bluuebunny/crossref_metadata_2025_split huggingface dataset:
Functional responses of different muscle types of the female rat urethra in vitro
Authors: ANDERSSON P. O. , MALMGREN A. , UVELIUS B. 
Published: December 2008

The influence of muscle type on functional responses of the female rat urethra was investigated using morphological and functional in‐vitro techniques. The urethral submucosa was found to contain longitudinally or obliquely oriented smooth muscle cells. The muscularis layer is composed of circularly oriented muscle cells. Near the bladder orifice smooth muscle fibres dominate, but in the mid‐urethra the vast majority is circularly oriented striated muscle cells.Circular preparations responded to electrical field stimulation in vitro with a rapid contraction. Stimulation with single impulses resulted in a twitch response; frequencies exceeding 5–10 Hz induced a summation and tetanus. The response was unaffected by phenoxybenzamine, propranolol and scopolamine and had a low sensitivity to calcium‐free solution but was sensitive to suxamethonium and tetrodotoxin. Using longer impulse trains stimulation evoked also a slow contraction, sensitive to calcium‐free solution.In longitudinal preparations stimulation induced a relaxation followed by a contraction, responses much smaller than those seen in the circular preparations.Both preparations relaxed on addition of calcitonin gene‐related peptide or capsaicin. The relaxation to calcitonin gene‐related peptide was larger than that to capsaicin in longitudinal preparations but equally large in the circular ones. Substance P and 5‐hydroxytryptamine contracted both preparations. The longitudinal urethra showed a larger contraction to 5‐hydroxytryptamine than to substance P, whereas both substances induced similar responses in the circular preparations.The study shows a similar muscle arrangement in the female rat urethra as described in humans and further points to a functional differentiation between the different types of muscle.
Endogenous nitric oxide as a probable modulator of pulmonary circulation and hypoxic pressor response in vivo
Authors: PERSSON M. G. , GUSTAFSSON L. E. , WIKLUND N. P. , MONCADA S. , HEDQVIST P. 
Published: December 2008

The objective of this study was to investigate the role of endogenous nitric oxide, formed from L‐arginine, in the regulation of pulmonary circulation in vivo, with special reference to the hypoxic pressor response. In artificially ventilated open‐chest rabbits, pulmonary vascular resistance at normoxic ventilation (F102= 21 %) was 78C 16 cmH2O ml‐l min 1000‐1 (mRUL). Hypoxic ventilation (F102= 10%) increased pulmonary vascular resistance to 117 ± 17 mRUL. Nw‐nitro‐L‐arginine methylester (L‐NAME), an inhibitor of nitric oxide synthase, increased pulmonary vascular resistance at normoxic ventilation to 192 ± 28 mRUL and during hypoxic ventilation to 462 ± 80 mRUL. During Nw‐nitro‐l‐arginine methylester infusion there was also an increase in mean arterial blood pressure as well as a decrease in cardiac output that was even more pronounced during hypoxic ventilation. L‐arginine reversed the effect of Nw‐nitro‐l‐arginine methylester on pulmonary vascular resistance at normoxic ventilation to 140 ± 26 mRUL and at hypoxic ventilation to 239 ± 42 mRUL.In spontaneously breathing closed‐chest rabbits, Nw‐nitro‐L‐arginine methylester evoked a marked decrease in arterial Po2, and increases in respiration frequency and central venous pressure, while blood pH, PCO2 and base excess remained unchanged. Taken together these findings indicate that endogenous nitric oxide, formed from L‐arginine, might be a regulator of ventilation‐perfusion matching at normoxic ventilation, and that nitric oxide acts as an endogenous modulator of the hypoxic pressor response.
Evidence from lack of decentralization‐induced supersensitivity that β2‐ adrenoceptors of the cat nictitating membrane are non‐innervated
Authors: BROADLEY K. J. 
Published: December 2008

The right superior cervical sympathetic trunk of cats was sectioned preganglionically under anaesthesia. Six days later the blood pressure, heart rate and contractions of the left (control) and right (decentralized) nictitating membranes were recorded under chloralose anaesthesia (80 mg kg‐1). The α‐adrenoceptor‐mediated contractile responses of the nictitating membrane to intravenous adrenaline were greater on the decentralized side than the control side, with a significant shift of the doseresponse curve to the left. After phentolamine (8 mg kg‐1i.v.), adrenaline administered intra‐arterially exerted β‐adrenoceptor‐mediated relaxation of the nictitating membranes. However, there was no difference in the sensitivity or magnitude of responses between decentralized and control sides.In a separate series of experiments, the α‐adrenoceptor‐mediated contractile responses of the nictitating membrane to intra‐arterial noradrenaline displayed supersensitivity on the decentralized side, the dose‐response curve being significantly shifted to the left. In the same animals, the β‐adrenoceptor‐mediated relaxation responses to intra‐arterial isoprenaline were non‐significantly greater on the decentralized side, presumably because of raised tone. However, when expressed as a percentage of the maximum relaxation, there was no difference in sensitivity. This study shows that the α‐adrenoceptor‐mediated contractile response of the nictitating membrane displays supersensitivity after preganglionic section of the sympathetic innervation. This is presumably because of an up‐regulation arising from loss of sympathetic traffic onto the receptor. The relaxation response is mediated via adrenoceptors of the β2‐ subtype and shows no supersensitivity. This suggests that these receptors are not under the influence of the sympathetic innervation.
Gentamicin inhibition of Na+, K+‐ATPase in rat kidney cells
Authors: FUKUDA Y. , MALMBORG A.‐S. , APERIA A. 
Published: December 2008

Na,K+‐ATPase activity is decreased in homogenized renal tissue from GM‐treated rats. This study examines whether the site of the active effect of GM on Na,K‐ATPase activity in the kidney can be localized to the proximal convoluted tubules (PCT) where the drug is taken up and where it will produce necrosis.In rats treated with gentamicin (50 μg. kg‐1.day‐1i.m.) for 7 days, PCT Na,K‐ATPase activity was reduced as compared to vehicle‐treated rats but returned to control levels 7 days after treatment withdrawal. In another nephron segment, the medullary thick ascending limb of Henle (mTAL), where GM induced lesions are uncommon, Na,K‐ATPase activity was the same in GM‐ and vehicle‐treated rats treatment. To study thein vitroeffect of GM, dissected PCT and mTAL segments from untreated rats were preincubated for 30 min with GM 10‐3m, a dose similar to the tissue concentration in chronically treated rats. In tubule segments that were permeabilized to allow the drug to enter the cells, GM 10‐3msignificantly inhibited Na,K‐ATPase activity both in PCT and mTAL. In non‐permeabilized mTAL segments GM did not inhibit Na,K‐ATPase activity. GM inhibition of Na,K‐ATPase activity in permeabilized PCT segments persisted after the tubules were rinsed in GM free medium. GM does not inhibit Na,K‐ATPase partly purified from the renal cortex. Conclusion. Gentamicin inhibits Na,K‐ATPase activity in renal tubule cells when it has access to the cytoplasm. Treatment with GM will therefore cause a selective inhibition of Na,K‐ATPase in the proximal tubule cells.
Changes in pitutary‐adrenal activity regulate the central vasodepressor responses induced by neuropeptide Y and adrenaline in the awake unrestrained male rat
Authors: AGUIRRE J. A. , FUXE K. , ANDBJER B. , ENEROTH P. , AGNATI L. F. 
Published: December 2008

The central cardiovascular responses induced by neuropeptide Y (0.25 nmol) and adrenaline (2.00 nmol) given i.c.v. in close to maximal doses in the awake, unrestrained male rat were studied following changes in the pituitary‐adrenal activity. Adrenalectomy (1 week) alone significantly reduced the vasodepressor response to i.c.v. adrenaline but not to i.c.v. neuropeptide Y. Corticosterone replacement treatment (5 mg kg‐1x 2, i.p., 1 week) significantly reduced both the maximal (peak) and overall (area) vasodepressor responses to i.c.v. adrenaline and neuropeptide Y (only overall responses) in the adrenalectomized rat. Corticosterone treatment alone in the sham‐operated rat highly significantly reduced the vasodepressor responses to both i.c.v. adrenaline and neuropeptide Y. The bradycardic action of centrally administered neuropeptide Y was no longer significant after alterations in pituitary‐adrenal activity.The present results suggest that corticosterone treatment can abolish the centrally evoked vasodepressor responses to close to maximal doses of adrenaline and neuropeptide Y, which may contribute to their hypertensive properties in man. Finally, after adrenalectomy the central vasodepressor responses to neuropeptide Y dominate, since the adrenergic vasodepressor responses are selectively reduced. This dominance is reduced by corticosterone replacement treatment. The results indicate an antagonistic role of adrenocortical steroids in control of centrally induced acute vasodepressor responses to neuropeptide Y and adrenaline.
Relaxation of sheep urethral muscle induced by electrical stimulation of nerves: involvement of nitric oxide
Authors: Garcia‐Pascual A. , Costa G. , Garcia‐Sacristan A. , Andersson K.‐E. 
Published: December 2008

Isolated smooth muscle preparations from the sheep urethra responded to electrical field stimulation with contraction when basal tension was low (5–6 mN), but with relaxation when the preparations were contracted with noradrenaline (NA), clonidine, or prostaglandin F2α. No relaxant response could be elicited in high K+ (124 mM) contracted preparations. Electrically induced relaxations had a threshold of less than 1 Hz and a maximum at 8 Hz. Both contractant and relaxant responses were abolished by tetrodotoxin, indicating that they were caused by transmitters released from nerves.The amplitude of the relaxant responses showed a highly significant correlation to the tension induced by noradrenaline. A coefficient (R/T) was calculated relating relaxation to noradrenaline‐induced tension. In this way it is possible to separate the effect of drugs on muscle tension (non‐specific effect) from their action on the electrically induced relaxation (specific effect). Chemical sympathectomy with 6‐OHDA did not significantly modify the relaxant response to 6 Hz in noradrenaline contracted strips, as evaluated by the R/T coefficient. The electrically induced relaxation was not affected by hexamethonium, propranolol, phentolamine, muscarinic receptor blockade, cocaine, indomethacin, or methysergide. Both nifedipine and Bay K 8644 inhibited significantly the response induced by electrical stimulation, decreasing its maximum. Nifedipine, but not Bay K 8644, significantly reduced the level of tension induced by noradrenaline, and its effect, evaluated by the R/T coefficient, was an increase in the electrically induced relaxation, whereas Bay K 8644 had a significant inhibitory effect. Pre‐treatment with NG‐nitro‐L‐arginine (L‐NOARG) for 30 minutes did not significantly change resting tension, but concentration‐dependently reduced the relaxant responses, and at the highest L‐NOARG concentration used, relaxation was changed into a contraction. NO (present in acidified solution of NaNO2) still produced relaxation. NG‐nitro‐D‐arginine (D‐NOARG) had no effects.It is suggested that in contracted sheep urethral muscle, the relaxation produced by electrical stimulation of nerves is mediated by NO.
Effect of felodipine on the myogenic response to dynamic stretch in vascular smooth muscle
Authors: Bülow A. , Johansson B. 
Published: December 2008

In the present experiments we examined the effect of felodipine, a vasoselective dihydropyridine calcium antagonist, on contractile responses to dynamic and static stretch of the isolated portal vein of the rat. Dynamic stretch was applied to the vascular smooth muscle at graded rates (from 0.5‐1.5% muscle length s‐1). Earlier observations (Johansson & Mellander 1975) of a rate‐dependent excitation of the vascular smooth muscle by dynamic stretch were confirmed. Addition of felodipine, 3 nM, reduced the spontaneous activity at static lengths to about 50% but resulted in much stronger inhibition of the dynamic stretch responses. Particularly the rate‐dependent increase in active force was no longer evident since the response at high rates of passive lengthening was most clearly reduced by felodipine.By contrast, lowering of the extracellular Ca2+concentration resulted in a comparable attenuation of the spontaneous contractile activity and of the dynamic stretch responses which still showed the typical rate dependence. Therefore, the pronounced inhibition by felodipine of the dynamic myogenic reactivity of the rat portal vein appeared to be a specific effect and not simply related to the overall reduction in contractile activity. We suggest that felodipine, in addition to its inhibition of action potentials and excitation‐contraction coupling may exert a special negative influence on the mechano‐electrical coupling, i.e. the process that couples dynamic stretch of the vascular smooth muscle to membrane excitation.
The effect of meal size on postprandial increase in cardiac output
Authors: WAALER B. A. , ERIKSEN M. , TOSKA K. 
Published: December 2008

Heart rate, stroke volume, cardiac output and mean arterial blood pressure were followed from the resting primal situation and for 2 hours after intake of standardized meals in four healthy individuals. Continuous records of stroke volume and cardiac output were achieved with an improved method of Doppler ultrasonography. A smallish meal and one 2 1/2 times larger were both given twice and in random order to each of the four test persons.The consumption of a meal invariably resulted in a cardiac output increase, which developed gradually to reach a maximum level 30 to 60 min after end of the meal. The postprandial cardiac output increase resulted from significant increases in both heart rate and stroke volume.There were distinct and significant differences between the circulatory responses to small and large meals. The increase in cardiac output after a large meal was considerably larger and lasted for longer than the increase after a small meal. Two hours after a small meal cardiac output was nearly or fully back to pre‐meal values, while cardiac output was still markedly elevated 2 hours after a large meal. Consequently, the total ‘extra’ amount of blood delivered by the heart over 2 post‐meal hours was significantly — about 100%— larger after the large meal than after the small one.Mean arterial blood pressure either fell or remained almost unchanged in the hour after a meal, so that total peripheral resistance was consistently and significantly reduced in the postprandial period — and considerably more so after a large meal than after a small one.
Juxtacellular histamine concentration governs histamine release from rat peritoneal mast cells
Authors: UVNÄS B. , ÅBORG C. ‐H. , LYSSARIDES L. , DANIELSSON L. G. 
Published: December 2008

Isolated rat peritoneal mast cells release histamine when superfused with isoosmotic salt or sucrose solutions. The release was ascribed by us to an intracellular ion exchange between potassium and histamine at granule sites, resulting from a flux of cytoplasmic potassium across the granules secondary to the disturbance of the ‘state of equilibrium’ at the cell surface caused by the superfusion (Uvnäset al. 1989). In the present article is shown that the histamine releasing effect is counteracted by the addition of histamine to the superfusion fluid. The inhibition is concentration‐dependent and accompanied by concomitant changes in the potassium efflux. A 50% inhibition of the histamine release requires an external histamine concentration of 40 μm and extrapolation of the equilibrium curve hints at a total inhibition at concentrations around 170 μm.The observations are taken to indicate that reduction of the juxtacellular histamine concentration caused by the superfusion disturbs the histamine equilibrium at the mast cell surface resulting in the activation of the histamine secretory mechanism. In other words, the secretory activity of the mast cell is checked by the juxtacellular concentration of histamine. When the juxtacellular histamine is removed e.g. on isolation procedures, other experimental situations such as superfusion, or by consumptionin vivothe mast cell delivers histamine to restore the juxtacellular equilibrium.
In vitro steroid production by follicles of frog Rana esculenta: mammaIian gonadotropin‐releasing hormone effects
Authors: ZERANI M. , GOBBETTI A. , POLZONETTI‐MAGNI A. 
Published: December 2008

The effects of mammalian gonadotropin‐releasing hormone on ovarian release of progesterone, androgens and estradiol‐17β were studied in vitro by a superfusion system carried out on follicles of adult female Rana esculenta, collected at different periods of the annual reproductive cycle.The follicles were superfused with medium alone, pituitary, mammalian gonadotropin‐releasing hormone, or pituitary plus mammalian gonadotropin‐releasing hormone. For follicles obtained in the prereproductive period, pituitary plus mammalian gonadotropin‐releasing hormone increased the estradiol values much more than pituitary alone. In the reproductive period, pituitary alone increased the estradiol values much more than pituitary plus mammalian gonadotropin‐releasing hormone. For follicles obtained in the recovery period, mammalian gonadotropin‐releasing hormone alone stimulated the highest estradiol production, and pituitary plus mammalian gonadotropin‐releasing hormone increased the estradiol values much more than pituitary alone.The results reported here suggest that mammalian gonadotropin‐releasing hormone and/or pituitary have a direct effect on ovarian estradiol secretion, and that this effect varies with the annual reproductive cycle.
Gut blood flow in the estuarine crocodile,Crocodylus porosus
Authors: AXELSSON M. , FRITSCHE R. , HOLMGREN S. , GROVE D. J. , NILSSON S. 
Published: December 2008

Simultaneous recordings of blood flow in the right and left aorta and carotid and coeliac artery were made in the crocodile,Crocodylus porosusat rest and during various stimuli. In resting animals the right aorta and carotid artery flow profiles resembled the recordings obtained in the caiman (Axelssonet al. 1989 a), with an anterograde blood flow throughout the cardiac cycle. As in the caiman, the left aorta flow profile was complex with both anterograde and retrograde blood flow during the cardiac cycle, and a net left aorta blood flow near zero at rest.The coeliac artery blood flow profile did not show the complex pattern seen in the upper aorta, immediately suggesting that most of the coeliac artery blood originates elsewhere. We believe that coeliac artery blood flow in the resting animal derives from the right aorta via the abdominal anastomosis between the two aortas. Feeding induced an increase in the coeliac artery and left aorta blood flow, probably due to a decrease in visceral vascular resistance, and hence coeliac arterial and the left aorta blood pressure, which facilitates blood flow (from right to left aorta) through the foramen of Panizza.During short ‘fright dives’, heart rate fell and there was a decrease in the recorded blood flows: carotid artery blood flow did not decrease to the same extent as the RAo and coeliac artery flow, indicating some capacity for redistribution of blood to the cephalic circuits during diving. Similarly, a near‐unimpaired carotid artery blood flow was maintained after adrenaline injection.Substance P increased the coeliac artery blood flow and produced a right‐to‐left cardiac shunt, probably by construction of the pulmonary vasculature.
Haemodynamic and humoral responses to repeated hypotensive haemorrhage in conscious sheep
Authors: HJELMQVIST H. , ULLMAN J. , GUNNARSSON U. , LUNDBERG J. M. , RUNDGREN M. 
Published: December 2008

Haemodynamic and humoral responses to two subsequent hypotensive haemorrhages, separated by 3 hours and each followed by retransfusion, were studied in unanaesthetized sheep. Haemorrhage was induced by removal of blood from a jugular vein at a rate of 0.7 ml kg‐1 min‐1 until the mean systemic arterial pressure suddenly decreased by 35 mmHg or more.In addition to the mean systemic arterial pressure, the cardiac output, the mean pulmonary arterial pressure, the central venous pressure and the pulmonary capillary wedge pressure decreased in response to each haemorrhage. The recovery of the systemic and pulmonary arterial pressure was slower and/or less efficient after the second haemorrhage, due to a less pronounced increase of the vascular resistance. Relative bradycardia, in association with the abrupt fall of the mean systemic arterial pressure, was more apparent during the first haemorrhage.The plasma levels of vasopressin, renin activity and angiotensin II were increased by each blood removal, but the vasopressin response to the second haemorrhage was significantly reduced. The plasma noradrenaline concentration was slightly and transiently elevated only in response to the second haemorrhage. The concentration of neuropeptide Y‐like immunoreactivity in plasma was unaffected by both haemorrhages.It is suggested that the reduced and delayed increase in the systemic vascular resistance, accompanied by impaired recovery of the arterial pressure, and the relative absence of ‘bleeding bradycardia’, during the second haemorrhage, were due to the diminished vasopressin response.
Effects of alpha2‐adrenoceptor blockade and thyrotropin‐releasing hormone (TRH) on the cardiovascular system in the rabbit
Authors: SELIGSOHN E. E. , KOSKINEN L.‐O. D. 
Published: December 2008

The effects of two different doses of thyrotropin‐releasing hormone on regional blood flows were studied in urethane‐anaesthetized rabbits pretreated with the α2adrenergic antagonists yohimbine and idazoxan. The effects of yohimbine were also studied using unanaesthetized rabbits. Blood flow measurements were performed using the tracer microsphere method. Thyrotropin‐releasing hormone was injected i. v. at a dose of either 0.1 mg kg‐1or 2.0 mg kg‐1. Yohimbine and idazoxan did not modify the effect of thyrotropin‐releasing hormone on mean arterial blood pressure. In the anaesthetized animals, blockade of the α2adrenoceptors resulted in a vasoconstriction in several peripheral organs and the vasoconstriction increased after thyrotropin‐releasing hormone administration. Pretreatment with yohimbine reduced total cerebral blood flow moderately and in such animals thyrotropin‐releasing hormone elicited only minor cerebral blood flow effects. Pretreatment with idazoxan did not reduce the total cerebral blood flow and in such animals it increased from 53± 1 to 75±4 g min‐1100 g‐1(P< 0.01) after the administration of the lower dose of thyrotropin‐releasing hormone and from 64±5 to 112±17 g min‐1100 g‐1(P< 0.01) after the higher dose.In the conscious animals, yohimbine caused an increase in mean arterial blood pressure and heart rate. Vascular resistance increased in several organs. The cerebral blood flow decreased in white matter (P<0.05) and the caudate nucleus (P< 0.05).The results indicate that there is a yohimbine‐sensitive mechanism involved in the cerebrovasodilating effect of thyrotropin‐releasing hormone in anaesthetized rabbits. There is also an activation of the sympathetic nervous system by thyrotropin‐releasing hormone which results in increased vascular resistance and mean arterial blood pressure. Its effect on the vascular resistance may be enhanced by α2adrenoceptor blockade. In conscious animals, there seems to be a yohimbine‐sensitive mechanism involved in the control of cerebral blood flow.