bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of age and streptozotocin‐induced diabetes on contents and effects of substance P and vasoactive intestinal polypeptide in the lower urinary tract of the rat
Authors: ANDERSSON P. O. , FAHRENKRUG J. , MALMGREN A. , UVELIUS B. 
Published: December 2008

Andersson, P. O., Fahrenkrug, J., Malmgren, A. & Uvelius, B. 1992. Effects of age and streptozotocin‐induced diabetes on contents and effects of substance P and vasoactive intestinal polypeptide in the lower urinary tract of the rat. Acta Physiol Scand144, 361–368. Received 29 January 1991, accepted 11 October 1991. ISSN 0001–6772. Departments of Physiology, Clinical Pharmacology and Urology, University of Lund, Lund, Sweden and Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, Denmark.The urinary bladder and urethral content of substance P and vasoactive intestinal polypeptide and the in vitro effects of the peptides on the bladder were studied at 6 weeks and 6 months of streptozotocin‐induced diabetes in the rat. The results were compared with those obtained in age‐matched control animals. Both short‐term and long‐term streptozotocin treatment induced a clearcut increase in bladder weight. Bladder substance P content was increased in both groups of diabetic animals but substance P concentration was similar in control and diabetic animals. Vasoactive intestinal polypeptide content was slightly higher in diabetic animals than in controls but vasoactive intestinal polypeptide concentration was significantly lower in the bladders from both short‐term and long‐term diabetic animals. The bladder contractile response to substance P was similar in all groups of animals and vasoactive intestinal polypeptide was found to be devoid of contractile or relaxatory effects in the rat bladder. No change in urethral weight was seen with diabetes. There were no clear‐cut changes in the urethral contents or concentrations of substance P and vasoactive intestinal polypeptide.The study also enabled comparisons between younger (3 months) and older (9 months) rats. This comparison showed a decrease in the concentrations and contents of substance P and vasoactive intestinal polypeptide between young and older rats. The changes were seen in both the bladder and the urethra and were similar in diabetic and normal animals.
Production of monoclonal antibodies against gastric parietal cell antigens
Authors: CABERO J. L. , SASAKI T. , SONG Y.‐H. , HOLMDAHL R. , MÅRDH S. 
Published: December 2008

Cabero, J. L., Sasaki, T., Song, Y.‐H., Holmdahl, R. & Mårdh, S. 1992. Production of monoclonal antibodies against gastric parietal cell antigens. Acta Physiol Scand144, 369–378. Received 19 July 1991, accepted 11 October 1991. ISSN 0001–6772. Department of Medical and Physiological Chemistry, Biomedical Centre, Uppsala University, Sweden.Two mice DBA/1 were each immunized with a single injection of one million enriched parietal cells in the hind foot pads. Monoclonal antibodies to be used as research tools in studies on regulatory mechanisms in gastric parietal cells were obtained after fusion of mouse myeloma cells (SP2) with cells from the popliteal lymph nodes of the mice. Twelve hybridomas produced antibodies reactive with structures only present in parietal cells as assessed by immunohistochemistry of oxyntic rnucosa sections. Three hybridomas were subcloned and the antibodies produced by them, designated as PC4, PC8, and PC117, were characterized. In an enzyme‐linked immunosorbent assay, all antibodies reacted with H, K‐ATPase‐containing vesicles. The antibody PC8 recognized a 94 kDa protein after immunoblotting of H, K‐ATPase‐containing vesicles and all antibodies precipitated a 94 kDa protein from [125I]H, K‐ATPase‐containing vesicles. The antibodies PC4 and PC117 recognized extracellular structures with a polarized distribution in viable, purified parietal cells. The results suggest that the structure recognized by all three antibodies is the a‐subunit of the H, K‐ATPase. The antibodies produced by another hybridoma, PC43, recognized a structure present in parietal and surface epithelial cells of the oxyntic mucosa. In an enzyme‐linked immunosorbent assay, they reacted with a high‐activity carbonic anhydrase which had been affinity‐purified from pig oxyntic mucosa and they recognized a 30 kDa protein after immunoblotting. Thus, monoclonal antibodies against both intracellular and extracellular parietal cell structures were obtained after immunization with a small number of parietal cells.
Observations on intra‐abdominal pressure and patterns of abdominal intra‐muscular activity in man
Authors: CRESSWELL A. G. , GRUNDSTRÖM H. , THORSTENSSON A. 
Published: December 2008

Cresswell, A. G., Grundström, H. & Thorstensson, A. 1992. Observations on intra‐abdominal pressure and patterns of abdominal intra‐muscular activity in man.Actri Physiol Scand144, 409418. Received 16 July 1991, accepted 11 October 1991. ISSN 0001–6772. Department of Physiology III, Karolinska Institute, and Department of Radiology, Danderyd Hospital, Stockholm, Sweden.The aim was to investigate possible relationships between activities of the individual muscles of the ventrolateral abdominal wall and the development of pressure within the abdominal cavity. Intra‐muscular activity was recorded bilaterally from transversus abdominis, obliquus internus, obliquus externus and rectus abdominis with fine‐wire electrodes guided into place using real‐time ultrasound. Intra‐abdominal pressure was measured intragastrically using a micro tip pressure transducer. Six males were studied during loading and movement tasks with varied levels of intra‐abdominal pressure. During both maximal voluntary isometric trunk flexion and extension, transversus abdominis activity and intra‐abdominal pressure remained constant, while all other abdominal muscles showed a marked reduction during extension. When maximal isometric trunk flexor or extensor torques were imposed upon a maximal Valsalva manoeuvre, transversus abdominis activity and intra‐abdominal pressure remained comparable within and across conditions, whereas obliquus internus, obliquus externus and rectus abdominis activities either markedly increased (flexion) or decreased (extension). Trunk twisting movements showed reciprocal patterns of activity between the left and right sides of transversus abdominis, indicating an ability for torque development. During trunk flexion‐extension, transversus abdominis showed less distinguished changes of activity possibly relating to a general stabilizing function. In varied pulsed Valsalva manoeuvres, changes in peak intra‐abdominal pressure were correlated with mean amplitude electromyograms of all abdominal muscles, excluding rectus abdominis. It is concluded that the coordinative patterns shown between the muscles of the ventrolateral abdominal wall are task specific based upon demands of movement, torque and stabilization. It appears that transversus ahdominis is the abdominal muscle whose activity is most consistently related to changes in intra‐abdominal pressure.
The effects of cortisol on insulin sensitivity in muscle
Authors: HOLMÄNG A. , BJÖRNTORP P. 
Published: December 2008

Holmäng, A. & Björntorp, P. 1992. The effects of cortisol on insulin sensitivity in muscle. Acta Physiol Scand144, 425–431. Received 12 September 1991, accepted 20 November 1991. ISSN 0001–6722. Department of Medicine I and The Wallenberg Laboratory, Sahlgren's Hospital, University of C., teborg, SwedenThe effects of cortisol on insulin sensitivity were examined in rats with the euglycaemic, hyperinsulinaemic clamp technique. Uptake of 2–deoxyglucose and incorporation of glucose into glycogen was followed in the white gastrocnemius, extensor digitorum longus, red gastrocnemius and soleus muscles as well as the liver (only glycogen synthesis). Maximal velocity and fractional velocity of the insulin‐sensitive part of glycogen synthase (FV %) was measured in the muscles, as well as muscle fibre composition and capillary density.After 24 h exposure to cortisol, insulin sensitivity was diminished in the clamp measurements. This was paralleled by a decrease in glycogen synthesis in the most insulin‐sensitive red gastrocnemius and Soleus muscles, but not in the white gastrocnemius or extensor digitorum longus muscles or the liver, and no effect was seen on 2–deoxyglucose uptake in muscles. FV % was markedly inhibited in all muscles. After 48 h exposure to cortisol, glycogen synthesis was markedly inhibited in all muscles, and 2–deoxyglucose uptake in all except the least insulin‐sensitive muscle, WG. No changes in muscle morphology were found.These results suggest that the insulin resistance caused by cortisol is elicited in a stepwise manner, starting with an inhibition in the glycogen synthesis system in insulin‐sensitive muscles, later including all muscles as well as 2–deoxyglucose uptake. This occurs without changes in morphology.
Overnight increases in haematocrit: additional evidence for a nocturnal fall in plasma volume
Authors: TALAN M. I. , ENGEL B. T. , KAWATE R. 
Published: December 2008

Talan, M. I., Engel, B. T. & Kawate, R. 1992. Overnight increases in haematocrit: additional evidence for a nocturnal fall in plasma volume. Acta Physiol Scand144, 473–476. Received 2 September 1991, accepted 20 November 1991. ISSN 0001–6722. National Institute on Aging, NIH, Gerontology Research Center, Baltimore, MD 21224, USA.Our previously published studies with monkeys describe a characteristic nocturnal haemodynamic pattern consisting of a monotonic decline in cardiac output and central venous pressure, and a concomitant rise in total peripheral resistance. These findings led us to hypothesize that there is a reduction in total plasma volume during the night. Since a fall in plasma volume should cause an increase in haemoglobin and plasma protein concentration, we designed this experiment to test the hypothesis that haematocrit levels would be significantly greater in the morning than in the evening. In a study of five monkeys, the levels of haematocrit were measured at 1700 h and at 0900 h the next morning for 14 days. The average morning haematocrit levels were 6S0h higher than the average evening values. Lower plasma volume and possibly greater blood viscosity could contribute to the pathophysiology of the morning increase in the incidence of ‘silen’ ischaemia and catastrophic vascular events such as sudden cardiac death, myocardial infarctions and strokes in man.
In vivomotor effects of loperamide on the rat urinary bladder
Authors: BERGGREN A. , SILLÉN U. , RUBENSON A. 
Published: December 2008

Bladder motility recordings were performed in anaesthetized rats and the effect of the peripherally active opiate agonist loperamide on urinary bladder function was studied. Regional intra‐arterial administration of loperamide (0.01–2 mg kg‐1) induced weak bladder contractionper se. Loperamide caused an effective dose‐dependent inhibition of bladder motility induced by regional injection of the receptor agonists acetylcholine (ACh) and substance P (SP), as well as by peripheral motor nerve stimulation (PNS).Pretreatment with naloxone (0.5 mg kg‐1) partially antagonized the inhibitory action of loperamide on the nerve‐mediated detrusor contraction. However, the depression of the motor responses induced by the receptor agonists ACh and SP was not influenced. It is suggested that the demonstrated inhibitory effect of loperamide on bladder motility is partially mediated by peripheral opioid receptors. The main non‐opioid part of the inhibition might be a direct smooth muscle action.
Sympathetic regulation of skeletal muscle blood flow in the pig: a non‐adrenergic component likely to be mediated by neuropeptide Y
Authors: MODINI A. , PERNOW J. , LUNDBERG J. M. 
Published: December 2008

The sympathetic regulation of blood flow in the skeletal muscle of the pig hind limb was investigated. Electrical stimulation of the lumbar sympathetic nerve with single impulses under control conditions decreased hind limb vascular conductance by 32%. After reserpine treatment combined with interruption of the sympathetic nerve activity in order to deplete the noradrenaline (NA) content, about 25% of the vasoconstrictor responses to single impulse stimulation still remained. In addition, an atropine sensitive dilatory component in the vascular response was also observed after reserpine treatment. Furthermore, intermittent stimulation with 20 Hz bursts (for 2 min) after reserpine caused a large vasoconstriction which was about 80% of the control response and lasted twice as long (about 15 min). This response was not affected by administration of the a‐adrenoceptor antagonist phenoxybenzamine or the stable ATP‐analogue α, β‐methylene‐ATP. Furthermore, in the reserpine pretreated pigs 20 Hz burst stimulation caused detectable overflow of neuropeptide Y (NPY)‐like immunoreactivity while NA release was reduced by 90%.Intra‐arterial administration of the NPY analogues [Leu31Pro34]NPY (Y1 receptor agonist) and NPY(13–36) (Y2‐receptor agonist) evoked dose dependent and long‐lasting vasoconstriction, whereby the Y1 agonist was about 10‐fold more potent than the Y2 agonist.In conclusion, the sympathetic regulation of the pig hind limb vasculature involves adrenergic, cholinergic and non‐adrenergic mechanisms. Several indirect lines of evidence suggest that the non‐adrenergic constrictor component, which is present even upon single impulse stimulation, is caused by NPY, possibly acting on Y1 receptors.
Breakdown of membrane choline‐phospholipids induced by endogenous and exogenous muscarinic agonist is potentiated by VIP in rat submandibular gland
Authors: DUNÉR‐ENGSTRÖM M. , FREDHOLM B. B. 
Published: December 2008

The outflow of tritium from rat submandibular gland fragments, pre‐labelled with [3H]choline, following electrical or pharmacological stimulation was studied. Electrical stimulation of the tissue increased the outflow of tritium in a frequency dependent manner. Atropine treatment decreased the electrically‐induced release, indicating that the outflow did not reflect acetylcholine from nerve endings, but was largely brought about by postsynaptic receptors. In agreement with this hypothesis, treatment with noradrenaline or carbachol induced a dose dependent increase in tritium outflow from the gland fragments which could be blocked by prazosin or atropine, respectively. Moreover, analysis of the tissue‐associated tritium revealed an incorporation primarily in the lipid fraction of the tissue (almost 80%), of which about 90% was in phosphatidylcholine, indicating that this was the source of the tritium outflow.Pre‐incubation with vasoactive intestinal polypeptide (VIP), which coexists with acetylcholine in the parasympathetic neurons innervating the submandibular gland, increased the carbachol‐induced tritium overflow significantly. The effect of VIP could be imitated by the adenylyl cyclase stimulator forskolin, which increased the carbachol‐stimulated tritium efflux in a dose dependent manner.Taken together, our results suggests that muscarinic‐ and α1‐receptor agonists may activate a phospholipase coupled to phosphatidylcholine hydrolysis in the rat submandibular gland. Endogenous acetylcholine released from parasympathetic nerve endings appear to activate this mechanism. Furthermore, VIP treatment, and the concomitant cAMP‐accumulation, potentiates the acetylcholine induced phosphatidylcholine hydrolysis, demonstrating a new type of interaction between the classical transmitter acetylcholine and the co‐stored neuropeptide VIP.
Significance of increased atrial pressure on stroke volume during atrial fibrillation in anaesthetized pigs
Authors: LEISTAD E. , CHRISTENSEN G. , ILEBEKK A. 
Published: December 2008

During atrial fibrillation synchronized atrial contraction is lost and cardiac output declines. Concomitantly, atrial pressure increases. The significance of the increase in atrial pressure on stroke volume was examined before and after blood volume expansion. Atrial fibrillation was induced by rapid atrial pacing in seven anaesthetized, open‐chest pigs. The increase in right atrial pressure subsequently was counteracted by an appropriate constriction of the inferior vena cava. To avoid the confounding effect of a rapid and irregular heart rate, ventricular rate was kept constant by separate His bundle pacing after complete atrioventricular block.When atrial fibrillation was induced, right and left atrial pressure at the top of the v‐wave increased both during normovolaemia and during hypervolaemia. Concomitantly, stroke volume declined. When the increase in atrial pressure was prevented during atrial fibrillation, stroke volume declined further: by 35 (21–50) and 9 (2–17)% (difference: P= 0.01), during normo‐ and hypervolaemia, respectively.Thus, the increase in atrial pressure counteracts the decline in stroke volume after induction of atrial fibrillation and thereby represents an important compensatory mechanism. This mechanism is more important with normal blood volume than during hypervolaemia.
Distribution of recurrent inhibition in the human upper limb
Authors: KATZ R. , MAZZOCCHIO R. , PÉNICAUD A. , ROSSI A. 
Published: December 2008

The distribution of homonymous and heteronymous recurrent inhibition among the motor nuclei innervating the main muscles of the human upper limb has been investigated in 25 healthy subjects.Homonymous recurrent inhibition was studied with a specially designed electrophysiological method with paired H‐reflexes, previously described by Bussel & Pierrot‐Deseilligny (1977), combined with a pharmacological study using a cholinergic agonist, the l‐acetylcarnitine (Rossi & Mazzocchio 1991). These methods were used to investigate the Flexor Carpi Radialis (FCR), Extensor Carpi Radialis (ECR), Opponens Pollicis (OP) and Abductor Digiti Minimi (ADM) motor nuclei. In the Deltoid, Triceps, Flexor Carpi Ulnaris (FCU) and Extensor Carpi Ulnaris (ECU) motor nuclei in which it was impossible to evoke clearly distinguishable H‐reflexes, homonymous recurrent inhibition was studied with the PSTH technique: homonymous recurrent inhibition was found in Deltoid, Triceps, FCR, FCU, ECR, ECU motor nuclei but not in OP and ADM motor nuclei.Heteronymous recurrent inhibition was studied with the PSTH technique in the Deltoid, Biceps, Triceps, FCR, ECR, FCU, ECU, Flexor Digitorum Communis (FDC), Extensor Digitorum Communis (EDC) motor nuclei as well as those innervating the intrinsic muscles of the hand. The following results were obtained: (1) motor neurones innervating muscles acting at digits do not receive any heteronymous recurrent inhibition; (2) motor neurones innervating muscles acting at the wrist give recurrent inhibition to motor nuclei of proximal muscles but do not receive any recurrent projections from the latter; and (3) motor neurones innervating proximal muscles (acting at shoulder or elbow) are interconnected by recurrent inhibition and receive heteronymous recurrent projections from some wrist muscles but not from intrinsic hand muscles.
Renal Na+, K+‐ATPase in Dahl salt‐sensitive rats: K+ dependence, effect of cell environment and protein kinases
Authors: NISHI A. , BERTORELLO A. M. , APERIA A. 
Published: December 2008

Na+, K+‐ATPase in renal epithelial cells plays an important role in the regulation of Na+ balance, extracellular volume and blood pressure. The function of renal Na+, K+‐ATPase in Dahl salt‐sensitive (DS) rats, an animal model for salt‐sensitive hypertension, and Dahl salt‐resistant (DR) rats has been studied. In Na+, K+‐ATPase partially purified from renal cortex, affinities and the Hill coefficients for Na+ and K+ activation were similar in DS and DR rats. Only one component of low ouabain affinity site was found in both strains, indicating the presence of the al isoform. Protein kinase C and cAMP‐dependent protein kinase phosphorylated Na+, K+‐ATPase α subunit in DS and DR rats, and the phosphorylation by protein kinase C was associated with an inhibition of enzyme activity. The kinetic parameters for K+ activation were also studied in a preparation of basolateral membranes and were found to be similar in DS and DR rats. In a preparation of cortical tubule cells, Na+, K+‐ATPase activity was determined as ouabain‐sensitive oxygen consumption (OS Qo2). Maximal OS Qo2, measured in Na+ loaded cells, was the same in DS and DR rats. The K06 for K+ was significantly lower in DS than DR rats (0.163 ±0.042 vs. 0.447 + 0.061 mM, P < 0.05), indicating that factors regulating Na+, K+‐ATPase activity in intact cells are altered in DS rats. Kinetic parameters for Na+ activation in cells were the same in both strains.In summary, the function of renal Na+, K+‐ATPase molecule is not altered in DS rats. The intracellular systems that regulate renal Na+, K+‐ATPase activity might be different in DS and DR rats.
Role of the L‐arginine/nitric oxide pathway in relaxation of isolated human penile cavernous tissue and circumflex veins
Authors: KIRKEBY H. J. , SVANE D. , POULSEN J. , T0TTRUP A. , FORMAN A. , ANDERSSON K.‐E. 
Published: December 2008

In human penile corpus cavernosum strips, pre‐contracted by noradrenaline, electrical stimulation of nerves evoked non‐adrenergic, non‐cholinergic (NANC) relaxant responses which could be inhibited by tetrodotoxin 10‐6M, NG‐nitro‐L‐arginine (L‐NNA) 10‐7‐10‐4M, and oxyhaemoglobin 10‐5M, but not by methylene blue (MB) 10‐5M. Acetylcholine‐induced relaxations were also inhibited by L‐NNA 10‐4M and oxyhaemoglobin 10‐5M, but were unaffected by pyrogallol 10‐4M, MB 10‐6M, and tetrodotoxin 10‐6M. MB 5 × 10‐4‐10‐4M significantly reduced the responses to both electrical stimulation and to acetylcholine. Nitric oxide (NO) 10‐7‐10‐4M and sodium nitroprusside 10‐9‐10‐4M caused concentration‐dependent relaxations. The NO‐induced relaxations were inhibited by oxyhaemoglobin 10‐5M, and the concentration‐response curve for sodium nitroprusside was shifted to the right by MB 10‐5M. The response to sodium nitroprusside was unaffected by L‐NNA 10‐4M, oxyhaemoglobin 10‐5M, and pyrogallol 10‐4M. In circumflex veins, pre‐contracted by noradrenaline, no NANC‐mediated relaxation was found in response to electrical stimulation; acetylcholine caused endothelium‐dependent relaxations, which were insensitive to L‐NNA 10‐4M and oxyhaemoglobin 10‐5M. NO and sodium nitroprusside caused concentration‐dependent relaxations; the concentration‐response curves for NO and sodium nitroprusside were shifted to the right by oxyhaemoglobin 10‐5M. Removal of the endothelium left the NO‐ and sodium nitroprusside‐induced relaxations unchanged.The results confirm previous observations that relaxations of human corpus cavernosum induced by both NANC nerve stimulation and exogenous acetylcholine involve an agent derived from L‐arginine. No NANC response to electrical stimulation was found in circumflex veins, where acetylcholine induced an endothelium‐dependent relaxation, apparently independent of the L‐arginine/nitric oxide pathway.