bluuebunny/crossref_metadata_2025 huggingface dataset:
Energy metabolism in type I and type II human muscle fibres during short term electrical stimulation at different frequencies
Authors: SODERLUND K. , GREENHAFF P. L. , HULTMAN E.
Published: December 2008

The degradation of adenosine triphosphate, phosphocreatine and glycogen was determined in type I and type II fibres of the human quadriceps femoris muscle during intermittent electrical stimulation at 20 and 50 Hz, (1.6 seconds stimulation, 1.6 seconds rest). Seven healthy volunteers took part in the study. Muscle biopsy samples were obtained at rest and after 10 and 20 seconds of stimulation (six and 12 contractions, respectively). The resting contents of adenosine triphosphate, phosphocreatine and glycogen were all higher (P < 0.05) in type II fibres compared to type I fibres. By the end of stimulation, whole muscle force production had declined to 84 and 77% of the initial force at 20 and 50 Hz, respectively. The phosphocreatine degradation rate after 10 and 20 seconds of stimulation was greater in type II fibres (P < 0.05) compared to type I fibres at both 20 and 50 Hz. The rates of glycogenolysis after 20 seconds stimulation in type II fibres were 3.18±1.1 and 6.31±1.39mmol glycosyl units kg‐1 s‐1. The corresponding rates in type I fibres were 0.46 ± 0.73 and 0.60 ± 0.39 mmol glycosyl units kg‐1 s‐1 which were not significantly different from zero. It is hypothesized that the decline in whole muscle force observed during electrical stimulation may be a consequence of the rapid loss of PCr stores in type II fibres.
Myocardial lactate extraction and release at rest and during heavy exercise in healthy men
Authors: KAIJSER L. , BERGLUND B.
Published: December 2008

The relationship between myocardial lactate extraction and blood lactate concentration and the possibility that simultaneous uptake and release of lactate occur in the normal human heart was investigated by measuring arterial‐coronary sinus differences of lactate and of labelled lactate during infusion of 14C lactate in 13 healthy young male volunteers. Measurements were done at rest, during increased cardiac work with unaltered arterial lactate concentration achieved by atrial pacing and during increased cardiac work and increased arterial lactate concentration achieved by supine cycle ergometer exercise. There was on no occasion a significant difference in 14C lactate specific activity between arterial and coronary sinus blood, i.e. no significant admixture of non‐labelled lactate occurred in the coronary sinus indicating that on no occasion was there any sign of lactate release. The myocardial extraction of lactate seemed to be a linear function of arterial lactate concentration. During exercise with an arterial lactate concentration of 6 mmol l‐1 and above, lactate could have covered approximately 75–100% of the oxidative metabolism. Thus, during short‐term heavy work myocardial lactate extraction dominates over other substrates (mainly free fatty acids and glucose) taken up by the heart, and used for oxidation by the heart muscle cells.
Adenosine receptor‐induced cAMP changes in D384 astrocytoma cells and the effect of bradykinin thereon
Authors: ALTIOK N. , BALMFORTH A. J. , FREDHOLM B. B.
Published: December 2008

In human D384 astrocytoma cells, cyclic AMP accumulation can be conveniently studied after labelling of the adenosine triphosphate pool (15 fmol cell‐1) with [3H]adenine. In this study, adenosine had a biphasic effect on cyclic AMP accumulation, which was scarcely altered by blocking adenosine uptake and metabolism. Low concentrations of adenosine led to an inhibition of cyclic AMP accumulation, and higher concentrations led to stimulation. No effect of adenosine on cyclic AMP was observed unless phosphodiesterase was inhibited by rolipram.

The A1receptor antagonist DPCPX attenuated the inhibitory phase of adenosine response, and enhanced the cyclic AMP accumulation induced by adenosine analogues. The cyclic AMP accumulation was stimulated by NECA > ADO > CGS 21680 > CV 1808 > CPA ≥ CHA, indicating mediation by A, receptors. The stimulatory effect of NECA was much more effectively blocked by the combined A1and A2receptor antagonist CGS 15943 (KB4 nmol I‐1) than by theA1antagonist DPCPX (KB110 nmol 1‐l). Treatment of the cells with pertussis toxin (0.2 μgml‐1for 2.5 h) potentiated the cyclic AMP response to adenosine analogues significantly. The cyclic AMP response to NECA was enhanced by the protein kinase C activator phorbol dibutyrate even after pertussis toxin treatment. By contrast, nanomolar concentrations of bradykinin, which increases Ca2+‐levels and protein kinase C activity in D384 cells, reduced NECA‐induced cyclic AMP accumulation in control and pertussis toxin‐treated cells.

Thus, D384 cells possess both A1and A2adenosine receptors influencing cyclic AMP in opposite directions. A2receptor‐mediated cyclic AMP accumulation can be stimulated by activating protein kinase C and inhibited by raising Ca2+. Neither the effects of protein kinase C activation nor those of bradykinin required pertussis toxin‐sensitive G‐proteins.
Intracerebroventricular immunization with TRH‐antiserum lowers blood pressure in spontaneously hypertensive rats
Authors: NURMINEN M.‐L.
Published: December 2008

Centrally administered thyrotropin‐releasing hormone exerts a well documented hypertensive effect. In this study, the possible physiological role of thyrotropin‐releasing hormone in the central cardiovascular regulation was evaluated in spontaneously hypertensive rats receiving long‐term (8–14 days) intracerebroventricular infusion of a heterologous antiserum to thyrotropin‐releasing hormone. The effect of this passive immunization on the blood pressure was monitored from conscious animals by the tail‐cuff method. Thyrotropin‐releasing hormone antiserum significantly decreased the systolic arterial pressure in adult rats with established hypertension. No alterations in serum thyroid hormone status were observed indicating that the antihypertensive effect of immunological blockade of thyrotropin‐releasing hormone was not due to changes in the serum thyroid hormone levels. These results provide evidence for a role of endogenous brain thyrotropin‐releasing hormone in the maintenance of hypertension in spontaneously hypertensive rats.
Plasma ANP during hypertonic NaCl infusion in man
Authors: ARJAMAA O. , KARLQVIST K. , KANERVO A. , VAINIONPÄÄ V. , VUOLTEENAHO O. , LEPPÄLUOTO J.
Published: December 2008

To determine the relationship between hyperosmolality and immunoreactive atrial natriuretic peptide of heart atrial plasma six healthy men were given 0.06 ml kg‐1 min‐1 855 mmol 1‐1 NaCI, i.v., for 2 h. The right atrial pressure and atrial plasma atrial natriuretic peptide were measured. During the infusion, right atrial pressure was kept constant by lowering the legs of the subject in a supine position downwards if any increase in the pressure was seen. There was a significant and linear increase in atrial serum osmolality, from 288 ± 3.3 to 307 ± 3.2mOsm kg‐l (P < 0.001). No statistically significant changes in right atrial pressure were seen. Regression analysis revealed that there was a statistically significant correlation between serum osmolality and plasma ANP in three subjects (responders) (r2: 0.5241, 0.8965, 0.6695). In three other subjects (nonresponders), there was no correlation between osmolality and ANP. The mean basal osmolality of responders was 280 mOsm kg‐1 and the mean basal osmolality of nonresponders was 295 mOsm kg‐1. In contrast, all subjects responded with an increase in plasma ANP (P < 0.05) after RAP had been increased by tilting the legs of the subject upwards for 30 min.

We conclude that the right atrial pressure regulates the release of atrial natriuretic peptide. Serum hyperosmolality may also contribute to the the regulation of atrial natriuretic peptide independently of the right atrial pressure in man.
Alternative spinal, somatosensory pathways investigated with the tactile orienting reaction in the cat
Authors: DANIELSSON I.
Published: December 2008

Previous results indicated the possibility of abolishing the orienting reaction to light tactile stimulation of specific areas below lesions encompassing three sectors of the transverse spinal plane, if all sectors were transected simultaneously. Hence presumably interrupting three different ascending pathways. Two sectors corresponded to the sites of the well known, somatosensory, dorsal column and spino‐cervical pathways. Single stage lesion technique now has been used to pinpoint the site of the third pathway.

Immediate orienting reactions to both sides were seen before surgery. The orienting reactions remained postoperatively to stimuli applied on the hind limb contralateral to the dorsal column and the spino‐cervical lesions. When the hind limb ipsilateral to the dorsal column and the spino‐cervical lesions was stimulated five cats showed an absence of orienting reactions. The cats' lesions included the dorsal column and the spino‐cervical on one side and the border area between the lateral and ventral funiculi on the other side of the cord. The remaining cats showed either partial or no deficiency of the orienting reactions. These cats' spinal lesions spared the area between the ventral and lateral funiculi.

The findings show the possibility of abolishing the tactile orienting reactions from one hind limb with single stage lesions, which include the dorsal column and the spino‐cervical pathway on one side, and a pathway located in the border area between the contralateral lateral, and ventral funiculi. This site corresponds to the morphological position of ascending spino‐mesencephalic and/or spino‐thalamic fibres. Consequently, all of these pathways might provide alternative routes for information about the place of tactile stimuli, which may evoke orienting reactions.
Response characteristics of tooth pulp‐driven postsynaptic neurons in the spinal trigeminal subnucleus oralis of the cat
Authors: HUOPANIEMI T. , JYVÄSJÄRVI E. , CARLSON S. , LINDROOS F. , PERTOVAARA A.
Published: December 2008

Neuronal activity in the spinal trigeminal subnucleus oralis in response to electrical tooth stimulation was recorded in the anaesthetized cat in order to compare the eiectrophysiological characteristics of the oralis neurons with those of subnucleus caudalis and interpolaris neurons recorded in previous studies. The most sensitive oralis neurons had lower thresholds and shorter latencies than the most sensitive caudalis and interpolaris neurons. The thresholds of the oralis neurons were lower and their strength‐duration curves flatter than those depicting liminal dental pain in man but similar to those depicting liminal jaw reflexes in the cat. Noxious conditioning stimulus elevated the threshold of only 1 of 10 neurons tested. The converging input from the skin and oral mucosa was from low‐threshold mechanoreceptors. The results indicate that the response properties of the subnucleus oralis neurons differ significantly from those of other spinal subnuclei. Human pain thresholds cannot be explained by the liminal response properties of oralis neurons. These neurons might be important in the mediation of liminal reflex events evoked by dental stimuli.
Sodium‐dependent regulation of sodium, potassium‐adenosine‐tri‐phosphatase (Na+, K+‐ATPase) activity in medullary thick ascending limb of Henle segments. Effect of cyclic‐adenosine‐monophosphate guanosine‐nucleotide‐binding‐protein activity and arginine vasopressin
Authors: FRYCKSTEDT J. , APERIA A.
Published: December 2008

This study examine the regulation Na+, K+‐ATPase activity in the medullary thick ascending limb of Henle Na+, K+‐ATPase activity was determined in medullary thick ascending limb of Henle (mtal) segments dissected from rat kidneys. The sodium concentration in the medium (Na,) was 20 or 70 mM. Since the segments were permeabilized, intracellular Na+ (Na,) was assumed to be the same as Na2. Dibuturyl cyclic adenosine monophosphate (dbcAMP) and forskolin inhibited Na+, K+‐ATPase activity independently of Nam. Arginine vasopressin (AVP) receptors coupled to adenylate cyclase have been identified in the medullary thick ascending limb of Henle. At Nam= 20 mMAVP caused a dose‐dependent inhibition of Na+, K+‐ATPase activity with a maximal effect (49%) at 10‐8 m. This inhibition was abolished in the presence of the adenylate cyclase inhibitor 2,5‐dideoxyadenosine (2, 5‐DDA). AVP had no effect on Na+, K+‐ATPase activity in the mTAL at Nam= 70 mM. The guanosine‐diphosphate analogue GDPβS inhibited Na+, K+‐ATPase activity at Nam= 70 mM but not at Nam= 20 mM.

We conclude that increased cyclic adenosine monophosphate (CAMP) levels inhibit Na+, K+, ATPase activity in mTAL. AVP can, depending on Na2 produce this effect by adenylate cyclase activation. The guanonine nucleotide binding protein G‐protein might be the site of Na+‐dependence.
Captopril and time dependent changes in post‐ to pre‐glomerular resistance ratios in remnant kidneys of pre‐hypertensive rats
Authors: WILKE W. LEE , PERSSON A. E. G.
Published: December 2008

Wilke, W. Lee & Person, A. E. G. 1992. Captopril and time dependent changes in post‐ to pre‐glomerular resistance ratios in remnant kidneys of pre‐hypertensive rats. Acta Physiol Scand144, 253–261. Received 26 June 1991, accepted 8 October 1991. ISSN 0001–6772. Department of Physiology, Colorado State University, Fort Collins, Colorado, USA and Department of Physiology and Biophysics, University of Lund, Sweden.

Micropuncture experiments were performed on intact and remnant kidneys of male Sprague‐Dawley rats before and after angiotensin converting enzyme inhibition with captopril (0.5 mg kg‐1 iv). Partially nephrectomized rats were studied at 2 and 8 weeks post‐surgery before the development of systemic hypertension. At 2 weeks, nephrectomized rats had a numerically higher tubular stop‐flow pressure than controls (43 ± 2 mmHg vs. 38 ± 2 mmHg; P = 0.08) and a higher post‐ to pre‐glomerular resistance ratio (Re/Ra) (0.40 ± 0.03 vs. 0.31± 0.03; P = 0.08). At 8 weeks, stop‐flow pressure and post‐ to pre‐glomerular resistance ratios were similar in remnant and intact kidneys. Captopril had no effect on stop‐flow pressure in 2 week post‐surgery nephrectomized rats or either control group, but it increased stop‐flow pressure in 8 week post‐surgery nephrectomized rats (40 ± 2 to 44 ± 2 mmHg, P= 0.04). This increase in stop‐flow pressure was associated with an increase in the post‐ to pre‐glomerular resistance ratio (0.33 ± 0.02–0.42 ±0.02, P = 0.009). Stop‐flow pressure was positively correlated with the post‐ to pre‐glomerular resistance ratio in 2‐week post‐surgery nephrectomized rats and their respective controls when combined (r = 0.89, P= 0.0001) and 8‐week post‐surgery nephrectomized rats and their respective controls combined (r= 0.78, P = 0.0001). Stop‐flow pressure was not significantly correlated with mean arterial pressures or welling‐point pressures in these groups. We conclude that stop‐flow pressure in remnant kidneys of pre‐hypertensive rats is primarily determined by the post‐ to pre‐glomerular resistance ratio, and increases in stop‐flow pressure and post‐ to pre‐glomerular resistance ratios in remnant kidneys are transient in the absence of systemic hypertension. The role of the renin‐angiotensin system in determining the ratio and stop‐flow pressure is dependent on time post‐nephrectomy. Captopril‐induced increases in stop‐flow pressure and post‐ to pre‐glomerular resistance ratio at 8 weeks, suggests that its primary effect at that time is not a preferential post‐gIomerular vasodilation subsequent to reductions in intrarenal angiotensin II.
Dopamine receptor blockade and synthesis inhibition during exaggerated natriuresis in spontaneously hypertensive rats
Authors: HANSELL P. , SJÖQUIST M.
Published: December 2008

Hansell, P. & Sjöquist, M. 1992. Dopamine receptor blockade and synthesis inhibition during exaggerated natriuresis in spontaneously hypertensive rats. Acta Physiol Scand 144, 269–276. Received 21 September 1990, accepted 11 October 1991. ISSN 0001–6772. Department of Physiology and Medical Biophysics, Biomedical Centre, University of Uppsala, Sweden.

The influence of dopamine receptor blockade and synthesis inhibition on natriuresis induced by isotonic saline volume expansion was investigated in anaesthetized spontaneously hypertensive rats and normotensive Wistar‐Kyoto rats. The aim of the study was to elucidate the mechanisms underlying the phenomenon of exaggerated natriuresis during volume expansion that has been observed in spontaneously hypertensive rats. Volume expansion, at 5 % of body weight, resulted in a larger and faster natriuretic response in spontaneously hypertensive rats than in Wistar‐Kyoto rats. Sixty minutes after commencement of volume expansion the natriuretic response (accumulated sodium excretion) in Wistar‐Kyoto rats (n = 8) was only 24% of that in spontaneously hypertensive rats (n = 17). When spontaneously hypertensive rats were pretreated with the dopamine receptor blockers haloperidol (n= 14, 1 mg kg‐1), SCH23390 (n = 8, 30 μg h‐1 kg‐1) or the dopamine synthesis inhibitor benserazide (n= 8, 50 mg kg‐1; n = 5, 100 mg kg‐1), the natriuretic response to volume expansion was only 16, 35, 59 and 42%, respectively, of that in untreated SHR. The corresponding proportion in the haloperidol‐treated (n= 8) compared with untreated Wistar‐Kyoto rats was 22%.

In conclusion, isotonic volume loading results in more pronounced natriuresis in spontaneously hypertensive than in Wistar‐Kyoto rats. Dopamine receptor blockade and synthesis inhibition attenuate the expansion of exaggerated natriuresis in spontaneously hypertensive rats and reduces the volume expansion natriuresis in Wistar‐Kyoto rats, indicating that the dopamine system plays an important role.
Characteristics of the carotid baroreflex in man during normal and flow‐restricted exercise
Authors: EIKEN O. , CONVERTINO V. A. , DOERR D. F. , DUDLEY G. A. , MORARIU G. , MEKJAVIC I. B.
Published: December 2008

EIKEN, O., CONVERTINO, V. A., DOERR, D. F., DUDLEY, G. A., MORARIU, G. & Mekjavic; I. B. 1992. Characteristics of the carotid baroreflex in man during normal and flow‐restricted exercise. Acta Physiol Scand144, 325–331. Received 27 May 1991, accepted 29 October 1991. ISSN 0001–6772. School of Kinesiology, Simon Fraser University, Burnaby, B.C., Canada.

Eight subjects were studied in the supine position at rest, during normal dynamic leg exercise (control exercise) and with blood‐flow restriction in the working legs (flow‐restricted exercise). Graded muscle blood‐flow restriction was accomplished by applying a supra‐atmospheric pressure of 50 mmHg to the working legs. During incremental‐load exercise, flow restriction reduced exercise performance and peak heart rate by 36% and 13%, respectively. The function of the cardiac branch of the carotid baroreflex was studied over its full operational range, at rest and during constant‐load control and flow‐restricted exercise, by measuring R‐R intervals during application of pulse‐synchronous graded pressures (40 to ‐65 mmHg) in a neck‐chamber device. Heart rate and arterial pressure were higher during flow‐restricted than control exercise, indicating that the flow restriction activated the muscle chemoreflex. Raising the carotid transmural pressure (systolic arterial pressure minus neck‐chamber pressure) was accompanied by increasing R‐R intervals in all conditions. The set point (point of baseline carotid transmural pressure and R‐R interval) coincided with the midportion of the pressure‐response curve at rest and with the threshold point of the curve during exercise. The maximal rate of change in relative R‐R intervals and the corresponding carotid transmural pressure range were higher during control exercise than at rest and highest during flow‐restricted exercise, indicating that exercise and especially flow‐restricted exercise increased carotid baroflex sensitivity, and shifted the carotid baroreflex optimal buffering range to higher pressures. The results suggest that the carotid baroflex attenuates exercise heart rate increases mediated by the muscle chemoreflex and/or by central command.
Influence of impulse pattern on noradrenaline release from sympathetic nerves in cerebral and some peripheral vessels
Authors: HARDEBO J. E.
Published: December 2008

Hardebo, J. E. 1992. Influence of impulse pattern on noradrenaline release from sympathetic nerves in cerebral and some peripheral vessels. Acta Physiol Scand144, 333–339. Received 18 June, accepted 7 November 1991. ISSN 0001–6772. Departments of Medical Cell research and Neurology, University of Lund, Lund, Sweden.

Earlier findings suggested that the physiological firing rate in sympathetic nerves did not exceed 10 Hz. Later recordings have revealed that this is a net value: impulses are usually not continuous but occur in bursts of high frequencies separated by quiet periods. The effects of continuous and burst‐like neurogenic activation in various isolated blood vessels were compared. In the first part of the study changes in vascular tone were registered. Electrical field stimulatory parameters were chosen to give tetrodotoxin‐blockable, neurogenic responses. From dose‐response experiments in rat caudal artery a net frequency of 6 Hz was chosen, for bursts usually designed as 30 Hz during 0.2 s followed by a quiet period of 0.8 s. In the rabbit ear artery the neurogenic contraction was enhanced by a mean of near 50% during stimulation with bursts. Now appeared a minor phentolamine‐resistant portion, which was nor due to release of NPY, 5–HT, histamine or ATP. Also in the rat caudal artery and monkey pial artery a significant enhancement of contraction was seen during burst stimulation, whereas in the rabbit facial vein no significant difference in dilatation through β‐receptor activation was obtained. In vessels that do not normally respond with purely neurogenic contractions/dilatations during continuous stimulation, like pial arteries from the rat and rabbit, not even bursts revealed a neurogenic response. In a second series of experiments the influence of continuous and burst‐like nerve activation on the release of [14C]noradrenaline was studied in monkey, rabbit and rat pial arteries, rat caudal artery and rabbit central ear artery and facial vein. In all vessels except rabbit pial artery a significantly higher release was obtained with burst‐like compared to continuous stimulation.
Calcium fluxes in rat thyroid FRTL‐5 cells. Evidence for a functional Na+/Ca2+ exchange mechanism
Authors: TÖRNQUIST K.
Published: December 2008

Törnquist, K. 1992. Calcium fluxes in rat thyroid FRTL‐5 cells. Evidence for a functional Na+/Ca2+ exchange mechanism. Acta Physzol Scand144, 341–348. Received 28 April 1991, accepted 30 October 1991. ISSN 0001–6772. Endocrine Research Laboratory, University of Helsinki, Minerva Foundation Institute for Medical Research, Helsinki, Finland.

The effect of extracellular Na+ on cytosolic free Ca2+ and on influx and efflux of Ca2+ was investigated in FRTL‐5 thyroid cells. Stimulating the cells with the purinergic agonist ATP induced a rapid efflux of 45Ca2+ from cells loaded with 4aCa2+. Replacement of extracellular Na+ with choline+, significantly decreased the adenosine triphosphate‐induced efflux of 45Ca2+. Furthermore, adenosine triphosphate‐induced uptake of 45Ca2+ was increased when extracellular Na+ was replaced with choline+, compared with the uptake seen in Na+ buffer. Replacing extracellular Na+ with choline+, increased resting levels of cytosolic free Ca2+ from 50 ± 2 nM (mean ± SE) to 81 ± 3 nM (P < 0.05) in Fura 2 loaded cells. In cells preincubated with 1 mM ouabain for 30 min, resting cytosolic free Ca2+ increased to 73 ± 3 nM (P < 0.05). In a Na+ buffer, the adenosine triphosphate‐induced transient increase in cytosolic free Ca2+ was 872 ± 59 nM, compared with 1070 ±63 nM in choline' buffer (P < 0.05). The plateau level of cytosolic free Ca2+ in response to adenosine triphosphate was 130±16 nM in Na+ buffer, compared with 209±9 nM in choline+ buffer (P < 0.05). Readdition of Na+ to the plateau phase decreased cytosolic free Ca+2 to 152 ± 5 nM. Stimulating the cells with 10 μM of the Na+‐selective monovalent ionophore monensin increased cytosolic free Ca2+ from 53 ± 9 nM to 12416 nM (P < 0.05). This increase in cytosolic free Ca2+ was dependent on both extracellular Na+ and extracellular Ca2+ If cells were first stimulated with monensin, and then with adenosine triphosphate, the transient increase in cytosolic free Ca2+ was 1027 ± 24 nM (P < 0.05, compared with control cells). The results thus indicate, that FRTL‐5 cells have a functional Na+/Ca2+ exchange mechanism and that this mechanism is of importance in restoring adenosine triphosphate‐induced transient increase in cytosolic free Ca2+ to resting cytosolic free Ca2+ levels.
The polycationic compound gentamicin inhibits the calcium paradox in guinea‐pig hearts
Authors: GÖDICKE J. , JACOBSEN L. , LÜLLMANN H. , MÜLDER G.
Published: December 2008

Gödicke, J., Jacobsen, L., Lüllmann, H. & Mülder, G. 1992. The polycationic compound gentamicin inhibits the calcium paradox in guinea‐pig hearts. Acta Physiol Scand144, 349–354. Received 2 July 1991, accepted 13 October 1991. ISSN 0001–6772. Department of Pharmacology, University of Kiel, Germany.

The polycationic drug gentamicin and two calcium antagonists were studied with respect to their protecting action against the calcium paradox in perfused guinea‐pig hearts. Besides the mechanograms the release of creatine kinase was recorded; in parallel experiments the Na+‐content of the hearts was measured before and at the end of the Ca2+lack period, and during re‐exposure to normal [Ca2+]0. The calcium paradox was induced by perfusion, for 50 s, with Ca2+‐free solution containing EGTA (3 × 10‐4 m). Nifedipine and verapamil in concentrations which reduced the equilibrium contractile force by 50%, only mitigated the extent of the calcium paradox, whereas gentamicin applied in a concentration also reducing the contractile amplitude by 50% was able to suppress the calcium paradox completely. The doseresponse curves for nifedipine, with respect to the reduction of contractile force and contracture, were identical. In contrast, gentamicin was more effective in attenuating the contracture of the paradox than in reducing the equilibrium contractile force. The large gain of Na+ during the Ca2+‐lack period was diminished by both nifedipine and gentamicin. The partial protection of calcium antagonists can be related to their interference with the uptake of Na+ through L‐type Ca2+‐channels during the Ca2+‐lack period, whereas gentamicin seems to act by an additional inhibition of the Na/Ca exchange during the re‐exposure to normal [Ca2+]0.
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, Sweden

The 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.
Myocardial potassium balance associated with regional ischaemia in the pig: effects of β‐adrenoceptor blockade, duration of ischaemia and preceding ischaemic periods
Authors: AKSNES G. , KIRKEBØEN K. A. , LANDE K. , ILEBEKK A.
Published: December 2008

The effects of β‐adrenoceptor blockade, duration of ischaemia and preceding ischaemic periods on ischaemia‐induced changes in myocardial K+balance were studied in 12 open‐chest pigs. Coronary venous blood was directed through a shunt from the coronary sinus to the right atrium. Continuous recordings of arterial, shunt blood [K+] and shunt flow enabled us to compute myocardial K+balance during and after consecutive 2‐, 2‐, 5‐, 10‐ and 2‐min periods of regional ischaemia separated by 30 min of reperfusion. β‐adrenoceptor blockade (propranolol 1 mg kg‐1i.v.) given between the first and second ischaemic period did not alter the effects of 2 min ischaemia on myocardial K+balance. Total K+losses induced by 2, 5 and 10 min of ischaemia were 67.1 (40.6–93.3), 106.7 (69.4–176.8) and 192.2 (117.7–332.6) μmol 100 g‐1respectively. Thus, the plateau observed in extracellular [K+] between 2 and 10 min of regional ischaemia could, at least partly, be explained by continuous drainage of K+from ischaemic myocardium into the surrounding normally perfused tissue. The total K+loss induced by the second and last 2‐min ischaemic period were 67.1 (40.6–93.3) and 35.6 (23.1–53.6) μmol 100 g‐1(P < 0.001), respectively. This reduction shows that ion homeostasis during ischaemia was greatly changed in myocardium which had been ‘preconditioned’ and ‘stunned’ by 5 plus 10 min of ischaemia. Total amount, maximal rate and duration of post‐ischaemic K+reuptake increased with the duration of the preceding ischaemia. Moreover, K+re‐uptake after 2 min of ischaemia and the number of sarcolemmal Na/K pumps ([3H]ouabain binding), were normal in stunned myocardium. From these observations we conclude that progressive stimulation of the Na/K‐pump occurred when ischaemia was prolonged from 2 to 10 min, and that Na/K‐pump function was preserved in stunned myocardium.
Water intake and its thermal energy cost in reindeer fed lichen or various protein rations during winter
Authors: SOPPELA P. , NIEMINEN M. , SAARELA S.
Published: December 2008

Captive reindeer were fed four different rations which supplied equal energy but varying amount of crude protein: lichens (3%), mixed hay plus lichens (10%) and two feed concentrates with medium (12%) or high (18%) protein content. Kinetics of total body water were measured with tritiated water from February to March 1985, and thermal energy cost of daily water intake was estimated. Biological half‐time of water was shorter, and daily water intake significantly higher on the hay plus lichens diet and on the medium‐ or high‐protein concentrates diet than on the lichens diet during March 1985. Similar differences were found between reindeer on medium‐protein concentrate and on lichens at the end of the corresponding feeding period during April 1986. Daily water inflow was positively correlated with a dietary supply of digestible crude protein (r = 0.916). Thermal energy costs of daily water intake were highest 1.9 MJ (3.7 1‐1) in reindeer on high‐protein concentrate during March 1985, and 2.0 MJ (3.91‐1) in reindeer on medium‐protein concentrate during April 1986. The reindeer fed on lichens had minimal and nearly twice as small thermal energy cost of daily water intake (mean 1.1 MJ 2.11‐1) as on either of the concentrates. Our results show that even a moderate feed protein ration can significantly increase free water intake and its thermal energy cost in reindeer as compared to dominant natural feed (lichens) during winter. Careful protein supplementation is recommended to support body condition with a concomitant addition of easily soluble carbohydrates to compensate for increased thermal costs of water intake.
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.
Effects of ischaemic training on local aerobic muscle performance in man
Authors: SUNDBERG C. J. , EIKEN O. , NYGREN A. , KAIJSER L.
Published: December 2008

The aim of the study was to compare the effects of ischaemic and non‐ischaemic training on aerobic performance. In 10 subjects, peak oxygen uptake (peak VO 2) and time to fatigue (TTF) for one‐legged exercise were measured before and after 4 weeks (4 times week‐1) of one‐legged training. Each training session started with one leg training for 45 min with 20% blood‐flow reduction induced by local application of a supra‐atmospheric external pressure of 50 mmHg (ischaemic leg; I‐leg). We have previously shown that this decreases leg blood flow by about 20%. The contralateral leg (nonrestricted‐flow leg; N‐leg), serving as a control, then trained with an identical power‐output profile for 45 min but without flow restriction. In the I‐leg the average training‐induced increments in TTF and peak VO 2 were 27 and 24%, respectively. In the N‐trained leg TTF and peak‐VO 2 increased 10 and 14%, respectively. Both increments were significantly greater (P < 0.05) in the I‐trained leg. Moreover, the performance increase in the I‐trained leg was exaggerated (P < 0.05) in the ischaemic test condition, i.e. there was a specificity in the training response. In conclusion, ischaemia acts as an additive stimulus to training leading to an exaggerated increase in endurance and peak‐VO2 compared to identical training without blood‐flow restriction. The main explanation is probably an enhanced local adaptation in the I‐trained leg.
Glutathione metabolism in skeletal muscle derived cells of the L6 line
Authors: SEN C. K. , RAHKILA P. , HÄNNINEN O.
Published: December 2008

Skeletal muscle derived L6 myoblasts possess a considerably high resting total glutathione (TGSH) pool. Exposure to l‐buthionine‐[S,R]‐sulphoximine resulted in a 90% depletion of the intracellular TGSH pool. All the key enzymes of glutathione metabolism, especially glutathione S‐transferase, were observed to be considerably active in the undifferentiated cells. Se‐dependent glutathione peroxidase activity appeared to account for most of the total GSH peroxidase activity of the cells. A significant contribution of γ‐glutamyl transpeptidase‐independent (5 mm acivicin insensitive) mechanism to the extracellular GSH uptake capacity of the muscle cells was evident. Efflux of oxidized glutathione from the cells exposed to t‐butyl hydroperoxide was rapid and appeared to be energy linked.
The influence of high salt intake on intestinal Na,K‐ATPase in Wistar and Dahl rats
Authors: PÁCHA J. , POHLOVÁ I.
Published: December 2008

The Na,K‐ATPase of intestinal mucosa was compared in Wistar (W), salt‐sensitive (DS) and salt‐resistant (DR) Dahl rats fed a low‐salt (LS) and high‐salt (HS) diet. ATPase activity and the kinetics of its activation by Na+were determined in three intestinal segments (jejunum, ileum, distal colon). There were demonstrated only small differences in the affinity for Na+among the strains studied but we found a considerable profile of Na,K‐ATPase activity along the intestine in all strains; the activity was higher in jejunum and lower in ileum and distal colon. Chronic salt loading decreased the affinity of Na,K‐ATPase for Na+but had no effect on Vmax. The changes in salt intake were accompanied by different response of plasma aldosterone in particular strains. According to the stimulation of aldosterone level by LS diet the sensitivity of the strains was DR > W > DS. HS diet suppressed aldosterone level to similar values in all strains. The data indicate that the kinetics of intestinal Na,K‐ATPase and its response to HS intake is independent of the genotype of the rats.