bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibition of the Cortisol response to systemic angiotensin II by forebrain lesions involving the anterior wall of the third ventricle
Authors: JUNKERGÅRD J. , ANDERSSON B. , JÓNASSON H. 
Published: December 2008

The influence of bilaterally narrow, medial forebrain lesions on the increase in plasma Cortisol concentration normally seen in response to intravenous angiotensin II was studied in five goats. For comparison, the pre‐ and post‐lesion Cortisol responses to intravenous endotoxin were also evaluated. The Cortisol response to angiotensin was extinguished in two goats, whereas a slightly attenuated response to endotoxin was still obtained post‐lesioning. In these animals the lesions embraced the subfornical organ (SFO), the organum vasculosum of the lamina terminals (OVLT) and the interjacent anterior wall of the third ventricle. In two other goats, in which the SFO was completely destroyed but the OVLT remained largely intact, the lesions caused about 50% reduction of the Cortisol response to angiotensin without any concomitant reduction of the response to endotoxin.It is concluded that ACTH‐cortisol release in response to systemic angiotensin II is not mediated exclusively by receptors for the octapeptide confined to the SFO. Angiotensin receptors in the OVLT seem to be equally important in this respect.
Muscarinic supersensitivity in the rat urinary bladder after capsaicin pretreatment
Authors: MALMGREN A. , EKBLAD E. , SUNDLER F. , ANDERSSON K.‐E. , ANDERSSON P.O. 
Published: December 2008

The effects of capsaicin on urinary bladder function have been investigated in adult rats. Ten days after capsaicin treatment immunocytochemical investigations showed a nearly complete disappearance of substance P (SP) and calcitonin gene‐related peptide (CGRP) in all parts of the bladder. Recordings of micturition patterns and cystometrical investigations in conscious animals revealed no functional effects of capsaicin treatment. In‐vitro experiments showed that the contractile response to substance P was similar before and after capsaicin treatment and CGRP exerted no contractile effects on the urinary bladder in either group of rats.The concentration–response curve to carbachol as well as the frequency‐response curve to electrical stimulation were significantly shifted to the left in bladder muscle after capsaicin treatment. However, the maximal responses were similar in control and capsaicin‐treated bladders. In the presence of scopolamine the maximal response to electrical stimulation was clearly lower in bladders subjected to capsaicin treatment than in controls.In conclusion, depletion of substance P and CGRP in the rat urinary bladder by capsaicin induced no supersensitivity to these peptides. However, the increased sensitivity to carbachol and to electrical stimulation seen after capsaicin treatment indicates the development of a supersensitivity to muscarinic receptor stimulation. Despite this supersensitivity in vitro no functional effects of capsaicin treatment were found in vivo.
Atropine treatment induced cholinergic supersensitivity at receptor and second messenger levels in the rat salivary gland
Authors: WESTLIND‐DANIELSSON A. , MÜLLER R. M. , BARTFAI T. 
Published: December 2008

Physiological, biochemical and morphological correlates of chronic treatment of rats with the classical muscarinic antagonist atropine for 14 days (20 mg kg‐1 day‐1 s. c.) were studied in submandibular salivary glands.The amount of saliva collected from submandibular glands following a single injection of isoproterenol (30 mg kg‐1 i. p.) was significantly larger and had higher protein concentration in rats treated with atropine than in saline‐treated animals. In the glands of atropine‐treated rats a conspicuous increase in the amount of rough endoplasmic reticulum (RER) along with a decrease in the mucous volume was observed in the acinus when examined by light microscopy.Several biochemical changes were observed in an enriched plasma membrane fraction from the submandibular gland of the atropine‐treated rats: (1) an increase in the number of muscarinic antagonist binding sites (31 ± 3.4%), (2) a decrease in the specific activity of basal adenylate cyclase, (3) a significantly lower Vmax of the adenylate cyclase in the presence of GTP (10 μM) and varying concentrations of Mg2+ (0–22.5 mM) with no apparent change in affinity of the enzyme for Mg2+ but (4) higher magnitude of stimulation in the presence of GTP (100 μM), vasoactive intestinal polypeptide (5 μM), isoproterenol (100 μM), NaF (10 mM) and forskolin (10μM). There was however no change in the density of β‐adrenergic receptors upon atropine treatment.In tissue slices from the submandibular glands of atropine‐treated rats we found lower basal cAMP levels (decrease 29 ± 6.9%) and no significant change in the phosphatidylinositol breakdown stimulated by carbachol (10‐6 to 10‐4 M).It appears that chronic blockade of an inhibitory muscarinic input to the adenylate cyclase system is compensated by lowered adenylate cyclase activity. Phosphoinositide metabolism is not subject to the same adaptation, suggesting that cAMP may be the pivotal second messenger in the supersensitive salivary response.
Endothelium‐independent potentiation by neuropeptide Y of vasoconstrictor responses in isolated arteries from rat and rabbit
Authors: GUSTAFSSON H. , NILSSON H. 
Published: December 2008

An endothelium‐dependent action of neuropeptide Y (NPY) has been implicated in studies on various vascular beds. In the present study, the requirement of an intact endothelium for NPY‐evoked potentiation of the response to sympathetic nerve stimulation was determined in the small mesenteric arteries of the rat and in the central ear artery of the rabbit. Further, NPY‐mediated inhibition of relaxing influences was determined in small mesenteric arteries of the rat.Vascular segments were mounted in a double myograph, where one of the two suspended vessels was denuded of endothelium by gently rubbing the intimal surface. Removal of endothelium was verified by en‐face silver staining.In both species, the response to bursts of transmural field stimulation eliciting 10% of maximal contraction was potentiated 2–4 times in the presence of ionM NPY, whether the endothelium was present or not.In small mesenteric arteries precontracted with noradrenaline, addition of acetylcholine (1 μM) caused relaxation only in vessels with an intact endothelium. Subsequent addition of ionM NPY enhanced vasoconstriction in both intact and endothelium‐denuded vessels. The endothelium‐independent β‐adrenergic agonist isoprenaline (1 μM) relaxed both intact and denuded small mesenteric arteries, and in both further addition of 10 nM NPY increased the contraction to about the same extent.The results demonstrate that NPY potentiates the responses to sympathetic field stimulation in small mesenteric arteries from the rat and in central ear artery from rabbit whether the endothelium is present or not. NPY inhibits both endothelium‐dependent and ‐independent relaxations in small mesenteric arteries from rat.
Amino acid stimulation of Na, K‐ATPase activity in rat proximal tubule after high‐protein diet
Authors: JAKOBSSON B. , LARSSON S. H. , WIESLANDER Å. , APERIA A. 
Published: December 2008

Ouabain‐sensitive (OS) O2 consumption was determined in proximal tubular cells from weanling rats fed 21 % (normal‐protein, NP) or 50% (high‐protein, HP) protein diet for 4 days. Butyric acid 10‐3 M was added as a substrate for mitochondrial respiration and the ionophore amphotericin B (10 μ ml‐1) was used to sodium‐load the cells. OS respiration was higher in HP than in NP cells in both DME and amino acid‐free electrolyte solution (ES). Amphotericin B significantly increased OS respiration in both NP and HP cells, implying that the Na‐K pump was activated by increased intracellular Na. In cells incubated in ES, addition of amino acids stimulated OS respiration significantly in HP cells (16.9 ± 1.4 vs 21.2 ± 1.1 nmol min ‐1 mg‐1 protein) and in NP cells (13.9 ± 0.3 vs 14.9 ± 0.6 nmol min‐1 mg‐1 protein). Stimulation was significantly higher in HP cells (26 ± 4%) than in NP cells (7 ± 4%) (P < 0.001). The amino acids did not stimulate ouabain‐insensitive respiration.The results indicate that an HP diet to weanling rats will increase proximal tubule cell Na, K‐ATPase‐dependent respiration by enhancing Na entry via the Na‐amino acid symports.
Exocrine and endocrine release of kallikrein after reflex‐induced salivary secretion
Authors: BERG T. , JOHANSEN L. , POULSEN K. 
Published: December 2008

Exocrine and endocrine release of rat submandibular gland kallikrein has been shown to be low after parasympathetic and β‐adrenergic stimulation but greatly increased after α‐adrenergic stimulation. In the present study, release of glandular kallikrein was investigated under conditions known to give a reflex‐induced salivary gland response.Heat stress induced a rich flow of saliva originating in the submandibular glands. Salivary kallikrein secretory rate was higher than after parasympathetic stimulation but lower than after sympathetic stimulation (P < 0.005). Only heat stress increased circulating glandular kallikrein (12.7 ± 0.8 ng ml‐1 before heat exposure and 53.3 ± 14.1 ng ml‐1 40 min afterwards, P < 0.005). There were no indications that the endocrine release of kallikrein was due to non‐specific leakage. Atropine abolished heatinduced salivation and endocrine kallikrein secretion, possibly through interference with central pathways (P < 0.05). However, phentolamine did not, which may indicate an as yet unidentified mediator of endogenous kallikrein release. The salivary gland response to acid and ether was comparable to that observed after parasympathetic nerve stimulation and was abolished by atropine (P < 0.005). Stimuli known to influence other salivary gland ductal cells, such as aggression and starvation followed by drinking, also did not increase the plasma concentration of glandular kallikrein. The fact that various conditions which induce salivation did not increase circulating glandular kallikrein, coupled with the fact that kallikrein concentration was the highest in animals that died from heat stress, may suggest that the increase in circulating glandular kallikrein seen after heat stress may be pathological and could contribute to the development of heat shock.
Atrial natriuretic peptide, renin activity, aldosterone, urine volume and electrolytes during a 24‐h sleep‐wake cycle in man
Authors: LEPPÄLUOTO J. , RUSKOAHO H. 
Published: December 2008

To investigate the diurnal variation in the plasma atrial natriuretic peptide (ANP) concentrations and its relation to renin activity, aldosterone, urine volume and electrolytes, blood samples from six healthy male subjects were collected and blood pressure and heart rate recorded every 4 h during a 24‐h sleep–wake period. Systolic blood pressure and heart rate were at the lowest during sleep. Plasma ANP, extracted on Sep‐Pak cartridges and measured by radioimmunoassay, had the highest concentration at midnight and lowest at 04.00 h (27 ± 18 vs 16 ± 18 ng I‐1, mean ± SD, P < 0.05 after normalization of the original values). Plasma renin activity and aldosterone were at the highest at 08.00 and 12.00 h, whereafter they both began to decrease (P < 0.001, also normalized). Urinary volume, sodium, potassium and chloride showed highest values (P < 0.05) between 08.00 and 16.00 h.Plasma ANP levels did not correlate with systolic blood pressure, heart rate, serum or urinary Na or plasma renin or aldosterone (r = 0.1–0.3, P > 0.05). Plasma renin activity correlated with aldosterone and aldosterone with urinary K (r = 0.66 and 0.58 respectively, P < 0.001).These results suggest that the low plasma ANP levels found in our subjects at 04.00 h may be associated to diminished atrial distension accompanied by the inactivity of the sleep period. In addition, ANP does not appear to affect the secretion of renin and aldosterone in a normal sleep–wake cycle.
Task specificity in the control of intrinsic trunk muscles in man
Authors: ODDSSON L. , THORSTENSSON A. 
Published: December 2008

The human trunk is a complex mechanical system comprised of large and small segments interconnected with several layers of muscles. An accurate control of this system is important during a variety of everyday tasks such as voluntary movements of the trunk, walking and running. This study was designed to investigate the interaction between muscles controlling the pelvis and the trunk during a variety of movements requiring a finely tuned coordination.Four subjects carried out seven different forms of fast oscillatory movements of the pelvis and trunk in the sagittal and transverse planes. Electromyographical activity (EMG) was recorded with surface electrodes from the abdominal muscles rectus abdominis (RA), obliquus externus (OE), obliquus internus (OI) and erector spinae (ES), from the hip flexor muscle rectus femoris (RF), the hip extensor muscle gluteus maximus (GM) and from the hip extensor/knee flexor muscles of the hamstrings group (HAM). Movements were recorded with an optoelectronic system (Selspot).The results indicate that during spontaneous flexion‐extension movements of the trunk there was a basic alternating activation between a pure flexor (RF‐RA‐OE‐OI) and an extensor synergy (ES‐GM‐HAM). Different mixed synergies appeared when more specific patterns of coordination of the pelvis and spine were performed. For example, during pelvic tilts in the sagittal plane, RA‐OE‐OI‐GM formed a synergy which was activated reciprocally with ES.The neural circuitry controlling muscles of the pelvis and trunk is apparently adaptable to a variety of different tasks. Individual muscles were shown to either cause, brake or prevent a movement and to be integrated in several different task‐specific motor synergies. Such a flexibility of the motor system is important for an accurate control of postural equilibrium and coordinative movements of the pelvis and trunk.
Effects of histamine H2‐receptor blockade on the cardiovascular reflex response to lower‐body negative pressure in man
Authors: SJÖVALL H. , JÖNSSON C. , HÄGGENDAL J. , OLBE L. 
Published: December 2008

The role of histamine H2‐receptors in cardiovascular control is unknown. In seven healthy volunteers, we studied how histamine H2‐receptor blockade affected the reflex response to hypovolaemia induced by lower‐body negative pressure (LBNP). In placebo‐treated individuals, LBNP down to ‐40 mmHg did not change systolic pressure but increased diastolic pressure, heart rate, forearm vascular resistance, plasma noradrenaline concentration and plasma renin activity. After pretreatment with ranitidine, a specific histamine H2‐receptor antagonist, the diastolic pressure rise no longer sufficed to maintain a constant systolic pressure during LBNP. Ranitidine pretreatment also attenuated the heart rate response and the rise in plasma renin activity induced by LBNP, but did not significantly change the reflex forearm vasoconstriction or the forearm plasma noradrenaline response.The results suggest that histamine H2‐receptor blockade attenuates the reflex vasoconstrictor response to lower‐body negative pressure. The mechanism behind this effect remains unknown, but the data do not support the idea that the effect is exerted in the skeletal muscle vascular bed.
Cardiovascular and sympathoadrenal responses to mental stress: a study of sensory intake and rejection reactions
Authors: FREYSCHUSS U. , FAGIUS J. , WALLIN B. G. , BOHLIN G. , PERSKI A. , HJEMDAHL P. 
Published: December 2008

Cardiovascular, sympathoadrenal and subjective responses to mental stress induced by two mental challenges eliciting sensory intake (word identification test = WIT) and sensory rejection (colour word conflict test = CWT) reactions were studied in 10 healthy males. Pressor responses to these stressors have been proposed to differ haemodynamically. Sympathoadrenal activity was assessed by arterial and femoral venous plasma catecholamine determinations and direct recordings of muscle sympathetic activity in the right peroneal nerve (MSA). Basal measurements differed little from those made during an active relaxation procedure, with the exception of MSA, which decreased. Both stress tasks elicited increases in heart rate, cardiac output, calf blood flow and brachial and pulmonary arterial blood pressures. WIT and CWT elicited qualitatively similar responses, but the amplitudes of the circulatory responses were lower with WIT, which also was rated as a weaker stressor.MSA increased during CWT, while marginal increases were seen during WIT. Arterial adrenaline showed a transient increase by 0.14 nmol 1‐1 during WIT. During CWT arterial adrenaline increased significantly by 50%. Increases in arterial adrenaline and subjective stress ratings were related to increases in cardiac output and reductions of systemic vascular resistance. Arterial and femoral venous noradrenaline increased during CWT, while changes during WIT were small. MSA and noradrenaline responses did not correlate to local vascular responses in the calf.Differences in the responses to mental challenges evoking sensory intake or rejection seem to be of a quantitative rather than a qualitative character.
Role of different serotonergic receptors in the long‐lasting blood pressure depression following muscle stimulation in the spontaneously hypertensive rat
Authors: HOFFMANN P. , CARLSSON S. , SKARPHEDINSSON J. O. , THORÉN P. 
Published: December 2008

In a previous study prolonged low‐frequency muscle stimulation in the hind leg of the spontaneously hypertensive rat (SHR) was shown to induce a reduction in blood pressure (about 15 mmHg) that lasted for many hours. We showed in that study that endorphin and serotonin systems were involved.In the present study drugs with selective affinity for the serotonin (5‐HT) receptors were used to analyse further the involvement of different serotonin systems. In one group of SHR, a prestimulatory dose of metitepine maleate (a 5‐HT1 and 5‐HT2 receptor antagonist) completely abolished the post‐stimulatory depressor response. The long‐lasting depressor response was still present, although less pronounced, after a bolus dose of the 5‐HT2 blocking agent ritanserin (R 55667) at the start of stimulation. The 5‐HT3 receptor antagonist ICS 205–930 did not influence the response at all, nor did the selective 5‐HT1a receptor agonist 8‐OH‐DPAT enhance the depressor response. These results indicate that the reduction in blood pressure after muscle stimulation is mainly mediated by the 5‐HT1 receptor.
The concentration of ouabain binding sites in biopsies of uterine muscle
Authors: EVERTS M. E. , SKAJAA K. , HANSEN K. 
Published: December 2008

The concentration of Na, K‐ATPase in biopsies of uterine muscle was determined bymeasurement of [3H]ouabain binding in the presence of vanadate. For this purpose amethod previously described for skeletal muscle (Norgaard et al. 1983) was modified. Biopsies were obtained from uterine muscle from pregnant women (during caesariansection), non‐pregnant women (during hysterectomy) and from adult, non‐pregnantguinea‐pigs and rats.The ouabain binding site concentration in uterine muscle of the pregnant women averaged 72 ± 2 pmol g‐1wet wt (n= 8), with an apparent dissociation constant (KD) for ouabain of 3 times 10‐9mol 1‐1. The ouabain‐binding capacity in uterine muscle of the non‐pregnant women amounted to 83 ± 9 pmol g‐1wet wt (n = 8). In uterine muscle of the guinea‐pig, two populations of ouabain binding sites were observed: one with a maximum binding capacity of 230 pmol g‐1wet wt and an apparent KDof 1.6 times 10‐6mol 1‐1, and one with a maximum capacity of 62 pmol g‐1wet wt and an apparent KDof 5 times 10‐8mol 1‐1.Immediate freezing of the biopsies in liquid N2and storage at‐60 °C for up to 6 weeks caused no change in ouabain‐binding capacity. The dry weight/wet weight ratio of the samples from different subjects showed values of around 20±.It is concluded that the concentration of Na‐K pumps in human uterine muscle can be quantified by [3H]ouabain binding using samples weighing 5–10 mg. The method may provide a useful approach in clinical studies, i.e. analysis of the changes in Na, K‐ATPase concentration that may occur as a basis for disturbances of labour.
Influence of serotonin on total intravascular capacity in the anaesthetized dog
Authors: HEDBERG P. A. , RUTLEN D. L. 
Published: December 2008

The influence of serotonin on intravascular volume in the total capacitance circulation has not previously been examined. Thus, blood was drained from the venae cavae to an extracorporeal reservoir and returned to the right atrium at a constant rate so that total intravascular volume changes could be recorded as the inverse of changes in reservoir volume in 31 anaesthetized dogs.Thus, serotonin causes a biphasic change in total intravascular volume. The initial decrease in intravascular volume is not mediated by a reflex or by 5‐HT1, 5–HT2, or α‐adrenergic receptor stimulation. The late intravascular volume increment appears to be mediated, at least in part, by preganglionic or ganglionic stimulation, which may well be at a 5–HT1receptor. In an animal with an intact circulation, the biphasic volume change might be expected to act via the Starling mechanism to first increase and then decrease cardiac output and thereby enhance the effect of the biphasic total peripheral resistance change on arterial pressure.Serotonin (588 ± 47 μg) in the left atrium was associated with an initial decrease in intravascular volume of 39 ± 12 ml(P < 0.01) followed by an increase of 129 ± 31 ml (P < 0.01) above control at 20 min. Mean arterial pressure increased from a control of 74 ± 4 mm Hg to 99 ± 7 mmHg (P < 0.01) initially and then decreased to 64 ±5 mm Hg (P < 0.05) at 20 min. Following ganglionic blockade with mecamylamine, serotonin caused only a decrease in intravascular volume, which was 73 ± 12 ml (P < 0.01) at 20 min. 5‐HT2and α‐adrenergic blockade with ketanserin did not attenuate the early decrease in intravascular volume. 5‐Carboxamidotryptamine (82 ± 39 μg), a 5‐HT1agonist, was associated with only an increase in intravascular volume, which was 82 ± 13 ml (P < 0.01) at 20 min and which was abolished after ganglionic blockade.
Testosterone elevates pituitary prolactin content of long‐term castrated rats under constant but not under periodic light
Authors: PORKKA‐HEISKANEN T. , LAAKSO M.‐L. , STENBERG D. , PEDER M. , JOHANSSON G. 
Published: December 2008

Intact and castrated male rats were kept for 1 week under constant or periodic light, during which time they received daily injections of either vehicle or testosterone propionate (125 or 250 μg day‐1). Immediately after the experiment the rats were decapitated and serum and pituitary prolactin were measured radioimmunologically. The pituitary prolactin content was decreased after castration in both lighting conditions. Daily testosterone injections elevated the pituitary prolactin content of the castrated rats to the level of the intact rats in constant‐light conditions but were ineffective under periodic light. Serum prolactin concentrations were not affected by constant light.We have previously shown that testosterone decreases the serum luteinizing hormone concentration of castrated rats more effectively under constant than under periodic light. In the present study we showed that serum prolactin was not elevated in constant light and thus could not be the cause of increased testosterone sensitivity. We also showed that testosterone elevates the pituitary prolactin content of castrated rats under constant but not under periodic light. This finding gives further support to the hypothesis that constant light sensitizes the hypothalamo‐pituitary axis of castrated male rats to the effects of testosterone.