bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mecamylamine pretreatment counteracts cigarette smoke induced changes in hypothalamic catecholamine neuron systems and in anterior pituitary function
Authors: ANDERSSON KURT 
Published: December 2008

ANDERSSON, K. 1985. Mecamylamine pretreatment counteracts cigarette smoke induced changes in hypothalamic catecholamine neuron systems and in anterior pituitary hormone function. Acta Physiol Scand125, 445–452. Received 8 January 1985, accepted 7 May 1985. ISSN 0001–6772. Department of Histology, Karolinska Institute, Stockholm, Sweden.We have studied the eifects of acute, intermittent exposure to tobacco smoke on discrete hypothalamic CA nerve terminal networks and on neuroendocrine function by means of quantitative histofluorimetrical determinations of catecholamine (CA) fluorescence in sections of rat brain and by radioimmunoassay procedures for hormones. Acute intermittent exposure to cigarette smoke induced a lowering of NA levels and increased NA turnover in discrete hypothalamic nerve terminal regions. This exposure also induced increases in DA turnover in the median eminence. The cigarette smoke lowered TSH, prolactin, LH and FSH serum levels, but induced an increase in serum corticosterone concentrations. To determine if the above mentioned changes in neuroendocrine function were nicotine mediated, a cholinergic nicotine‐like blocking agent, mecamylamine, was administered prior to exposure to cigarette smoke. Pretreatment with mecamylamine (1.0 mgkg‐1) counteracted the cigarette smoke induced changes in CA levels and turnover in all hypothalamic CA nerve terminal regions as well as the changes in serum levels of the pituitary hormones and corticosterone. It is suggested that acute intermittent exposure to cigarette smoke, via its nicotine component, lowers TSH, prolactin, LH and FSH secretion at least in part through activation of the tubero‐infundibular DA neurons. Furthermore, the nicotine component of the cigarette smoke is suggested to induce the increase in corticosterone serum levels via increasing NA turnover in the paraventricular hypothalamic nucleus.
Evaluation of the ‘stretched pore phenomenon’ in isolated rat hindquarters
Authors: RIPPE BENGT , HARALDSSON BÖRJE , FOLKOW BJÖRN 
Published: December 2008

RIPPE, B., HARALDSSON, B., FOLKOW, B. 1985. Evaluation of the ‘stretched pore phenomenon’ in isolated rat hindquarters. Acta Physiol Scand125, 453–459. Received 5 March 1985, accepted 7 May 1985. ISSN 0001–6772. Department of Physiology, University of Göteborg, Sweden.In order to study the changes in capillary permeability occurring upon marked elevations in microvascular pressure, capillary filtration coefficient (CFC) and diffusion capacity (PS) for Cr‐EDTA were repeatedly measured ‘on‐line’ before and after brief periods (3 min) of large venous pressure (Pv) elevations in maximally vasodilated perfused rat hindquarters. First at Pv's ≥ 55 mmHg, increases in CFC and Ps‐Cr‐EDTA were observed immediately after the pressure elevations. While the CFC increases were then always pronounced (up to 4‐ to 5‐fold), the concomitant increases in PS‐Cr‐EDTA were small (at most 30–40%). For Pv≥ 55 mmHg there was a rough proportionality between Pv and CFC. While PS for Cr‐EDTA showed little reversibility with time upon Pv normalization, CFC was usually almost completely reversed after 10–20 min. The mentioned CFC and PS increases at Pv's ≥ 55 mmHg were quantitatively similar to those induced by histamine‐type mediators in the same preparation. It is concluded that capillary hydraulic conductivity can increase markedly but reversibly upon large Pv elevations, and that this is mainly due to forceful opening of ordinarily closed ‘large pores’ in the microvascular membrane, rather than being caused by lesional rifts in the endothelium,
Inhibition of the cholinergic neurotransmission in human airways via prejunctional alpha‐2‐adrenoceptors
Authors: GRUNDSTRÖM N. , ANDERSSON R. G. G. 
Published: December 2008

GRUNDSTRÖM, N. & ANDERSSON, R.G.G. 1985. Inhibition of the cholinergic neurotransmission in human airways via prejunctional alpha‐2‐adrenoceptors. Acta Physiol Scand 125, 513–517‐ Received 1 February 1985, accepted 29 May 1985. ISSN 0001–6772. Department of Pharmacology, Linköping University, Sweden.Previous investigations on guinea‐pig airways indicate that the excitatory, cholinergic neurotransmission can be inhibited via prejunctional alpha‐2‐adrenoceptors. The aim of this study was to investigate whether a similar inhibition of the cholinergic neurotransmission is present in human airways. Ring preparations of human bronchi were mounted for recording of isometric tension and immersed in oxygenated Krebs solution. Electrical field stimulation of the preparations elicited atropine‐sensitive twitch contractions. Exogenous noradrenaline (in the presence of cocaine and propranolol) inhibited the electrically evoked contractions. The noradrenaline‐induced inhibition could be antagonized by yohimbine whereas prazosin was ineffective, indicating that the inhibition was mediated by alpha‐2‐adrenoceptors. Contractions evoked by exogenous acetylcholine (in the presence of cocaine and propranolol) was unaffected by the addition of noradrenaline, which suggests that the alpha‐2‐adrenoceptors have a prejunctional localization. In conclusion, this report gives evidence that the human bronchial, cholinergic neurotransmission can be inhibited by stimulation of prejunctional alpha‐2‐adrenoceptors.
The influence of extrasegmental mechanical vibratory stimulation and transcutaneous electrical nerve stimulation on histamine‐induced itch
Authors: EKBLOM A. , HANSSON P. , FJELLNER B. 
Published: December 2008

EKBLOM, A., HANSSON, P. & FJELLNER, B. 1985. The influence of extrasegmental mechanical vibratory stimulation and transcutaneous electrical nerve stimulation on histamine‐induced itch. Acta Physiol Scand125, 541–545. Received 16 April 1985, accepted 13 June 1985. ISSN 0001–6772. Department of Physiology II, Karolinska Institutet, and Department of Dermatology, Karolinska Sjukhuset, Stockholm, Sweden.The effect of peripheral conditioning stimulation on experimentally induced pruritus was studied in 12 healthy volunteers. Itch was induced by intradermal injections of histamine on the upper arms. Vibration at 100 Hz and transcutaneous electrical nerve stimulation (TENS) at 2 and 100 Hz were applied extrasegmentally (dorsal aspect of the lower part of the leg, ipsilateral to the injected arm) for a period of 5 min following induction of itch. The effect of a 5 and 30 min stimulation period before itch elicitation was also studied as well as the influence of placebo stimulation. No significant effects were obtained with 100 Hz vibration and 100 Hz TENS, and none with placebo stimulation, whereas significant itch reduction was seen using 2 Hz TENS. The local skin flare response following histamine injections was not altered following conditioning stimulation of any type.
On the hormonal regulation of lipolysis in isolated reindeer adipocytes
Authors: LARSEN TERJE S. , NILSSEN KJELL J. 
Published: December 2008

LARSEN, T.S. & NILSSEN, K.J. 1985. On the hormonal regulation of lipolysis in isolated reindeer adipocytes. Acta Physiol Scand125, 547–552. Received 19 December 1984ac cepted 12 June 1985. ISSN 0001–6772. Department of Arctic Biology and Department of Physiology, Institute of Medical Biology, University of Tromsø, Norway.The effects of insulin and bovine growth hormone (bGH) on lipolysis (basal and/or adrenaline‐stimulated) were investigated in isolated adipocytes from the Norwegian reindeer. Addition of 100 nmol 1‐1 adrenaline to the cells increased lipolysis 20‐fold above basal lipolytic rate. Insulin (0.1 and 1 nmol l‐1) depressed lipolysis significantly at submaximal adrenaline stimulation but had no effect when lipolysis was stimulated maximally. Bovine GH (25 and 100 ng ml‐1) inhibited basal lipolysis during the first 2 h of incubation, whereas refractoriness to this action was induced during the third and fourth hour of incubation. These effects were not influenced by inclusion of a small amount of glucocorticoid (dexamethasone, 25 ng ml‐1). Addition of 0.1 and 1 nmol 1‐1 insulin together with bGH (100 ng ml‐1) prevented the initial antilipolytic effect of the latter and resulted in the expression of normal basal lipolytic rates. Preincubation with bGH (100 ng ml‐1) for 2 h did not alter the lipolytic response of the adipocytes to adrenaline. These findings lend support to the conclusion that insulin exerts a major control of lipolysis in reindeer adipose tissue. The significance of the antilipolytic effect of bGH is difficult to evaluate since this effect was transient and was abolished during the third and fourth hour of incubation.
Changes in isometric force‐ and relaxation‐time, electromyographic and muscle fibre characteristics of human skeletal muscle during strength training and detraining
Authors: HÄKKINEN K. , ALÉN M. , KOMI P. V. 
Published: December 2008

HÄKKINEN, K., ALÉN, M. & KOMI, P.V. 1985. Changes in isometric force‐ and relaxation‐time, electromyographic and muscle fibre characteristics of human skeletal muscle during strength training and detraining. Acta Physiol Scand 125, 573–585. Received 26 January 1985, accepted 9 May 1985. ISSN 0001–6772. Department of Biology of Physical Activity and Department of Health Sciences, University of Jyväskylä, Jyväskylä, Finland.Eleven male subjects (20–32 years) accustomed to strength training went through progressive, high‐load strength training for 24 weeks with intensities ranging variably between 70 and 120% during each month. This training was also followed by a 12‐week detraining period. An increase of 26.8% (P < 0.001) in maximal isometric strength took place during the training. The increase in strength correlated (P < 0.05) with significant (P < 0.05–0.01) increases in the neural activation (IEMG) of the leg extensor muscles during the most intensive training months. During the lower‐intensity training, maximum IEMG decreased (P < 0.05). Enlargements of muscle‐fibre areas, especially of fast‐twitch type (P < 0.001), took place during the first 12 weeks of training. No hypertrophic changes were noted during the latter half of training. After initial improvements (P < 0.05) no changes or even slight worsening were noted in selected force‐time parameters during later strength training. During detraining a great (P < 0.01) decrease in maximal strength was correlated (P < 0.05) with the decrease (P < 0.05) in the maximum IEMGs of the leg extensors. This period resulted also in decreases (P < 0.05) of the mean muscle‐fibre areas of both fibre types. It was concluded that improvement in strength may be accounted for by neural factors during the course of very intensive strength training. Selective training‐induced hypertrophy also contributed to strength development but muscle hypertrophy may have some limitations during long‐lasting strength training, especially in highly trained subjects.
Dissociation between renal prostaglandin E2and renin release. Effects of glucagon, dopamine and cyclic AMP in dogs
Authors: VIKSE ARILD , BUGGE JAN , DAHL ELLEN , KIIL FREDRIK 
Published: December 2008

VIKSE, A., BUGGE, J., DAHL, E. & KIIL, F. 1985. Dissociation between renal prostaglandin E2and renin release. Effects of glucagon, dopamine and cyclic AMP in dogs.Acta Physiol Scand125, 619–626. Received 14 March 1985, accepted 10 May 1985. ISSN 0001–6772. University of Oslo, Institute for Experimental Medical Research, Ullevaal Hospital, Norway.To examine the relationship between prostaglandin E2(PGE2) and renin release, glucagon, dopamine and dibutyryl cyclic AMP (DB‐cAMP) were infused into dog kidneys during autoregulatory dilation of preglomerular vessels. Autoregulatory vasodilation, which enhances PGE2and renin release, was induced by renal arterial constriction or ureteral occlusion. Glucagon infusion increased both PGE2and renin release during autoregulatory vasodilation, and renin release was almost abolished after inhibiting PGE2release by indomethacin. In contrast, dopamine and DB‐cAMP infused during autoregulatory vasodilation increased renin release without significantly changing PGE2release. Stimulation of renin release was not dependent on vasodilatory effects, which for all drugs were greatly diminished during autoregulatory vasodilation. Hence, glucagon stimulates both PGE2and renin release. Most of the increase in renin release during glucagon infusion is prostaglandin‐dependent since indomethacin greatly reduced the stimulatory effect. In contrast, dopamine and DB‐cAMP stimulate renin release without increasing PGE2release as previously found for β‐adrenergic stimulation.
Cyclic AMP potentiates glucose‐induced insulin release from mouse pancreatic islets without increasing cytosolic free Ca2
Authors: RORSMAN PATRIK , ABRAHAMSSON HÅKAN 
Published: December 2008

RORSMAN P. & ABRAHAMSSON, H. 1985. Cyclic AMP potentiates glucose‐induced insulin release from mouse pancreatic islets without increasing cytosolic free Ca2+. Acta Physiol Scand 125, 639–647. Received 18 March 1985, accepted 28 May 1985. ISSN 0001–6772. Department of Medical Cell Biology, Biomedicum, University of Uppsala, Sweden.The effects of various stimulants of insulin release on cytosolic free Ca2+, [Ca2+]i, in dispersed and cultured pancreatic β‐cells from ob/ob‐mice were studied using the indicator quin‐2, which in itself has only slight effects on the glucose‐induced insulin release and the metabolism of the sugar. The resting [Ca2+]i was 158 ± 7 nM. After increasing glucose to 20 mM there was a lag‐period of 1–2 min before [Ca2+]i gradually rose, reaching a new plateau 60% higher after 5–6 min. Increasing intracellular cyclic AMP by adding forskolin did not further increase [Ca2+]i; on the contrary there was a slight temporary reduction despite a doubling of insulin secretion. The maintenance of the β‐cell function was evident from a marked increase of cytosolic [Ca2+]i after depolarization evoked by high extracellular K+. Also dibutyryl cyclic AMP and theophylline lacked the ability to raise [Ca2+]i beyond that obtained by glucose. The results suggest that cyclic AMP potentiates glucose‐induced insulin release by sensitizing the secretory machinery to changes of [Ca2+]i rather than by increasing the cytosolic concentration of the ion.
Effects of shape and size on red blood cell deformability: a static bending analysis
Authors: ENGSTRÖM GUNNAR , TÄLJEDAL INGE‐BERT 
Published: December 2008

ENGSTRÖM, G. & TÄLJEDAL, I.‐B. 1985. Effects of shape and size on red blood cell deformability: a static bending analysis. Acta Physiol Scand 125, 669–679. Received 16 April 1985, accepted 19 June 1985. ISSN 0001–6772. Department of Histology and Cell Biology, University of Umea, Sweden.When flowing down a tapered tube, such as a narrow capillary, red blood cells (RBCs) are subject to deformation, the first event of which is folding in a pancake manner. The RBC deformability is reduced during cell ageing, a phenomenon that may reflect alterations in intracellular viscosity, membrane rigidity or RBC shape. Age related shape changes and their importance for increased RBC rigidity were theoretically analysed. The average empirically observed RBC profile is shown to offer little resistance to bending as compared to other, theoretically possible profiles of the same membrane area and RBC volume. Because of a decrease in projected area (diameter size), and therefore in pressure load, the pressure needed to initiate folding of an old RBC is between 20 and 55% higher than that required to fold a young one if, during RBC ageing, membrane area to cell volume ratio is constant as empirically observed. This difference exists whether the RBC is mathematically treated as a solid body or as a membrane shell.
Pre‐ and postjunctional modulation of cholinergic neuroeffector transmission by adenine nucleotides. Experiments with agonist and antagonist
Authors: WIKLUND N. PETER , GUSTAFSSON LARS E. , LUNDIN JAN 
Published: December 2008

WIKLUND, N.P., GUSTAFSSON, L.E.&LUNDIN, J. 1985. Pre‐and postjunctional modulation of cholinergic neuroeffector transmission by adenine nucleotides. Experiments with agonist and antagonist.Acta Physiol Scand125, 681–691. Received 27 May 1985, accepted 26 June 1985. ISSN 0001–6772. Departments of Physiology and Toxicology, Karolinska Institute, and The Swedish National Laboratory of Environmental Medicine, Stockholm, Sweden.Adenosine, 2‐chloroadenosine, AMP, AMPNH2, ADP, ATP, AMPPNP and β, γmeATP dose‐dependently and reversibly inhibited contractile responses to nerve stimulation in longitudinal plexus‐containing muscle preparations of guinea pig ileum. All the purines, except for 2‐chloroadenosine, were virtually equipotent and elicited maximal inhibition within 2 min after application. Adenosine deaminase abolished inhibition by adenosine but did not block the effect of 2‐chloroadenosine or the adenine nucleotides. During transmural nerve stimulation, the nucleotidase‐resistant analogues α, βmeADP and AMPPNP significantly depressed acetylcholine release measured by gas chromatography‐mass spectrometry. The inhibitory effect of all the purines was competitively, reversibly and at comparable pA2values antagonized by 8‐φ‐sulphophenyltheophylline. The results indicate that nucleotidesper secan inhibit neurotransmission via a prejunctional receptor common to nucleosides and nucleotides. An excitatory effect by all the di‐ and triphosphate nucleotides was also observed. The excitation was unaltered by atropine, tetrodotoxin and 8‐φ‐sulphophenyltheophylline, thus suggesting an action at postjunctional ADP‐ and ATP‐like receptive sites.
Transcapillary extravasation rate of albumin in rat skeletal muscle. Effect of motor activity
Authors: REED ROLF K. 
Published: December 2008

REED, R.K. 1985. Transcapillary extravasation rate of albumin in rat skeletal muscle. Effect of motor activity. Acta Physiol Scand 125, 719–725. Received 6 December 1984, accepted 19 July 1985. ISSN 0001–6772. Department of Physiology, University of Bergen, Bergen, Norway.Transcapillary extravasation of albumin in hindlimb and neck skeletal muscle of rats was determined as extra vascular plasma equivAlént volumes (I‐HSAev), 1–168 h after a single intravenous injection of radiolabelled human serum albumin (I‐HSA). One experimental group was immobilized in pentobarbital anaesthesia for the first 8 h after injection of I‐HSA. With longer extravasation periods, the rats then woke up and moved freely. In the other experimental group, injections were made in ether anaesthesia allowing the rats to move freely within 10 min after injection. One hour after injection, I‐HSAev in the immobilized group averaged 1.5 10‐3 ml g‐1 in neck and hindlimb muscle. In the mobile group, I‐HSAev was two to three times higher than in the immobilized rats up to 12 h in both muscle groups (P < 0.05). At 24 h and later I‐HSAev was similar in mobile and immobile rats (P > 0.05). The I‐HSAev increased up to 48 h, levelling off at about 0.06 and 0.08 ml g_I in hindlimb and neck skeletal muscle, respectively. Corresponding interstitial albumin concentration, calculated from steady‐state I‐HSAev and interstitial fluid volume (51Cr‐EDTA space), averaged 48% and 34 % of plasma albumin concentration, respectively.
Effects of atrial natriuretic peptide (ANP) during converting enzyme inhibition
Authors: HANSELL P. , ULFENDAHL H. R. 
Published: December 2008

Effects of atrial natriuretic peptide (ANP) during converting enzyme inhibition.Acta Physiol Scand130, 393–399. Received 1 December 1986, accepted 10 February 1987. ISSN 0001–6772. Department of Physiology & Medical Biophysics, Biomedical Centre, University of Uppsala, Sweden.Studies were performed on anaesthetized adult Münich‐Wistar rats to investigate the role of angiotensin 11 in the natriuretic response to synthetic atrial natriuretic peptide (ANP, 28 amino acids). For this purpose the whole kidney glomerular filtration rate (GFR) and urinary excretion of electrolytes were measured in groups of animals pretreated with the converting enzyme inhibitor captopril (3 mg h‐1kg‐1body wt) or vehicle and then given a continuous intravenous infusion of ANP at 10 μg h‐1kg‐1body wt. In the vehicle‐pretreated animals, 45 min of ANP infusion did not change GFR (control value 1.17 ± 0.11, experimental value 1.17 ± 0.06 ml min‐1g‐1kidney wt). Sodium excretion (UNaV) increased more than three‐fold from 0.036 ± 0.010 to 0.134 ± 0.058 pmol min‐1g‐1kidney wt (p0.05) and potassium excretion (UKV) increased from 0.481 ± 0.055 to 0.946 ± 0.068 μmol min‐1g‐1kidney wt (P0.05). Urine osmolality (UOsm) remained unchanged, while the blood pressure (BP) decreased by 15%. In animals pretreated with captopril, ANP infusion led to a decrease in GFR from 1.27 ± 0.11 to 1.05 ± 0.09 ml min‐1g‐1kidney wt (P0.05). Despite this effect,UNaVincreased more than two‐fold from 0.076 ± 0.020 to 0.193 ± 0.087 μmol min‐1g‐1kidney wt (P0.05). TheUKVwas not statistically significantly elevated (change from 0.623 ± 0.156 to 0.859 ± 0.146 μmol min‐1g‐1kidney wt) andUOsmremained unaltered, while BP decreased by 15% (P0.05). The captopril‐pretreated animals had a higher UNaVvalue during the control period than vehicle‐pretreated ones, but there was no statistical difference in this variable between the groups after ANP infusion. The captopril treatment decreased BP by 6%. It is concluded that converting enzyme inhibition induced by captopril does not interfere with either the natriuretic or with the hypotensive response to ANP, which suggests that angiotensin II does not participate in the generation of the acute effects of ANP. Atrial natriuretic peptide increases sodium excretion predominantly by affecting tubular transport processes, and not by increasing GFR.
Release of vasoactive intestinal polypeptide anally of a local distension of the feline small intestine
Authors: SJÖQVIST A. , FAHRENKRUG J. 
Published: December 2008

Release of vasoactive intestinal polypeptide anally of a local distension of the feline small intestine. Acta Physiol Scand 130, 433–438. Received 12 February 1987, accepted 27 February 1987. ISSN 0001–6772. Department of Physiology, University of Göteborg, Sweden, and Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, Denmark.The peristaltic reflex is elicited by a local distension of the intestine and consists of an ascending contraction and a descending inhibition of the smooth muscle layer. The transmitter mediating the inhibition of the smooth muscle cells is not known but vasoactive intestinal polypeptide (VIP) has, among others, been proposed to mediate the descending inhibition of a distension. An in vivo preparation of a segment of the feline intestine was designed to allow collection of the venous effluent and determination of the VIP release orally and anally of a distension. The release of VIP rose significantly more on the anal side of the intestinal distension, and so did the blood flow. Division of the myenteric plexus prevented the asymmetry of the VIP release to a large extent. These effects of distension on the release of VIP are consistent with the hypothesis that VIP mediates the descending inhibition of the peristaltic reflex.