bluuebunny/crossref_metadata_2025_split huggingface dataset:
The dopamine receptor antagonist haloperidol blocks natriuretic but not hypotensive effects of the atrial natriuretic factor
Authors: HANSELL P. , FASCHING A. , SJÖQUIST M. , ANDÉN N.‐E. , ULFENDAHL H. R. 
Published: December 2008

The dopamine receptor antagonist haloperidol blocks natriuretic but not hypotensive effects of the atrial natriuretic factor.Acta Physiol Scand130, 401–407. Received 11 December 1986, accepted 10 February 1987. ISSN 0001–6772. Department of Physiology & Medical Biophysics and Department of Pharmacology, Biomedical Centre, University of Uppsala, Sweden.Studies were performed on anaesthetized male Münich‐Wistar rats to investigate the influence of the dopamine (DA) receptor antagonist haloperidol on the natriuretic response to infusion of a synthetic atrial natriuretic factor. The whole kidney glomerular filtration rate (GFR), urinary excretion of electrolytes, and arterial blood pressure (BP) were therefore measured in groups of animals pretreated with haloperidol or vehicle and given a continuous intravenous infusion of atrial natriuretic peptide (ANP; 28 amino acids). Forty‐five minutes of ANP infusion at 10 μg h‐1kg‐1body wt did not increase GFR (change from 1.14 ± 0.08 to 1.15 ± 0.05 ml min‐1g‐1kidney wt). Sodium excretion (UNaV) increased more than four‐fold from 0.037 ± 0.008 to 0.165 ± 0.070 μmol min‐1g‐1kidney wt (P0.01). Potassium excretion (UKV) increased by 86% (P0.001) and the urine flow rate (V) increased transiently by 63% (P0.05) and did not differ from the control value during the last 15 min of ANP infusion. The urinary sodium concentration (UNa) increased almost three‐fold, while BP decreased by 14%. There was no change in urine osmolality. In animals pretreated with haloperidol (I mg kg‐1body wt), 45 min of ANP infusion did not significantly alter GFR (from 1.10 ± 0.08 to 0.98 ± o.09 ml min‐lg‐1kidney wt). TheUNaVdid not increase significantly (change from 0.026 ± 0.006 to 0.030 ± 0.009 μmolmin‐1g‐lkidney wt). TheUKVwas not elevated by ANF infusion. The urine flow rate was transiently elevated by 45% but was not different from the control during the last 15 min of infusion. BothUNaandUosmremained unchanged, but BP was reduced by 11%. In conclusion, the DA receptor blocking agent haloperidol blunts the natriuretic effect of ANP. This action is probably exerted by inhibiting the postulated tubular effects of ANP through an unknown mechanism, but not the vascular ones, since the hypotensive effect of ANP is unaltered. Atrial natriuretic peptide increases sodium excretion not, mainly, by increasing GFR but by affecting tubular transport processes.
Synthesis and secretion of amylase in the rat parotid gland following autonomic nerve stimulation in vivo
Authors: ASKING B. , GJÖRSTRUP P. 
Published: December 2008

Synthesis and secretion of amylase in the rat parotid gland following autonomic nerve stimulation in vivo. Acta Physiol Scand 130, 439–445. Received 10 November 1986, accepted 9 February 1987. ISSN 0001–6772. Department of Physiology and Biophysics, University of Lund, Sweden.Parasympathetic and sympathetic nerve stimulation in vivo, individually and in combination, was used to study secretion and synthesis of amylase in the rat parotid gland. After 30 min with sympathetic nerve stimulation (3 Hz) a decrease in glandular amylase was seen, which corresponded approximately to the salivary output. On the other hand, after parasympathetic stimulation (10 Hz), chosen to obtain comparable amylase output, there was no decrease in glandular amylase, which points to synthesis during such activation. Experiments with incorportation of [3H]leucine, reflecting amylase synthesis, showed that both types of nerve stimulations increased such uptake in parotid protein. These results indicate that beside sympathetic activity, which is the main stimulus for granular amylase secretion, parasympathetic nerve impulses can evoke considerable amylase secretion because amylase synthesis is stimulated and amylase is rapidly available from a special, possibly non‐granular pool. As expected from previous experiments an augmentation of amylase secretion was found, and the present experiments also indicated an augmentation at the level of synthesis when the two nerves were stimulated at the same time.
The effect of amiloride on biliary HCO‐3secretion in the anaesthetized pig
Authors: GROTMOL T. , BUANES T. , RÆDER M. G. 
Published: December 2008

The effect of amiloride on biliary HCO‐3‐secretion in the anaesthetized pig.Acta Physiol Scand130, 447–455. Received 20 October 1986, accepted 23 February 1987. ISSN 0001–6772. Institute for Experimental Medical Research, University of Oslo and Surgical Department, Ullevaal Hospital, Oslo, Norway.The present study was performed on 29 anaesthetized pigs and shows that the bile acid ursodeoxycholic acid (UDCA) produces a flow of bile rich in HCO‐3compared with taurocholic acid (TCA). The slope relating biliary HCO‐3secretion to bile acid secretion was 0.59 (0.44–0.82) and 0.33 (0.29–0.38) during venous infusion of UDCA and TCA, respectively. We next wanted to evaluate the importance of Na+/H+ion exchange for biliary HCO‐3secretion. High doses of amiloride were employed in order to impair the hepatic Na+/H+ion exchanger. It was reasoned that any reduction in H+efflux through the hepatic Na+/H+ion exchanger involved in causing biliary HCO‐3secretion would be translated into an equimolar fall in biliary HCO‐3secretion. We found that amiloride (2.0 ± 10‐‐4mol l‐1plasma) reduced UDCA‐dependent canalicular HCO‐3secretion by 26 (14–35)% without concurrently reducing bile acid secretion. Amiloride (2.9 ± 10‐‐4mol 1‐‐1plasma) did not significantly reduce secretin‐dependent ductular HCO‐3secretion. In this group of animals amiloride reduced bile acid secretion by 13 (5–22)%. It is concluded that Na+/H+ion exchanger is essential for UDCA‐dependent canalicular HCO‐3secretion, but not for secretin‐dependent ductular HCO‐3secretion.
Endurance, what is it? Muscle morphology after an extremely long distance run
Authors: SJÖSTRÖM M. , FRIDÉN J. , EKBLOM B. 
Published: December 2008

Endurance, what is it? Muscle morphology after an extremely long distance run. Acta Physiol Scand 130, 513–520. Received 26 July 1984, revised 4 January 1987, accepted 16 February 1987. ISSN 0001–6772. Department of Neurology and Anatomy, University of Umeå, and Department of Physiology III, Karolinska Institute, Stockholm, Sweden.Biopsies of m. vastus lateralis of a well‐trained 46‐year‐old man were analysed before and after an extremely long distance run (3529 km in 7 weeks). After the period of running, both a decrease of fibre size and a neuromuscular pathology were found. Muscle fibre degeneration and regeneration, especially of type 2 (fast‐twitch) fibres, was seen as well as signs of damage to the peripheral nerves. The relative amount of type I (slow‐twitch) fibres was higher after the run. The relationships between light and electron microscopical characteristics normally present could not be found in the specimens of this man. The changes in fibre size as well as the other microscopical characteristics may express an adaptation through more or less complete fibre transformation. However, we could not rule out that a selective elimination of fibres also contributed to the observed changes. In that case, the underlying pathophysiology might have been a peripheral arterial insufficiency which was related to the extreme functional demands. These disturbances may have affected type 2 fibres more than type I fibres. Endurance may, on this basis, express an adaptation of the muscle through elimination of weak fibres, that is, fibres related to limited functional capacities.
Binding and degradation of vasoactive intestinal peptide in prolactin‐producing cultured rat pituitary tumour cells (GH4C1)
Authors: BJøRO T. , WIIK P. , OPSTAD P. K. , GAUTVIK K. M. , HAUG E. 
Published: December 2008

Binding and degradation of vasoactive intestinal peptide in prolactin‐producing cultured rat pituitary tumour cells (GH4C1). Acta Physiol Scand 130, 609–618. Received 17 October 1986, accepted 2 March 1987. ISSN 0001–6772. Hormone Laboratory, Aker Hospital, Oslo, Norwegian Defence Research Institute, Division for Environmental Toxicology, Kjeller, and Institute of Medical Biochemistry, University of Oslo, Norway.Vasoactive intestinal peptide (VIP) stimulates prolactin (PRL) secretion from cultured rat pituitary cells (GH cells) (Bjero et al. 1984). This study demonstrates the presence of specific receptors for 125I‐VIP on the GH4C1 cells. Specific binding was rapid and biphasic giving a transient plateau lasting from 7 to 30 min. Thereafter specific binding declined to about one‐third after 90 min. This coincided with enhanced degradation of 125I‐VIP. The degradation was mainly cell‐mediated and only partly receptor dependent. Trichloroacetic acid precipitation and absorption chromatography indicated that the degradation products were either 125I‐ and/or small labelled peptide fragments. Bioassay, RIA and rebinding studies also demonstrated degradation of VIP. Pretreatment of GH4C1 cells with trypsin decreased the rate of degradation of 125I‐VIP, but also reduced the amount of specific binding. Scatchard analysis of binding data indicated the existence of two independent classes of receptors, one with Kd= 2.2 nM and Bmax= 15 fmol per 106 cells and another with Kd= 180nM and Bmax= 550 fmol per 106 cells. The IC50 for VIP, PHI and secretin were 4, 5 and 500 nM, respectively. We conclude that the high affinity receptor is the most probable mediator of VIP on PRL secretion. The effect of VIP and PHI on PRL secretion in GH4C1 cells is mediated through one common receptor.
Mechanical, morphological and pharmacological properties of oesophageal varices and small mesenteric veins in portal hypertensive rabbits
Authors: JENSEN L. S. , JUHL C. O. , MULVANY M. J. 
Published: December 2008

Mechanical, morphological and pharmacological properties of oesophageal varices and small mesenteric veins in portal hypertensive rabbits. Acta Physiol Scand 130, 649–656.The properties of isolated small oesophageal and mesenteric veins were investigated in a rabbit model subjected to a 4–week period of portal vein stenosis. The animals developed oesophageal varices and these together with the small mesenteric veins were mounted on a myograph. Compared with sham‐operated controls portal hypertension resulted in an increased normalized inner radius and media thickness of the oesophageal veins resulting in a non‐significant increase in the media to lumen ratio, while the inner radius decreased as media thickness increased in mesenteric veins resulting in a significant (P 0.01) increase in the media to lumen ratio. When activated, the active wall tension of both the oesophageal and mesenteric veins was increased following portal hypertension, but the active media stress was unchanged. The EC50 for noradrenaline and angiotensin I1 did not change in portal hypertensive vessels compared with controls and was equal in oesophageal and mesenteric vessels. The ability of isoprenaline and serotonin to relax pre‐contracted vessels of both types was reduced by the portal hypertension. The results of these studies suggest that the development of oesophageal varices is not only due to increased portal venous pressure.
Sprinters and marathon runners. Does is kinetic knee extensor performance reflect muscle size and structure?
Authors: JOHANSSON C. , LORENTZON R. , SJÖSTRÖM M. , FAGERLUND M. , FUGL‐MEYER A. R. 
Published: December 2008

Sprinters and marathon runners. Does isokinetic knee extensor performance reflect muscle size and structure?Acta Physiol Scand130, 663–669.In order to evaluate relationships between structure and concentric function of the quadriceps muscle, isokinetic maximum knee extensor output at different velocities of angular motion (30–180 degrees s‐1), integrated electromyographic activity (iEMG), cross‐sectional area (CSA) of m. quadriceps and fibre composition of m. vastus lateralis were analysed in five sprinters and five marathon runners (all males). Both output and input parameters, concerning peak torque (PT), instantaneous power (IP), contractional work (CW) and the summed iEMG were closely correlated to the m. quadriceps CSA, as well as to the calculated absolute type II (A + B), IIA and IIB fibre areas of m. vastus lateralis. When PT, IP, CW and the summed iEMG were corrected for CSA, such relationships were found only at 180 degrees s‐1 and only for type IIA fibre area. The electromyographic findings indicate that m. vastus lateralis was representative for the total mechanical output. The calculated mean power output (CW s‐1) and output/input balance (CW/iEMG) describe similar relationships with the velocity of angular motion and were not related to the CSA or to the absolute area of any fibre type. The calculated optimal CW per second and CW/EMG occur for sprinters at about 450 degrees s‐1 and for marathon runners at about 270 degrees s‐1, that is, velocities well above the capacity of the isokinetic dynamometer. Our observations indicate that the peak torque or instantaneous power, during single maximum knee extensions, at least at 180 degrees s‐1, express characteristics of the muscle structure.
Neuropeptide Y (NPY) induced inhibition of preganglionic nerve stimulation evoked release of adrenalin and noradrenaline in the pithed rat
Authors: DAHLÖF P. , PERSSON K. , LUNDBERG J. M. , DAHLÖF C. 
Published: December 2008

NPY, a peptide with 36 amino acid residues, is co‐stored together with noradrenaline (NA) in cardiac and sympathetic perivascular nerves as well as with adrenalin (A) in adrenal chromaffin cells. NPY is released together with NA from sympathetic nerves and with A from the adrenal glands and appears to be involved in the control of sympathetic neurotransmission.The aim of the present study was to analyse the effect of NPY on the preganglionic nerve stimulation (PNS) evoked increases in plasma A and NA concentrations in pithed rats. In the first part of the study (I) only one PSN period (2 Hz for 45 s) was performed in each rat and the control group was compared to the NPY treated group. In the second part of the study (II) two PNS periods (1 Hz for 45 s) were performed in each rat, which either received saline or NPY before the second PNS. Thus, interindividual changes between the responses to the first and second PNS in control and NPY rats could be compared.In both study I and II, systemic infusion of NPY (2 μg kg‐1 min1 i.v.) significantly reduced the PNS‐induced increase in plasma A by 26% and 42%, respectively (P < 0.05). However, the increase in plasma NA elicited by PNS was significantly reduced only in study II by 23% (P < 0.05). Infusion of NPY did not affect basal heart rate in either of the studies, but significantly increased basal blood pressure by about 10 mmHg. The blood pressure responses to PNS were significantly greater in NPY treated rats.It is concluded that PNS‐evoked release of A and NA is under inhibitory control of NPY. The inhibition of NA release from the sympathetic nerve terminals is most probably due to a prejunctional site of action, whereas the reduced secretion of A could be due to a local effect of NPY in the adrenal medulla,. The negative influence of NPY on A and NA release appears to be compensated for by the additional facilitatory action of NPY on the postjunctioned responses to these catecholamines.
Studies on terminal differentiation of rat renal proximal tubular cells in culture: ouabain‐sensitive K and NA transport
Authors: LARSSON S. H. , APERIA A. , LECHENE C. 
Published: December 2008

We have studied the ontogeny of Na‐K ATPase‐mediated Na and K transport in rat renal proximal tubular cells using electron probe analysis. The cells were cultured from kidneys of 10‐day‐old, young (Y), and 40‐day‐old, adult (A) rats. Before an experiment cells were Na‐loaded and K‐dcpleted by incubation in K‐free medium. The maximum rate of ouabain‐sensitive Na and K transport was measured after reactivating the Na‐K pump by transferring the cells from K‐free medium to medium containing 5 mM K. In cells cultured for 2 days, ouabain‐sensitive Na and K net initial transport rates were significantly higher in A than in Y cells. Between 2 and 4 days in culture there was a significant decrease in ouabain‐sensitive Na and K transport rates in both Y and A cells. From 2 to 4 days of culture there was, in Y but not in A cells, a significant decrease in K/Na ratio. The decrease in K/Na ratio was due to a significant increase in Na content. After incubation in K‐free medium, net intracellular solute accumulation was observed in A and Y cells cultured for 4 days but not in A and Y cells cultured for 2 days.In conclusion, maximal Na‐ and K‐pump‐mediated transport increases during terminal differentiation. This increase can be measured in cells cultured for 2 days. With longer time in culture, Na K pump activity decreases and the difference between A and Y cells is not measurable. We had previously observed that net Na and K permeabilities decrease from 2 to 4 days in culture in A but not in Y cells. In Y cells cultured for 4 days, a decrease in pump activity without a change in Na and K permeability causes an increase in intracellular Na content.
Acidosis, hypoxia and stress hormone release in response to one‐minute inhalation of 80% CO2 in swine
Authors: FORSLID A. , AUGUSTINSSON O. 
Published: December 2008

The study pertains to a series of investigations on the effects of CO2 inhalation as used for pre‐slaughter anaesthesia in swine.Acid/base parameters, blood oxygen tension, plasma Na, K, Ca and stress hormone concentrations were monitored in Yorkshire swine before, during, and for 10 min after the animals were descended for 1 min into 80% CO2 in air.Severe respiratory acidosis (Paco2˜ 50 kPa, arterial pH ˜ 6.6) and hypoxia (Pao2˜ 4 kPa) had developed after 45 s of the CO2 inhalation. The corresponding changes in venous blood were less drastic (PvCO2˜ 17 kPa, pH 7.1, Pvo2˜ 4 kPa). Readjustment to PaCO2˜ 11 kPa, arterial pH 7.2, and Pao2˜ 13 kPa had occurred at 1 min post CO2. Four minutes later the respiratory acidosis had become converted into metabolic acidosis subjected to partial respiratory compensation (arterial pH 7.3 in the presence of moderate hypocapnia and hyperoxaemia). The cause of this metabolic acidosis (present also at 10 min post CO2) was apparently hypoxia‐induced anaerobic metabolism (= lactic acid production). Apparently due to hydrogen ion transport into the cells in exchange for other cations, hyperkalaemia (K˜ 6.6 mmol 1‐l), and a 7 mmol 1‐1 increase in plasma Na had developed at 1.5 min later. The CO2 inhalation did not change the total plasma Ca significantly.The transport of the swine from the stable to the immediate pre‐experimental situation induced a 3‐fold increase in plasma Cortisol concentration (PC, to ˜ 130 mmol 1‐1). No further increase in PC occurred in response to the CO2 inhalation. It indicates that no additional emotional strain was imposed upon the animals during the CO2 exposure. Another possibility is that a maximal secretion of Cortisol was here reached already before the descent into the CO2.The transport procedure caused only minor increases in plasma adrenalin (A) and noradrenaline (NA). However, during the CO2 exposure plasma A and NA exhibited 15‐ and 50‐fold rises, respectively (to 3.5 and 22 mmol l‐1, respectively). The main cause of the A/NA elevation seems to have been the severe respiratory acidosis.
Peak torque and OBLA running capacity in male orienteers
Authors: JOHANSSON C. , LORENTZON R. , RASMUSON S. , REIZ S. , HAGGMARK S. , NYMAN H. , FUGL‐MEYER A. R. 
Published: December 2008

The isokinetic (30, 60, 120 and 1800 s‐1) peak torque of m. quadriceps femoris and m. triceps surae, and the running velocity at the onset of blood lactate accumulation (V0BLa) were determined at three different occasions (November, April and September) during a year in 15 male elite orienteers. The amount and type of training for each individual was also registered.At the first test (November) there was no significant intra‐individual correlation between peak torque of m. quadriceps and m. triceps surae. A negative correlation was found between V0BLA and peak torque of m. quadriceps at the lower velocities of angular motion, but not at the higher. The peak torque of m. triceps surae increased during the training period and decreased during the competition period back to the original level. Over the whole year the peak torque of m. quadriceps increased while no changes could be demonstrated within the two periods of the study. The running velocity at the onset of blood lactate accumulation increased during both training and competition periods. The changes in V0BLawere negatively associated with the changes in peak torque of m. quadriceps at 1800 s‐1 during the training period. During the competition period the changes in VOBLA were, for the majority of the orienteers, negatively correlated to the ratio of quality: quantity running, i.e. to a high content of forest running.
Optimal and actual end systolic pressure‐volume relations in dogs and rabbits. Including new method of Emax determination
Authors: PIENE H. , MYHRE E. S. P. , WINNEM B. 
Published: December 2008

Under the assumption that a ventricle and its arterial load are normally matched according to work optimization, a relation between left ventricular (LV) mechanical performance as described by the slope (Emax) of the end systolic pressure‐volume relationship (ESPVR), mean systolic pressure during ejection (mSLVP), and stroke volume (SV), is proposed: optimum Emax=E=mSLVP/SV.Slope (Emax) was obtained, in 6 dogs and 9 rabbits, by establishing relations among ejected volume and LV diameter squared (D2) in control beats, and among pressure and D2 at end systole (ES) in series of beats of varying load, accomplished either by acute aortic constriction (AOC) or inferior caval occlusion (IVCO). Slope in dogs was also obtained by direct measurements of ventricular volume by a conductance catheter and the results were compared with the above method. A dimensionless index, α= Emsx/E', (optimal value = 1.0) was calculated to indicate how well the ventricle and arterial system were matched. In dogs, E= 10.9 ± 2.1 mmHg ml‐1, Emax= 8.1 ± 2.6 (AOC) and 7.1 ± 2.5 (IVCO), hence α= 0.79 ± 0.23 (AOC) and 0.68 ± 0.15 (IVCO). In rabbits, E= 54.1 ± 20.0 mmHg ml‐1, Emax= 64.8 ± 15.9 (mmHg ml‐1), hence a = 1.23 ± 0.33. α=1.0 fell outside the 95% confidence interval only in experiments of dogs subjected to IVCO.
The release mechanism for atrial natriuretic factor during blood volume expansion and tachycardia in dogs
Authors: CHRISTENSEN G. , ILEBEKK A. , AAKESON I. , KIIL F. 
Published: December 2008

Atrial natriuretic factor (ANF) is released during blood volume expansion and tachycardia, but only blood volumer expansion causes atrial distension, which presumably promotes ANF release. Our study was undertaken to search for a common release mechanism. In five anaesthetized, closed‐chest dogs, plasma immunoreactive (IR) ANF was measured at three levels of blood volume, which were obtained by infusing a Ringer's solution. At each level of blood volume, plasma IR‐ANF was measured at three pacing frequencies. Plasma IR‐ANF increased as mean right atrial pressure (mRAP) was raised from 2 to 10 mmHg by volume expansion, whereas pacing tachycardia (at heart rates (HR) 50 ± 3 and 98 ± 1 beats min‐1 above control) at each level of blood volume expansion increased plasma IR‐ANF and systolic RAP (sRAP) at constant mRAP. Plasma IR‐ANF was more strongly correlated to sRAP (r= 0.83) than to mRAP (r = 0.69), but the product sRAP x HR had the highest correlation coefficient (Y= 0.86). According to the multiple regression equation:plasma IR‐ANF = k1+ k2 mRAP + k3 sRAP + k4 sRAP × HR, the product sRAP × HR had the highest coefficient of determination (r2= 0.75) and was the only significant determinant. We conclude that atrial tension or stress, developing during each atrial systole, is an important determinant of ANF release. Since atrial diastolic and systolic dimensions do not increase during pacing tachycardia, ANF release is not dependent on atrial distension.