bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of angiotensin II, α‐ and β‐adrenoceptors on peripheral noradrenergic neurotransmission in canine gracilis musclein vivo
Authors: SCHWIELER J. H. , KAHAN T. , NUSSBERGE J. , JOHANSSON M.‐C. , HJEMDAHL P. 
Published: December 2008

Interactions between angiotensin II and adrenoceptor‐mediated effects on peripheral sympathetic neurotransmission were investigated in constant flow blood‐perfused canine gracilis musclein situ, without and with pretreatment by non‐competitive α‐ adrenoceptor blockade.Angiotensin converting enzyme (ACE)‐inhibition by benazeprilat increased nerve stimulation (2 Hz, 4 min)‐evoked noradrenaline (NA) overflow (+21 ± 5 yo) with α‐ adrenoceptors intact, but reduced NA overflow (– 18 ± 6%) when α‐adrenoceptors were blocked. Vasoconstrictor responses were slightly reduced by benazeprilat. Subsequent infusion of angiotensin II (Ang 11, 20 and 500 ng kg‐1min‐1i.v., raising arterial concentrations from 0.6 ± 0.2 PM to 1390 ± 240 and 25 110 ± 3980 PM, respectively) failed to increase NA overflow or to enhance stimulation‐evoked vasoconstriction. Adrenaline (0.4 nmol kg‐1min‐1i.v.) did not change evoked NA overflow before or after benazeprilat, either with or without α‐adrenoceptor blockade, despite high concentrations (± 10 nM) in arterial plasma. Following benazeprilat, propranolol reduced NA overflow (–24 ± 3 yo) only if the α‐adrenoceptors were blocked.In conclusion, benazeprilat reduced evoked NA overflow in the presence of α‐ adrenoceptor blockade to a similar degree as previously shown in the presence of neuronal uptake inhibition in this model. However, contrasting to our previous findings, benazeprilat enhanced NA overflow and reduced the post‐junctional response to nerve stimulation in the absence of α‐adrenoceptor blockade. This could be related to bradykinin accumulation during ACE‐inhibition, in addition to the reduction of Ang II generation. Our data are not compatible with facilitation of NA release by circulating Ang II even at pharmacological dose levels. Although activation of prejunctional β‐adrenoceptors may facilitate evoked NA overflow in this model, circulating adrenaline is ineffective under physiological conditions even after α‐adrenoceptor blockade. Also, β‐adrenoceptor‐mediated prejunctional effects do not seem to involve Ang II in canine skeletal musclein vivo.
Effects of Amrinone on shortening velocity, force development and ATPase activity of demembranated preparations of rat ventricular myocardium
Authors: MÖRNER S. E. J. N. , CANEPARI M. , BOTTINELLI R. , CAPPELLI V. , REGGIANI C. 
Published: December 2008

This study analyses the effects of Amrinone (bipyridine derivative with phosphodiesterase inhibitor properties) on the myofibrillar apparatus of rat myocardium.Thin trabeculae were isolated from the right ventricle and chemically demembranated. Force development and shortening velocity were measured during maximal calcium activations (pCa = 4.45) in control conditions and in the presence of 1–3 mM Amrinone. Maximum shortening velocity was obtained both from extrapolation of the force‐velocity curve and with the slack test method. Amrinone was found to significantly reduce maximum shortening velocity and force development.Myofibrils and myosin were prepared from rat ventricular myocardium and their ATPase activity was assessed in control conditions and in the presence of Amrinone (0.3–6 mM). Ca–Mg dependent myofibrillar ATPase activity which was determined at low ionic strength was depressed by Amrinone in a dose‐dependent way. Ca‐stimulated ATPase activity determined at high ionic strength in myofibril or myosin preparations was not affected. Furthermore, Amrinone did not influence the pCa‐ATPase activity curve of the myofibrillar preparations. A comparison between the inhibitory effects of Amrinone on myofibrils prepared from euthyroid rats and myofibrils prepared from hypothyroid rats was carried out. The ATPase activity was significantly less depressed in myofibrils prepared from hypothyroid rats than in those prepared from euthyroid rats.These results provide the first evidence of an effect of Amrinone on ATP splitting and force generation in the myofilament system of cardiac muscle.
Adrenergic and non‐adrenergic cardiovascular effects of thyrotropin‐releasing hormone (TRH) in the anaesthetized rabbit
Authors: SELIGSOHN E. E. 
Published: December 2008

The effects of thyrotropin‐releasing hormone (TRH) on regional blood flows were studied in urethane‐anaesthetized rabbits. Experiments were performed both with and without adrenergic antagonist pretreatment. The tracer microsphere method was used to measure blood flow. TRH (0.1 mg kg‐1) caused an increase in mean arterial blood pressure (MAP) from 9.8 ± 1 to 11.8 ± 0.8; a higher dose (1 mg kg‐1) increased the blood pressure to 15.2±1 kPa (P < 0.001). Total cerebral blood flow (CBFtot) increased to 137 ± 10% (P< 0.05) of control at the lower dose and to 214±16% (P< 0.001), at the higher dose. A reduction in blood flow at both doses of TRH in several peripheral organs indicates that the pressor effect was mainly due to an effect on the peripheral vascular resistance. In prazosin‐pretreated animals in which the MAP was normalized by ligation of the thoracic aorta, TRH elicited an increase in the CBFtotto 131 ± 12% (P< 0.05) of control. In the iris, TRH caused vasodilation in prazosin‐pretreated animals. In experiments with combined α‐ and β‐adrenergic blockade, a non‐adrenergic vasoconstricting effect of TRH was seen in some peripheral organs.The results indicate that TRH activates the sympathetic nervous system thus causing an increased vascular resistance and MAP; these effects are mediated mainly by an α1‐adrenergic mechanism. In the spleen, the gastric mucosa and the adrenal glands, the vasoconstriction caused by TRH was partly non‐adrenergic. The vasodilation seen in the small intestine and the anterior uvea after TRH treatment and adrenoceptor blockade may be explained by effects on the parasympathetic nervous system. The vasodilating effect of TRH in the brain does not seem to involve α‐ or β‐adrenergic mechanisms.
Different ion channel mechanisms between low concentrations of capsaicin and high concentrations of capsaicin and nicotine regarding peptide release from pulmonary afferents
Authors: LOU Y.‐P. , FRANCO‐CERECEDA A. , LUNDBERG J. M. 
Published: December 2008

Vagal nerve stimulation (1 Hz for 1 min), capsaicin (10‐8M and 10‐6M), resiniferatoxin (3 × 10‐10M) and nicotine (10‐4M) evoked a non‐cholinergic bronchoconstriction in the isolated perfused guinea‐pig lung preparation. Simultaneously there was an increase in the perfusate levels of calcitonin gene‐related peptide‐like immunoreactivity, suggesting release from sensory nerves. Both the bronchoconstriction and peptide release evoked by a low concentration of capsaicin (10‐8M) and that evoked by nerve stimulation were depressed by tetrodotoxin, suggesting involvement of Na+channel dependent depolarization. Since the effects of capsaicin (10‐8M) and vagal nerve stimulation were inhibited by ω‐conotoxin but not influenced by nifedipine, the Ca2+‐channel involved is probably of N‐type. Furthermore, the capsaicin analogue resiniferatoxin also evoked ω‐conotoxin sensitive peptide release and bronchoconstriction. At the higher capsaicin concentration (10‐6M), the functional response was only slightly inhibited by wconotoxin or tetrodotoxin indicating that capsaicin at this concentration evoked peptide release and functional effects through other mechanisms, probably involving Ca2+fluxes in the non‐selective cation channel associated with the proposed capsaicin receptor. The nicotine (10‐4M) evoked peptide release and bronchoconstriction were only marginally influenced by ω‐conotoxin or tetrodotoxin.It is concluded that the ion‐channel mechanisms underlying the peptide releasing properties of antidromic nerve stimulation and low concentrations of capsaicin are similar and depend on action potential propagation, whereas capsaicin in high, toxic concentration and nicotine mainly act via receptor operated channels.
In vivoandin vitrostudies on effects of β‐endorphin and naloxone on sex steroids in the water frog,Rana esculenta
Authors: ZERANI M. , GOBBETTI A. 
Published: December 2008

The effects of β‐endorphin and its receptor antagonist, naloxone, on progesterone, androgens, and oestradiol‐17β release in male and femaleRana esculentawere studiedin vivoandin vitro. In thein vivoexperiments the frogs underwent hypophysectomy, gonadectomy or both, or were left intact; the animals were injected with β‐endorphin or naloxone and killed after 15, 30, 90 and 240 min. In thein vitroexperiments inter‐renal, testis and ovary, all with and without added pituitary, were incubated with β‐endorphin or naloxone for 10, 20, 40 and 80 min. Thein vivoandin vitrodata from males and females were in agreement. In vivo β‐endorphin increased progesterone in all experimental groups and oestradiol in intact and hypophysectomized frogs, while it decreased androgens in all experimental groups. In vitro β‐endorphin increased progesterone in inter‐renal and gonadal tissue, and oestradiol in gonads only, while it decreased androgens in inter‐renals and gonads. In vivo andin vitronaloxone induced opposite effects to β‐endorphin.These data suggest that inRana esculenta, opioids are involved in the modulation of hypothalamo‐pituitary‐inter‐renal and gonadal axes. In particular, the data indicate a direct effect of opioids on inter‐renal and gonadal sex steroid production.
Post‐prandial cardiovascular responses in man after ingestion of carbohydrate, protein or fat
Authors: WAALER B. A. , ERIKSEN M. 
Published: December 2008

Changes in cardiac output and in superior mesenteric arterial flow were followed with Doppler ultrasound techniques in five young, healthy persons for 2 h after ingestion of medium‐sized (4 MJ), fluid meals containing either carbohydrate, protein, fat or water only. Measurements were carried out before meals and at regular post‐meal intervals, during which mean arterial blood pressure was also followed.All energy‐containing meals caused marked and gradually developing post‐prandial increases in cardiac output as well as in superior mesenteric arterial flow. The maximum flow levels were reached in the course of 30–60 min and maintained until the observations ended after 2 h. The intake of water caused no such flow increases.There were considerable interpersonal variations in the size and in the speed of development of the flow increases after the three types of energy‐containing meals. The flow‐increasing effects of the three meal types were not significantly different, even if the most marked increases (median values about 1 1 min‐1 for both cardiac output and superior mesenteric arterial flow) occurred after carbohydrate meals.The marked effects on circulation of the three food components were also revealed in the calculated, integrated amounts of ‘extra’ cardiac output and superior mesenteric arterial flow observed in the course of the 2 h following the meal. Values of more than 100 1 for such ‘extra’ flows were seen after carbohydrate meals.The marked ingestion‐released increase in blood flow to the splanchnic organs is apparently partly met by an increase in cardiac output, and partly by some redistribution of flow, which benefits the digestive system.
Vagally mediated release of gastrin and cholecystokinin following sensory stimulation
Authors: UVNÄS‐MOBERG K. , LUNDEBERG T. , BRUZELIUS G. , ALSTER P. 
Published: December 2008

The aim of the present study was to investigate whether gastrin, cholecystokinin (CCK) and somatostatin secretion can be influenced by sensory stimulation and if so, whether such effects are mediated via the vagal nerves. Male rats anaesthetized with chloral hydrate were exposed to three different stimuli, i.e. to low frequency (2 Hz) electrical stimulation of muscles via needles (electro‐acupuncture), to thermal stimulation at 40 °C or to vibration at 100 Hz. The two former stimuli activate mainly small and medium sized myelinated fibres from muscles and skin respectively, whereas vibration activates large myelinated fibres from skin, subcutaneous tissue and muscles. Experiments were also performed on animals that were vagotomized or exposed to prior treatment with atropine (0.5 mg kg‐1). Blood was collected at various time intervals and plasma levels of gastrin, CCK and somatostatin were measured with radioimmunoassay (RIA).All three stimuli, i.e. electro‐acupuncture, vibration and thermal stimulation caused significant elevations of gastrin (103 ± 11–151 ± 16 pm, 105 ± 8–140 ± 12 pm and 105 ± 14–162 ± 4 pm) and cholecystokinin (9 ± 0.8–15 ± 2.8 pm, 8 ± 0.5–10 ± 1.5 pm and 8.0 ± 0.5–10.5 ± 1.5). Somatostatin was raised in response to electro‐acupuncture (10 ± 1–14 ± 3 pm). Vagotomy and atropinization abolished the release of gastrin and CCK in response to all three stimuli. CCK levels were significantly reduced following electro‐acupuncture in atropinized rats. In conclusion, gastrin and cholecystokinin release is stimulated by activation of sensory afferent, originating in skin, subcutaneous tissue as well as in muscle. Some of these effects are vagally mediated.
Renal interstitial pressure and tubuloglomerular feedback control in rats during infusion of atrial natriuretic peptide (ANP)
Authors: MORSING P. , STENBERG A. , CASELLAS D. , MIMRAN A. , MÜLLER‐SUUR C. , THORUP C. , HOLM L. , PERSSON A. E. G. 
Published: December 2008

Atrial natriuretic peptide (ANP), injected at physiological concentrations, is known to induce both natriuresis and diuresis. It has been suggested by some investigators that these changes result from an increasing glomerular filtration rate (GFR), but others have been unable to demonstrate an increased GFR. The tubuloglomerular feedback (TGF) mechanism is an important regulator of GFR, and the sensitivity of TGF is decreased during ANP administration. Furthermore, resetting of TGF is, in most instances, related to changes in renal interstitial hydrostatic and oncotic pressures. It is also known that ANP may increase capillary permeability which may change renal interstitial pressure.The present study was performed to examine renal interstitial pressures and the TGF mechanism during ANP infusion. In accordance with previous studies, TGF sensitivity was found to be decreased. The tubular flow rate which elicited half the maximal drop in stop‐flow pressure (Psf) was increased from 18.5 to 25.7 nl min‐1. In contrast, ANP infusion resulted in a decreased interstitial hydrostatic pressure and an increased interstitial oncotic pressure. From previous experiments, such changes in interstitial pressures would be expected to increase TGF sensitivity. The changes in interstitial pressure cannot, therefore, directly explain the resetting of the feedback mechanism.In conclusion, the present paper shows a decreased renal net interstial pressure after intravenous administration of ANP.
Changes in myocardial capillary diffusion capacity during infusion of vasoactive drugs
Authors: WÅHLANDER H. , FRIBERG P. , HARALDSSON B. 
Published: December 2008

The present study investigated how variations in coronary vascular resistance and metabolic demand affected myocardial capillary diffusion capacity. Hearts from Wistar rats were perfused with Krebs‐Henseleit‐albumin buffer in a Langendorff preparation, where heart rate (HR), contractility (dP/dtmax) and myocardial oxygen consumption (MVO2) were recorded continuously. Myocardial capillary diffusion capacity was measured as the permeability surface area product (PS) for Cr‐EDTA and vitamin B12by the single injection colorimetric indicator dilution method. After base‐line recordings without drugs, angiotensin II + arginine‐vasopressin was infused, which increased coronary vascular resistance by 90%, stimulated HR by 11%, decreased dP/dtmaxby 21% and reduced MVO2by 4%. PSCr‐EDTAand PSB12, decreased by 24 and 27%, respectively, leaving the ratio PSCr‐EDTA/PSB12unchanged indicating unaltered capillary permeability. Moreover, the reductions in MVO2and PS correlated significantly. During vasodilation: (1) nitroprusside‐NA stimulated HR by 7% and decreased dP/dtmaxby 14%; (2) adenosine reduced dP/dtmaxby 37% and decreased MVO2by 9%; and (3) isoproterenol increased HR, dP/dtmaxand MVO2by 53, 76 and 9%, respectively. However, all three vasodilators reduced PSCr‐EDTAand PSB12in parallel by 7–25% leaving PSCr‐EDTA/PSB12unchanged.Thus, maximal estimated diffusion capacities were obtained during spontaneous coronary vascular tone, most likely reflecting maximal capillary recruitment in the Krebs‐Henseleit‐albumin perfused heart. The derecruiting effects of the vasoconstrictors were partly overridden by metabolic factors, while the reductions of PS after vasodilation more likely were due to increased heterogeneity in coronary flow.
Endothelin contracts human uterine myometrium by a partly dihydropyridine‐sensitive mechanism
Authors: FRIED G. , LIU Y. A. , ANDERSSON E. 
Published: December 2008

The effect of endothelin (ET), a recently discovered 21‐amino‐acid polypeptide with powerful vasoconstrictor properties, was examined on human uterine myometrial stripsin vitro. ET dose‐dependently (10‐‐11‐‐10‐‐7m) increased the contractile force (monitored as contraction amplitude) of the myometrium with significant effects at 10–8and 10‐‐7M. ET (10‐‐8m and up) also increased the basal tone of the myometrium.The calcium channel blocking agents nifedipine (10‐‐7m) and diltiazem (10‐‐6m) both inhibited the spontaneous tonic contractions of the myometrium. When ET was given in the presence of nifedipine, the tonic contractions were further inhibited, whereas the ET‐induced increase in basal tone remained. The same result was obtained with diltiazem (10‐‐6m). The results indicate that the contractility of human myometrium may be modulated by ET, and that the effects of ET on the human myometrium are only partly mediated by dihydropyridine‐sensitive calcium channels.
5‐Hydroxytryptamine receptor characterizations of human cerebral, middle meningeal and temporal arteries: regional differences
Authors: JANSEN I. , OLESEN J. , EDVINSSON L. 
Published: December 2008

We have studied the regional distribution of 5‐hydroxytryptamine (5‐HT) receptor subtypes in fresh circular segments of human cerebral, middle meningeal, and temporal arteries. Vasomotor responses induced by a series of 5‐HT agonists and antagonists with some degree of selectivity were studied by using a sensitivein vitrosystem.Nine 5‐HT agonists were examined for contractile effects on the arteries. In cerebral and meningeal arteries 5‐carboxamidotryptamine (5‐CT) was more potent than 5‐HT. The opposite order of potency (5‐HT‐5‐CT) was found in temporal arteries. In the cerebral arteries 5‐methoxytryptamin (5‐MeOHT) was more potent than sumatriptan while sumatriptan was more potent than 5‐MeOHT in meningeal and temporal arteries.The 5‐HT1, receptor antagonist, methiothepin, competitively antagonized 5‐CT‐induced contractions in cerebral arteries, with aPA2, value of 9.05. 5‐HT‐induced contractions were competitively antagonized by ketanserin (5‐HT2) in the temporal arteriesPA2, value of 9.06). Methiothepin and ketanserin had non‐competitive antagonistic effects in the middle meningeal arteries. The 5‐HT3, selective antagonist ondansetron did not cause any shift of the contractions induced by 2‐methyl‐5‐HT in the temporal, cerebral and middle meningeal arteries.These results suggest that the cerebral arteries mainly contain 5‐HTid., or 5‐HT1,‐like receptors, and the temporal artery 5‐HT2, receptors; the data further indicate the presence of both receptor subtypes in the middle meningeal artery.
Dynamics of transcapillary fluid transfer and plasma volume during lower body negative pressure
Authors: LUNDVALL J. , BJERKHOEL P. , EDFELDT H. , IVARSSON C. , LÄNNE T. 
Published: December 2008

Lower body negative pressure (LBNP) is a stimulus frequently used to study reflex circulatory responses in humans. Studies have provided data on LBNP‐induced blood pooling; however, the possibility that LBNP also might be associated with an important loss of plasma fluid has attracted little attention. Therefore this problem was analysed in male volunteers exposed to prolonged (10 min) high (70–75 mmHg) LBNP. Data on LBNP‐induced blood pooling that were more reliable than in previous literature were also provided.LBNP caused early pooling of more than 870 ml of blood. Rapid filtration of plasma into the exposed tissues occurred throughout LBNP. The cumulative oedema in the legs and buttocks averaged as much as 460 ml, and additional quite large volumes of plasma apparently accumulated in other parts of the lower body. Concomitantly, there was compensatory absorption of extravascular fluid in the upper body. The net decrease in plasma volume (PV) was still large and averaged 491 2 29(SE) ml.Two aspects of the demonstrated process of transcapillary fluid fluxes and PV decline may be emphasized. Firstly, in conjunction with the primary large redistribution of intravascular volume, it certainly implies that LBNP is a potent stimulus as also indicated by a progressive increase in heart rate (HR) and a progressive decline in systolic pressure throughout experimental intervention. In fact, LBNP‐induced circulatory stress clearly has bearings on the extreme hypovolaemic situation provided by the pressure‐bottle haemorrhage technique used in animals. Secondly, it not only offers an interesting example of the dynamics of PV but appears to have more general validity with regard to states characterized by gravitational shifts of blood (hydrostatic load), like upright exercise and quiet standing.
Lung to blood passage of albumin and a nona‐peptide after intratracheal instillation in the young developing pig
Authors: FOLKESSON H. G. , WESTRÖM B. R. , PIERZYNOWSKI S. G. , SVENDSEN J. , KARLSSON B. W. 
Published: December 2008

The passage via the lower respiratory tract of the macromolecule, bovine serum albumin (BSA, mol. wt = 67000) and the nonapeptide, l‐deaminocysteine‐8‐d‐arginine vaso‐pressin (dDAVP, mol. wt = 1067), was assessed for 240 h after intratracheal instillation in young, developing pigs.The plasma levels of immunoreactive BSA increased with time, reaching a maximum between 36–86 h after instillation, and the main portion of BSA in plasma appeared intact, as assessed by crossed immunoelectrophoresis. The dDAVP levels reached a maximum after 1–3 h. The time to reach maximal plasma levels increased with the age of the pig for BSA, while no such effect was observed for dDAVP. The total lung passage, as calculated by dividing the area under the plasma level‐time curve obtained after intratracheal instillation with that obtained after intravenous administration (elimination curve), showed no significant differences with age for BSA (21.8 ± 90% in the newborn, 15.1 ± 8.0% in the 2‐day‐old and 16.1±4.2% in the 70‐day‐old pigs). For dDAVP, a significant decrease in the total passage was obtained with age, from 74.6 ± 9.4% in the newborn pigs to 44.1 ± 13.3%, in the 2‐day‐old pigs (P < 0.001), and to 23.6 ± 7.1% (P< 0.01) in the 70‐day‐old pigs.The study showed that the marker molecules, BSA and dDAVP, passed over the porcine lung into the blood circulation in high amounts, apparently inversely related to their molecular size. The total lung passage of dDAVP, but not that of BSA, was affected by changes with age, indicating that these two markers might traverse the lung epithelium via different routes that are differently affected during postnatal development.