bluuebunny/crossref_metadata_2025_split huggingface dataset:
Upper and lower bounds on capillary permeability ratios of Cr‐EDTA to cyanocobalamine in rat hindquarters
Authors: HARALDSSON B. , RIPPE B. 
Published: December 2008

The single injection indicator dilution technique, often used for assessing capillary permeability, was employed for estimations of the equivalent pore radius of skeletal muscle microvessels according to the theory of restricted diffusion. There are, however, certain important sources of error that must be considered in order to allow conclusions regarding the degree of restricted diffusion. In this study, we have recalculated previously published data in order to minimize the effect of heterogeneity of the second kind, i. e. a transit‐time dependence of the fractional extraction values. The method used makes it possible to calculate reliable intervals of confidence for the permeability surface area products, and hence for the permeability surface area product‐ratios (and equivalent pore radius), taking into account the maximal theoretical impact of back diffusion on measured extraction data.After correction for transit‐time dependent effects of heterogeneity, the permeability surface area product‐ratio of Cr‐EDTA to cyanocobalamine (vit. B12) from 48 measurements in eight rats was found to have a theoretical ‘upper bound’ of 2.63±0.06 and a lower bound of 2.10±0.07, corresponding to an equivalent pore radius of 60 to 109 Å. This minimum pore radius estimate was even further reduced by corrections for plasma flow dependent reductions in overall extraction fraction (heterogeneity of the first kind) to 45 Å, whereas the upper bound on pore radius was reduced to 60 Å. These data strongly support the presence of marked restricted diffusion of small solutes in the maximally vasodilated rat hindquarter microvasculature.
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.
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.
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.