of compensatory renal hypertrophy.5. The renal contents of adenosine‐3′,5′‐monophosphate (cyclic AMP) and of guanosine‐3′,5′‐monophosphate (cyclic GMP) in rats hypophysectomized for 2 days were of the same order as those in normal rats, but were markedly lower in rats hypophysectomized for 23 days.6. In contrast to what had been observed in normal rats, in hypophysectomized (2 or 23 days) rats, unilateral nephrectomy did not affect significantly the levels of cyclic nucleotides in the remaining kidney.7. Cross‐circulating anephric normal rats with 2 day hypophysectomized animals resulted in an increase of cyclic GMP content in their kidneys. The cross‐circulation between anephric normal rats and 23 days hypophysectomized rats had no effect on the level of renal cyclic GMP of the latter.8. When rats hypophysectomized for either 2 or 23 days and which had been nephrectomized were cross‐circulated with normal rats, there were no changes in the content of cyclic GMP in the kidneys of the latter.
Diencephalic efflux of calcium ions in the monkey during exercise, thermal stress and feeding
Authors: Gisolfi C. V. , Mora F. , Myers R. D. 
Published: December 2014

1. The diencephalon of the unanaesthetized macaque monkey was radio‐labelled with calcium by a microinjection of 6‐8 μC 45Ca2+ into the third cerebral ventricle through a permanently implanted cannula. Successive 5 min push—pull perfusions of the mid‐line hypothalamic region with an artificial
C.S.F. were carried out at a rate of 28 μl./min every 20 min. A washout curve of declining 45Ca2+ radioactivity was thus generated.2. When the monkey exercised strenuously on a special ‘rowing machine’ to obtain highly palatable banana pellets, its body temperature rose sharply. As the monkey exercised, during a sequence of push—pull perfusions, the concurrent efflux of 45Ca2+ ions increased markedly in the corresponding samples of diencephalic perfusate. This enhanced activity of calcium ions continued throughout a 30 min work period and persisted as long as the monkey's temperature was elevated in the interval immediately following exercise.3. Exposure of the monkey's trunk, between neck and thigh to cold air of 5 °C likewise augmented the amount of 45Ca2+ ions in the diencephalic push—pull perfusates; however, a similar exposure to air warmed to 35 °C failed to alter the pattern of 45Ca2+ efflux from the animal's diencephalon. If a fasted monkey consumed only the banana pellets but was not exercised, the level of 45Ca2+ in the perfusate also increased transiently, just at the onset of feeding.4. We conclude that a local change in calcium transport, binding or other cellular activity of the cation within the diencephalon could play an important role in the central mechanism underlying the set‐point rise in a primate's temperature which accompanies vigorous exercise. Further, the results support the idea that this cation functions in the diencephalic control of metabolic heat production as well as in the overall processes of energy metabolism, particularly in relation to feeding.
Octanol reduces end‐plate channel lifetime
Authors: Gage Peter W. , McBurney Robert N. , Van Helden Dirk 
Published: December 2014

1. Post‐synaptic effects of n‐octanol at concentrations of 0·1‐1 m
M were examined in toad sartorius muscles by use of extracellular and voltage‐clamp techniques.2. Octanol depressed the amplitude and duration of miniature end‐plate currents and hence depressed neuromuscular transmission.3. The decay of miniature end‐plate currents remained exponential in octanol solutions even when the time constant of decay (τD) was decreased by 80‐90%.4. The lifetime of end‐plate channels, obtained by analysis of acetylcholine noise, was also decreased by octanol. The average lifetime measured from noise spectra agreed reasonably well with the time constant of decay of miniature end‐plate currents, both in control solution and in octanol solutions.5. Octanol caused a reduction in the conductance of end‐plate channels. Single channel conductance was on average about 25 pS in control solution and 20 pS in octanol.6. In most cells the normal voltage sensitivity of the decay of miniature end‐plate currents was retained in octanol solutions. The lifetime of end‐plate channels measured from acetylcholine noise also remained voltage‐sensitive in octanol solutions. In some experiments in which channel lifetime was exceptionally reduced the voltage sensitivity was less than normal.7. In octanol solutions, τD was still very sensitive to temperature changes in most cells although in some the temperature sensitivity of τD was clearly reduced. Changes in τD with temperature could generally be fitted by the Arrhenius equation suggesting that a single step reaction controlled the decay of currents both in control and in octanol solutions. In some cells in which τD became less than 0·3 ms, the relationship between τD and temperature became inconsistent with the Arrhenius equation.8. As the decay of end‐plate currents in octanol solutions remains exponential, and the voltage and temperature sensitivity can be unchanged even when τD is significantly reduced, it seems likely that octanol decreases τD by increasing the rate of the reaction which normally controls the lifetime of end‐plate channels.
Calcium‐dependent repolarization in Paramecium
Authors: Brehm Paul , Dunlap Kathleen , Eckert Roger 
Published: December 2014

1. Intracellular injection, recording and current‐passing methods were used to investigate the role of intracellular Ca in the modulation of electrical behaviour in the ciliate Paramecium caudatum.2. Injection of EGTA converted graded regenerative responses ascribed to Ca inward current to all‐or‐none action potentials. The EGTA injection also caused a discontinuity in the steady state I—V relations to outward current, but had little effect on hyperpolarizing current—voltage responses.3. The overshoot of the all‐or‐none spike produced by the EGTA‐injected cell followed an approximate 29 mV increase for a tenfold increase in external Ca concentration and was independent of changes in external K and Na concentrations.4. The EGTA‐induced all‐or‐none action potential tended to produce plateaus that could last up to 20 sec. During the plateau the membrane slowly repolarized to a critical potential, upon which repolarization occurred precipitously.5. Injection of 10−6
M‐free Ca2+ as a Ca‐EGTA buffer hyperpolarized the membrane and decreased the potential shifts to inward current pulses. These responses are consistent with an increase in K conductance.6. During EGTA plateaus reversed beating of the cilia indicated a rise in intracellular Ca, and thus an inability of the EGTA to complex the Ca as rapidly as it entered the cilia. Reversal of the motile apparatus thus appears to be activated at lower concentrations of intracellular Ca than are required to activate the inferred Ca‐dependent K system.7. In uninjected cells removal of the cilia, which results in a loss of the voltage‐activated Ca channels (Dunlap, 1977), or addition of extracellular Ba both tended to linearize the steady state I—V relations.8. Injections of Cs and TEA tended to linearize the steady state I—V relations, but did not result in either a conversion to an all‐or‐none spike or a discontinuity in the depolarizing steady‐state I—V relations.9. It is concluded that in Paramecium a Ca‐activated K conductance short‐circuits the inward current of the regenerative Ca response, preventing all‐or‐none behaviour. The occurrence of plateau spikes following EGTA injection indicates that the Ca conductance inactivates very slowly in face of a maintained depolarization. Such slow Ca‐inactivation is consistent with the slow relaxation of Ca‐dependent ciliary reversal that occurs during maintained depolarization.10. The possibility is discussed that injection of EGTA may also enhance the Ca conductance.
Uptake of [14C]urea by the in vivo choroid plexus—cerebrospinal fluid—brain system: identification of sites of molecular sieving
Authors: Johanson Conrad E. , Woodbury Dixon M. 
Published: December 2014

1. The time course of the uptake of [14C]urea by the lateral ventricular choroid plexus of the adult rat in vivo was analysed to delineate further the permeability characteristics of the epithelial membrane of this secretory tissue.2. Eight hours after
I.P. injection, [14C]urea attained a steady‐state distribution in 78% of the tissue water of lateral ventricular choroid plexus; similarly, approximately 8 hr was required for radiourea to reach a steady‐state concentration in both the cerebral cortex and cerebrospinal fluid (c.s.f.).3. Results obtained for compartment analysis were used to calculate the concentration of [14C]urea in the epithelium of the lateral ventricular plexus during the approach to and at steady‐state distribution. Even after 1 hr of distribution, the [14C]urea concentration in choroid cell water was less than 15% of that in plasma water.4. Although the concentration of radiourea in choroid cell water continually increased after 3 hr, it remained in equilibrium with the concentration of [14C]urea in c.s.f. water. At the steady state (i.e., 8 hr), the distribution of [14C]urea between the water of plasma and that of the choroidal epithelium was considerably away from equilibrium (i.e., by 25‐30%).5. An analysis of the concentration gradients for [14C]urea across both the apical (c.s.f.‐facing) and basolateral (plasma‐facing) membranes of the epithelium of the lateral ventricular plexus suggests that the movement of urea is hindered to a greater extent by the basolateral membrane than by the apical membrane.6. Only a single half‐time component (1·3 hr) can be resolved from analysis of the curve describing the time course of uptake of radiourea by the choroid epithelial cell compartment.7. The concentration gradient data suggest that urea penetrates from blood to c.s.f. via the choroid plexus by a transcellular pathway; however, it is not possible to rule out a paracellular pathway for urea movement.8. At the steady state, radiourea distributes into 88% of the water of cerebral cortex. This observation, together with the finding of a steady‐state concentration gradient for [14C]urea from cortical tissue to c.s.f., constitutes evidence that urea movement is hindered at the blood‐brain barrier as well as at the blood—c.s.f. barrier.
A bilateral antidiuresis to renal artery infusion of prostaglandin E1 in dogs treated with phenylbutazone
Authors: Hall W. J. , Hensey O. J. , O'Neill P. , Sheehan J. D. 
Published: December 2014

1. In acute experiments, high levels of endogenous prostaglandins, provoked by operative stress, could obscure or alter the actions of infused prostaglandins on the kidney. For this reason we decided to compare the effects of infusing prostaglandin E1 into the renal artery of the dog before and after the administration of phenylbutazone, a prostaglandin synthetase inhibitor.2. Infusion of prostaglandin E1 into the left renal artery of the pre‐phenylbutazone treated dog undergoing a mannitol diuresis increased renal plasma flow, glomerular filtration rate and the excretion of salt and water. The findings are in general agreement with those reported by others.3. Following phenylbutazone administration the vascular and saluretic actions of prostaglandin E1 were unchanged but a reduced diuretic effect was observed. The response to a low dose of prostaglandin E1 (0·05 μg/min) was reduced from 1·46 ± 0·15 to 0·96 ± 0·16 ml./min (P < 0·001) and the response to a high dose (0·5 μg/min) from 1·82 ± 0·19 to 0·99 ± 0·31 ml./min (P < 0·002).4. A significantly less dilute urine was excreted during prostaglandin infusion in the dog after phenylbutazone treatment than before. The reduction in the diuretic response was of the same order as the decrease in the free water clearance response, while the increase in osmolar clearance was unchanged.5. In water‐loaded dogs treated with phenylbutazone, infusion of prostaglandin E1 into the left renal artery had a biphasic effect on urine output from the left kidney. An initial diuretic response to a low dose of prostaglandin E1 disappeared with the infusion of higher doses, and antidiuresis developed in the immediate post‐infusion period.6. As prostaglandin was infused into the left kidney progressive antidiuresis was seen in the non‐infused right kidney.7. It is concluded that endogenous prostaglandins do not obscure or alter the vascular and saluretic actions of intrarenal prostaglandin E1. The findings question the proposed link between the vascular and saluretic actions of this compound.8. It is suggested that the reduced diuretic effect of prostaglandin E1 in series no. 1, and the antidiuresis in the water‐loaded dogs, are caused by the release of endogenous ADH. It is further suggested that phenylbutazone unmasks this release by removing the endogenous prostaglandins. If these deductions are correct, the findings support the anti‐ADH role assigned to endogenous prostaglandins by Anderson, Berl, McDonald & Schrier (1975).
Effect of luminal pH on acid secretion from Heidenhain pouches evoked by topical and parenteral stimulants
Authors: Carter David C. , Grossman Morton I. 
Published: December 2014

1. An apparatus for intragastric titration has been devised and its validity tested. Both when attached to a beaker simulating a pouch and when attached to a pouch whose secretion was suppressed by infusing cimetidine, the apparatus accurately measured added acid when the endpoint setting was between pH 3·0 and 9·0. At pH 2·0 and 1·0 with liver extract and at pH 1·0 with saline, the amount of acid added was markedly underestimated.2. In dogs with vagally denervated pouches, during stimulation by
I.V. infusion of histamine or pentagastrin, the rate of acid secretion as measured by intrapouch titration was uninfluenced by changes in luminal pH between 2·0 and 9·0. The apparent decrease in acid secretion at pH 1·0 could be shown to be due entirely to artifact in that no change in acid secretion was found when the gain in mass of acid was simultaneously measured by using a non‐absorbable dilution indicator to measure volume gain and titration of samples to pH 7·0 to measure acid concentration.3. During stimulation of acid secretion by solutions of liver extract or of
L‐histidine instilled into the pouch, the rate of acid secretion was found to increase markedly as pH was increased from 3·0 to 9·0 thus confirming our earlier findings.4. We conclude that while stimulation of acid secretion by topical stimulants is highly dependent on luminal pH, secretion increasing as pH increases, stimulation by parenteral agents such as histamine and pentagastrin is not influenced by luminal pH in the range from pH 1·0 to 9·0.
The effect of pituitary‐adrenal function in the modulation of pain sensitivity in the rat
Authors: Heybach John P. , Vernikos-Danellis Joan 
Published: December 2014

1. The relationship between adrenalcortical hormones, adrenocorticotrophic hormone (ACTH), and pain sensitivity was investigated in the rat. Pain sensitivity was assessed by measuring paw‐lick and jump latencies in response to being placed on a grid at 55 °C.2. Bilateral adrenalectomy increased the sensitivity to pain, but adrenal demedullation had no effect.3. Pain sensitivity was inversely related to the circadian changes in circulating corticosterone and was greater at 7 a.m. than at 7 p.m. However, the same variation in pain sensitivity existed if the adrenals were removed, suggesting that the increase in pain sensitivity after adrenalectomy was not related directly to the levels of corticosteriods.4. The time course of the increase in pain sensitivity after adrenalectomy paralleled that of the changes in circulating ACTH. Adrenalectomy markedly increased pain sensitivity at 9 and 18 days following surgery when circulating ACTH levels were markedly elevated and corticosterone was absent, but not at 3 days following adrenalectomy when ACTH levels were lower and corticosterone was absent.5. Hypophysectomy decreased the sensitivity to pain.6. The results indicate that ACTH can alter pain sensitivity and that the effect of corticosteroids on the sensitivity to pain is an indirect one by virtue of their negative feed‐back action on the hypothalamic‐pituitary system.
Topography of cutaneous mechanoreceptive neurones in dorsal root ganglia of skin‐grafted frogs
Authors: Baker R. E. , Corner M. A. , Veltman W. A. M. 
Published: December 2014

1. Topographical distribution patterns of dorsal root ganglion (d.r.g.) cutaneous neurones providing innervation to various body surfaces were examined in doublypithed Discoglossus pictus frogs.2. Using electrophysiological methods, sensory neurones innervating back skin were observed to predominate on the dorsal ganglionic surfaces, while belly skin neurones were most prevalent in the caudal half of the d.r.g. ventral surfaces. Flank neurones clustered in the medial half of d.r.g. ventral surfaces.3. Cutaneous neuronal distribution patterns within the d.r.g. of 180° skin grafted animals were indistinguishable from those observed in control frogs.4. Sensory neurone distribution patterns were found to be altered in all animals with single skin type grafts. Projection patterns were always heaviest towards the autograft, which was on the opposite body surface (i.e. dorsally located d.r.g. sensory neurones projected to back skin on the frog's ventrum, while ventrally located neurones projected to belly skin on the frog's dorsum).5. The results are discussed in the light of several selective outgrowth mechanisms which have been proposed as a possible underlying basis for the development of misdirected wiping reflex behaviour in skin grafted anurans. The findings indicate that none of the proposed selective growth mechanisms can account adequately for the development of misdirected wiping reflexes, at least in the species studied.6. It is suggested that selective cell replacement, based upon competition among prespecified cutaneous neurones, might best account for the development of normal and misdirected wiping reflexes in frogs.
Mobilization of colonic kallikrein following pelvic nerve stimulation in the atropinized cat
Authors: Fasth S. , Hulten L. , Johnson B. Julienne , Nordgren S. , Zeitlin I. J. 
Published: December 2014

1. Pelvic nerve stimulation (p.n.s.) in cats induces atropine‐resistant colonic vasodilatation and colonic contraction. The effects of this on cat colon are mimicked by synthetic bradykinin infusions. The present study examines the effect of p.n.s. on the activation of kallikrein, the kinin‐forming enzyme present in colonic tissue and its effects on the plasma kinin system in the atropinized cat.2. Mean level (±
S.D.) of mucosal kallikrein was found to be about 37 times higher in unstimulated colonic mucosa (300 ± 100 ng bradykinin equivalents min−1g−1) than in the underlying muscle (8·2 ± 6·3 ng bradykinin equiv min−1g−1).3. After a p.n.s. of 5 min, mean kallikrein level in colonic muscle was 7·3 ± 3·5 ng bradykinin equiv min−1g−1, which was not significantly different from the control muscle kallikrein. However, there was an 86% fall in mucosal kallikrein to 41·3 ± 34·7 ng bradykinin equiv min−1g−1 after 5 min p.n.s., indicating a rapid activation and secretion of mucosal kallikrein.4. Secretion of mucosal kallikrein was paralleled by specific depletion of plasma kininogen, the precursor of active kinin in blood draining the colon. The mean plasma kininogen level fell to 79 and 68% of the prestimulated value (3·1 ± 1·1
S.D. μg bradykinin equiv per ml. plasma) after 5 and 10 min p.n.s. respectively. Total plasma protein and haematocrit remained unaltered excluding non‐specific changes due to protein extravasation or haemodilution and indicating utilization of the plasma kinin precursor.5. Following 2 hr p.n.s., raised levels of kallikrein were detected in both colonic muscle (28 ± 2·0 bradykinin equiv min−1g−1) and mucosa 434 ± 118 ng bradykinin equiv min−1g−1). Preliminary studies using a kallikrein inhibitor indicated that the increased kallikrein levels originated from plasma.6. Direct stimulation of the parasympathetic pelvic nerve in the atropinized cat thus produced activation of the plasma kinin system in the colon and formation of free kinins may be responsible for the mucosal vasodilatation and strong motor contraction which is not blocked by large doses of atropine. The observation that prolonged stimulation causes extravasation of plasma kallikrein, a potential inflammatory mediator, into the tissues may be of clinical significance.