bluuebunny/crossref_metadata_2025_split huggingface dataset:
On the role of polyamines in bone resorption induced by parathyroid hormone
Authors: LJUNGGREN Ö. , FREDHOLM B. B. , LERNER U. H. 
Published: December 2008

In order to elucidate the possible role of polyamines in the mobilization of mineral from long‐term bone cultures stimulated with parathyroid hormone we have measured the activity of ornithine decarboxylase in osteoblasts, the levels of polyamines in calvarial bone and determined the effect of added polyamines and inhibitors of polyamine biosynthesis on calcium mobilization.Parathyroid hormone (10nmoll‐1) stimulated omithine decarboxylase activity by approximately 50% in both cultured bone cells of osteoblastic phenotype, UMR 106 and in mouse calvarial osteoblast‐like cells. In mouse calvaria the levels of putrescine and spermidine were increased by parathyroid hormone after 24 hours. The levels of spermine were very low and were unchanged by parathyroid hormone.The two polyamine synthesis inhibitors alpha‐difluoromethylornithine (DFMO; 2 mmol 1‐1) and methylglyoxal‐bis‐guanylhydrazone (MGBG; 50 μ mol 1‐l) did not significantly affect the mobilization of 45Ca from parathyroid hormone‐stimulated bones. All three polyamines, putrescine, spermidine and spermine, inhibited the mobilization of 45Ca induced by parathyroid hormone in a dose‐dependent manner. The inhibition induced by putrescine was reversible.In summary, we have shown that parathyroid hormone increases the accumulation of polyamines in bone, but the effect is small. Furthermore, inhibition of polyamine biosynthesis does not reduce parathyroid hormone‐induced mineral mobilization and the addition of polyamines leads to a reduced rather than a stimulated mineral mobilization. Thus, polyamines do not seem to be critically involved in the changes in bone resorption induced by parathyroid hormone. However, polyamines are themselves potent inhibitors of parathyroid hormone effects and an examination of the mechanism underlying this effect may help to define critically important elements in the signal transduction from parathyroid hormone receptor to bone resorption.
Myogenic responsiveness in rat hindquarter vessels during constant‐flow and constantpressure perfusion in vitro; effects of various potassium concentrations and of endothelial nitrous oxide blockade
Authors: JOHNSSON E. , FOLKOW B. , KARLSTRÖM G. 
Published: December 2008

An in vitro constant‐flow, alternatively constant‐pressure, perfusion method for studying microvascular myogenic responsiveness in otherwise intact rat hindquarters was used to explore how three types of influences affect the pressure‐flow induced enhancements of myogenic tone: (1) Changes of potassium concentration over the range 2–50 mmol; (2) Whether myogenic responsiveness, which is fairly weak during these conditions of high shear rates, is enhanced by blockade of endothelial prostacycline and nitrous oxide formation; (3) Whether some of the drawbacks of the constant‐flow technique, like rapid edema formation, is offset by a constant‐pressure variant.The result can be summed up as follows. (1) Myogenic responsiveness is also during in nitro conditions markedly influenced by even modest potassium concentration changes around the physiological resting level, e.g. showing a fourfold difference between potassium concentrations of 2.5–4.5 mmol. It was entirely suppressed above 7–8 mmol potassium concentration but also when potassium concentration values above 20 mmol increasingly depolarize and constrict the resistance vessels. (2) While blockade of prostacycline synthesis was without effect, suppression of endothelial nitrous oxide production could increase myogenic responsiveness up to fourfold, suggesting that shear‐stress dependent release of this agent serves to suppress myogenic activity. These effects were, however, quite variable suggesting that also other endothelial inhibitory influences are involved. (3) The constant‐pressure variant reduces some of the methodological drawbacks, particularly the oedema formation which can be further reduced by increasing perfusate colloid osmotic pressure. However, interferences by the mentioned, partly unknown endothelial mechanisms still tend to suppress myogenic responsiveness to a varying extent, which hampers quantitative analyses particularly of other inhibitory influences.
Segmental heterogeneity of the rat colon in the response to activators of secretion on the cAMP‐, the cGMP‐ and the Ca2+‐pathway
Authors: NOBLES M. , DIENER M. , MESTRES P. , RUMMEL W. 
Published: December 2008

The electrolyte transport was compared in proximal and distal segments of the rat colon under control conditions and after induction of secretion on the CAMP‐, the cGMP‐ and the Ca2+‐pathway.Baseline short‐circuit current was decreased by indometacin and tetrodotoxin in the distal colon, indicating a spontaneous production of neuronally acting prostaglandins. In contrast, baseline short‐circuit current in the proximal colon was decreased only by indometacin, but not by tetrodotoxin. Unidirectional flux measurements revealed that in the distal colon sodium and chloride were absorbed, while the proximal colon secreted chloride.A morphological comparison between the distal and proximal epithelium revealed that the zonulae occludentes and the microvilli were longer in the distal colon. The size of the Golgi apparatus was several times larger in the crypt than in the surface region without differences between proximal and distal colon.Distal segments were more sensitive to an activator of the Ca2+‐pathway, carbachol, or activators of the CAMP‐pathway such as forskolin and a CAMP‐analogue. In contrast, the activation of the cGMP‐pathway by a cGMP‐analogue or by the heat‐stable enterotoxin of E. coli (STa) was more effective in the proximal colon. The results give evidence for a segmental specificity with regard to the intracellular pathways responsible for the activation of secretion.
Flashed pattern‐induced activity in the visual system: I. The short latency evoked response recorded from the cat visual cortex
Authors: SJÖSTRÖM A. , ABRAHAMSSON M. , NORRSELL K. , HELGASON G. , ROOS A. 
Published: December 2008

Previous methods for estimating visual acuity have used the visual evoked response conventionally the late visual evoked response components or the steady‐state potential. The present experiments were undertaken to evaluate the possible use of short latency flashed pattern evoked responses in estimating pattern dependent activity in the cat visual system.Recordings were made from the skull bone and the dura above the primary visual cortex and intracortically.The visual evoked responses to patterned (checks) and non‐patterned light flashes of high intensity and short duration were recorded. The visual evoked response activity recorded from the cortical surface had an onset latency of 14–15 ms. The initial positive‐negative potential sequences of the responses were similar for patterned and non‐patterned stimuli, however a difference was recorded from 35–40 ms after stimulus. The smallest check size which separated a pattern from a non‐pattern VER was in the order of 10 min of arc. The results indicate that the short‐latency cortical VER may be used to estimate visual resolution.
The possible role of prostaglandin D2 in the long‐lasting airways vasodilatation induced by allergen in the sensitized pig
Authors: ALVING K. , MATRAN R. , LUNDBERG J. M. 
Published: December 2008

Allergen‐induced nasal and bronchial vasodilatation and bronchoconstriction were studied in ascaris‐sensitized pigs with and without pretreatment with diclofenac sodium, to evaluate the contribution of prostanoids in these responses. The bronchoconstriction induced by allergen aerosol challenge was enhanced by diclofenac, whereas the duration of the bronchial vasodilatation was reduced from 80 to 30 min, without changing the maximal effect. However, both the maximal effect and the duration of the nasal vasodilatation were reduced upon nasal allergen challenge by 60% (P < 0.01) and from 72 to 16 min (P < 0.05), respectively. Bronchial challenge with the allergen also induced nasal vasodilatation of long duration and this response was highly sensitive to diclofenac pretreatment. I.v. injections of prostaglandins (PG) E1, E2, I2 and D2 revealed that only PGD2 induced vasodilatation of long duration in the airways without major effects on the systemic arterial blood pressure. Nebulization of PGD2 (0.7‐1.4 μmol) into the pig airways also induced marked vasodilatation of long duration (40 min), especially in the nasal circulation. The vasodilatory responses to PGD2 were not changed by systemic pretreatment with capsaicin or diclofenac. Challenge in the airways with platelet‐activating factor (PAF) produced bronchial and vascular responses similar to those seen with the allergen and the vasodilatory responses to PAF were partly sensitive to diclofenac.We propose that a long‐lasting component of the allergen‐induced vasodilatation in the pig airways, especially in the nasal mucosa, may be caused by the release of PGD2, acting independently of sensory nerves. Allergen and PAF aerosol challenge in the lung may also induce the release of a vasodilatory prostaglandin, possibly PGD2, into the systemic circulation, thereby inducing nasal vasodilatation.
The ‘initial burst’ of human primary muscle spindle afferents has at least two components
Authors: EDIN B. B. 
Published: December 2008

Ten muscle spindle primary afferents from the extensor digitorum communis muscle of man were studied with single unit afferent recordings. Responses to slow test stretches with three different pre‐history conditions were assessed to investigate the contribution of rapid stretches to the stretch sensitization phenomenon. In two of the conditions, the slow test ramps were preceded by rapid stretch after which the parent muscle of the receptor was either (a) kept short for 5 seconds or (b) kept long for 3.2 seconds and then returned to the short muscle length for 5 seconds. The third condition (c) consisted of a slow stretch from short to long muscle length followed by a rapid return to the short muscle length, in turn followed by 5 seconds at the short muscle length.Afferent responses were depressed when the muscle had been kept at the long length after the rapid stretches (condition b) and enhanced when the muscle had been kept at the short length (conditions a & c). A prominent ‘initial burst’ was only present in the afferent discharge when the parent muscles of the primary endings had been kept short (condition a). A second, more prolonged burst was present for conditions (a) and (c) but was lacking or inconspicuous when the muscle had been kept long after rapid stretches (condition b). The rapid stretches in the stretch sensitization paradigm appear to be a primary factor not only for the enhanced responses of sensitized primary afferents but also for the depressed responses of desensitized primary afferents.
Acute but not chronic gastric sodium administration regulates vasoactive intestinal peptide metabolism by the liver
Authors: HAWLEY C. M. , DUGGAN K. A. , MacDONALD G. J. , SHELLEY S. 
Published: December 2008

We have shown previously that gastric sodium loading releases vasoactive intestinal peptide from the intestine and in rabbits on a low sodium diet it appears to decrease vasoactive intestinal peptide metabolism by the liver. To determine the contributions of the low sodium diet and the acute sodium load to changes in vasoactive intestinal peptide metabolism, metabolic clearance studies of vasoactive intestinal peptide infused intraportally were performed. These studies were performed in male New Zealand white rabbits equilibrated on normal and low sodium diets before and after an acute gastric sodium load of 1.5 mmol kg‐1. No difference was detectable in metabolic clearance rates between normal and low salt diets, however, decreases in metabolic clearance rates were observed in response to the sodium load (normal diet P < 0.005, low salt P < 0.0005). Secretion rates also decreased following the gastric sodium load (normal P < 0.005, low salt P < 0.05).We conclude that hepatic VIP metabolism is decreased by acute gastric sodium loading but it is not affected by chronic sodium intake.
Effects of the nitric oxide synthase inhibitor NG‐nitro‐L‐arginine on the erectile response to cavernous nerve stimulation in the rabbit
Authors: HOLMQUIST F. , STIEF C. G. , JONAS U. , ANDERSSON K‐E. 
Published: December 2008

Using a rabbit model, the involvement of the L‐arginine/nitric oxide pathway in penile erection was investigated. The mean basal intracavernous pressure was 21 cm H2O. Cavernous nerve stimulation (4–8 V, 20–30 Hz) increased the pressure to approximately 130 cm H2O. This response was highly reproducible and usually associated with full penile erection. The pressure increase could be quantified in terms of: (1) the slope of the initial, ascending part of the pressure increase; (2) ΔP, which was defined as the maximal pressure obtained by the stimulation minus the basal pressure before the stimulation; (3) T90, which was defined as the time to reach 90 per cent of ΔP. Intrapenile administration of the L‐arginine/nitric oxide synthesis inhibitor NG‐nitro‐L‐arginine had no effect on systemic arterial blood pressure. However, NG‐nitro‐L‐arginine (0.22 and 2.19 mg), administered via the same route, abolished the erectile response induced by cavernous nerve stimulation; T90 increased and slope and ΔP decreased significantly. NG‐nitro‐D‐arginine (2.19), on the other hand, had no inhibitory effect. L‐arginine (21.07 mg), given either directly or after NG‐nitro‐L‐arginine had no consistent effect on the functional response to cavernous nerve stimulation.The results suggest that pharmacologically induced effects on intracavernous pressure in the rabbit can be described quantitatively, and that this model may be useful to study the mechanisms controlling penile erection in vivo. The pronounced inhibitory action of NG‐nitro‐L‐arginine demonstrates the important role of the arginine/nitric oxide pathway in mediating relaxation of penile smooth muscles necessary for erection.
Parotid secretion of fluid, amylase and kallikrein during reflex stimulation under normal conditions and after acute administration of autonomic blocking agents in man
Authors: JENSEN J. L. , BRODIN P. , BERG T. , AARS H. 
Published: December 2008

The purpose of this work was to study the effect of graded mechanical and gustatory stimulation on the secretion of the acinar products fluid and amylase and the ductal product kallikrein from the human parotid gland (n= 9). The involvement of parasympathetic and sympathetic nerves in the salivary reflexes was subsequently examined using receptor blocking agents (n= 4).Chewing elevated the secretion of all products as compared to rest (P < 0.013). When increasing the length of the chewing object, secretion of fluid (P < 0.013), but not enzymes, further increased. The shift from mechanical to gustatory stimulation with 0.5% citric acid enhanced significantly the secretion of amylase and kallikrein (P < 0.009), while application of 5.0% citric acid increased the secretion of both acinar products (P < 0.009) more than kallikrein. A differentiated reflex control of salivation both with regard to input and output was thereby indicated.The muscarinic‐cholinergic antagonist oxyphencyclimin reduced median fluid secretion between 54 and 76% depending on the stimuli. During citric acid stimulation, but not during chewing, fluid secretion was reduced about 40% by the beta1‐adrenergic antagonist metoprolol, and about 20% by the alpha1‐adrenergic antagonist prazosin. Median amylase secretion was reduced 30% during chewing and 75% during gustatory stimulation by metoprolol.It was concluded that the masticatory‐salivary reflex mainly activated parasympathetic pathways producing saliva of low protein content. The gustatory‐salivary reflex activated sympathetic pathways to a higher extent, resulting in saliva with higher protein content. Using this reflex model, kallikrein secretion seemed not to be mediated by any of the tested receptors.
Somatostatin inhibition of phospholipase G activity in isolated rat pancreatic islets
Authors: MALM D. , GIÆVER A. , VONEN B. , BURHOL P. G. , FLORHOLMEN J. 
Published: December 2008

We have assessed the effect of somatostatin on the phospholipase C activity in isolated rat pancreatic islets. The phospholipase C activity was measured as the generation of inositol 1,4,5‐trisphosphate and its metabolite inositol 1,3,4‐trisphosphate from the hydrolysis of polyphosphoinositides. Inositol phosphates were measured using anion‐exchange fast protein liquid chromatography analysis of extracts from islets prelabelled with myo‐[3H]inositol.Somatostatin (1–1000 nmol l‐1) significantly inhibited the glucose‐induced (12 mmol l‐1) phospholipase C activity in a concentration‐dependent manner. The Ca2+ channel blocker verapamil (25 μmol l‐1) also inhibited the glucose‐induced (12 mmol l‐1) phospholipase C, whereas the combination of somatostatin and verapamil did not induce any additional inhibition. At 3.3 mmol l‐1 glucose, the hypoglycaemic sulphonylurea, tolbutamide (1 mmol l‐1), increased the phospholipase C activity. This effect was reversed by somatostatin (100 nmol l‐1). Tolbutamide did not further increase the glucose‐induced (12 mmol l‐1) phospholipase C activity.However, the somatostatin inhibition of glucose‐induced (12 mmol l‐1) phospholipase C was reversed by tolbutamide. The activator of adenylyl cyclase, forskolin (20 μmol l‐1), did not exert any effect on the PLC‐inhibition of somatostatin, whereas forskolin alone inhibited the phospholipase C activation at 12 mmol l‐1 glucose.Our study demonstrates that somatostatin inhibits the hydrolysis of polyphosphoinositides in pancreatic islets, apparently via a mechanism dependent on Ca2+ and not on cAMP.
Effects of detraining following short term resistance training on eccentric and concentric muscle strength
Authors: COLLIANDER E. B. , TESCH P. A. 
Published: December 2008

Healthy males were examined before and after 12 weeks of accommodated resistance training (three week‐1) and after 12 weeks of detraining. Training consisted of four to five sets of six coupled maximum voluntary bilateral concentric and eccentric (Grp ECCON; n= 10) or 12 concentric (Grp CON; n= 8) quadriceps muscle actions. Concentric and eccentric peak torque at various constant angular velocities and three repetition maximum half‐squat and vertical jump height were measured.Grp ECCON showed greater (P < 0.05) overall increase in peak torque after training and detraining than Grp CON. Thus, concentric peak torque (0.52 rad s‐1) increased more (P < 0.05) over the experimental period in Grp ECCON and increases in eccentric peak torque were preserved in Grp ECCON only. Increases in peak torque in response to training were greater (P < 0.05) at 0.52 than at 2.62 rad s‐1. Alterations in the torque‐velocity patterns induced by training remained after detraining in Grp ECCON but not in Grp CON. The retained increases (P < 0.05) in half‐squat were 12 and 18% in Grps CON and ECCON, respectively. Neither group showed increased vertical jump height after detraining.This study showed greater preservation of concentric and eccentric peak torque after detraining following coupled concentric and eccentric than concentric resistance training. Only the former regime induced a change in the shape of torque‐velocity curves that was manifest after detraining. These results suggest that the performance of eccentric muscle actions is critical to optimize increases in muscular strength in response to heavy resistance training, because it probably induce greater and more long‐lived neural adaptations than the performance of concentric actions.
Na+‐H+ exchange is not important for pancreatic HCO‐3 secretion in the pig
Authors: VEEL T. , VILLANGER O. , HOLTHE M. R. , JR. E. J. CRAGOE , RÆDER M. G. 
Published: December 2008

Veel, T., Villanger, O., Holthe, M.R., Cragoe jr., E.J. & Reder, M.G. 1992. Na+‐H exchange is not important for pancreatic HCO‐3 secretion in the pig. Acta Physiol Scand144, 239–246. Received 13 September 1991, accepted 14 November 1991. ISSN 0001–6772. University of Oslo, Institute for Experimental Medical Research and Surgical Department, Ullevaal Hospital, Oslo, Norway.Pancreatic inter‐ and intralobular duct cells extrude H+‐ions to interstitial fluid when they secrete HCO‐3 to pancreatic juice. This study assesses the potential importance of Na+‐H+‐ion exchange for H+‐ion extrusion and secretion of HCO‐3 using the Na+‐H+ exchange blockers amiloride and hexamethylene‐amiloride. Intracellular pH (pH,) in inter‐ and intralobular pancreatic duct epithelium was measured using BCECF fluorescence. H+‐ion efflux was measured using a NH4Cl prepulse, acid‐loading technique. In HCO‐3‐free media, pH1 recovery following acid loading was blocked by amiloride (10‐4 m) and hexamethylene‐amiloride (10‐6 m), demonstrating amiloride‐and hexamethylene‐amiloride‐sensitive Na+‐H+ exchange. However, 5 × 10‐6 M hexamethylene‐amiloride did not reduce secretin‐dependent pancreatic HCO, secretion in vivo. Maximal H+‐efflux through Na+‐H+ exchange was 1.5 ± 0.2μmol min‐1 ml cell volume‐l, i.e. less than 1 % of estimated net H+‐ion efflux during HCO‐3 secretion. Conclusion: amiloride‐ and hexamethylene amiloride sensitive Na+‐H+ exchange is not important for secretin‐dependent pancreatic HCO‐3 secretion in the pig. Other mechanisms for H+ extrusion dominate.
Myogenic vasoconstriction in the rat kidney elicited by reducing perirenal pressure
Authors: CLAUSEN G. , ØIEN A. H. , AUKLAND K. 
Published: December 2008

Clausen, G., Øien, A. H. & Aukland, K. 1992. Myogenic vasoconstriction in the rat kidney elicited by reducing perirenal pressure. Acta Physiol Scand 144 277–290. Received 17 April 1991, accepted 2 September 1991. ISSN 0001–6772. Departments of Physiology and Mathematics, University of Bergen, Norway.Autoregulation of renal blood flow is generally believed to result from tubuloglomerular feedback and/or a vascular myogenic mechanism, but there is no consensus on the relative importance of these mechanisms. We designed an experiment in which tubuloglomerular feedback would tend to oppose a myogenic response: the denervated kidney in sits was enclosed in an airtight chamber and exposed to a 35 mmHg subatmospheric pressure for 1 to 10 minutes. Renal blood flow recorded by an electromagnetic flowmeter fell by 33 % in the course of a few seconds. Renal venous concentration of inulin showed no consistent change, indicating similar reduction in glomerular filtration rate. Since urine flow also fell, it is likely that the tubular flow rate was reduced. The kidney volume expanded by 10–20%, and subcapsular interstitial fluid pressure was reduced from 6.8 to — 8.6 mmHg. Arterial pressure remained unchanged, while renal venous pressure inside the chamber fell from 9.4 to 5.8 mmHg. Normalization of perirenal pressure gave rapid normalization of all parameters. Elevation of ureteral pressure attenuated or even prevented the renal blood flow reduction. Renal decapsulation or sympathetic blockade by phentolamine, or infusion of furosemide or 0.9% NaCl to inactivate tubuloglomerular feedback, did not prevent the renal blood flow reduction. We interpret the results to indicate that myogenic vasoconstriction greatly overpowered TGF and even surpassed the constriction predicted by a mathematical model based on maintenance of the preglomerular wall tension as estimated from transmural pressure.