ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1988.tb08373.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

When adenine nucleotides were administered to isolated guinea pig ileum longitudinal muscle, two immediate effects were observed: a contractile effect and a concomitant inhibition of the responses elicited by transmural nerve stimulation. At concentrations up to 10‐4mthe order of potency for the contractile effect was α,β‐MeADP =α,β ‐MeATP>ADP = ATP = AMPPNP =β,t‐MeATP>2′‐deoxy AMP = 2′‐deoxy ADP. AMP and adenosine did not show any contractile effect, whereas both compounds dose‐dependently and reversibly inhibited the nerve‐induced contractile responses. ADP, ATP, β,t‐MeATP and AMPPNP also inhibited contractile responses to transmural nerve stimulation, whereas 2′‐deoxy AMP, 2′‐deoxy ADP, α,β ‐MeADP and α,β ‐MeATP showed but weak inhibitory effects, 2′‐deoxyadenosine, IMP, IDP, ITP, 8‐BrATP and TDP lacked significant contractile effects and did not exert a significant inhibition on nerve‐induced contractions.p‐chloromercuribenzene sulphonic acid (PCMBS) irreversibly antagonized the contractile effects of ADP, ATP and the α,β ‐methylene derivatives, whereas dantrolene sodium, tetrodotoxin, scopolamine and 8‐p‐sulphophenyltheophylline were without effect on nucleotide‐induced contractions.The contractile effect of ADP or ATP was unaffected by indomethacin, whereas the contractile effect by α,β ‐methylene derivatives was abolished by indomethacin. ADP, ATP and α,β ‐MeADP enhanced contractile responses to exogenous acetylcholine, α,β‐MeADP being most effective. This enhancement was blocked by indomethacin. We suggest that ADP and ATP contracted the guinea pig ileum by an action at postjunctional P2‐purinoceptors with different characteristics from prejunctional P1‐purinoceptors. The α,β‐methylene analogues seemed to act at least at one different excita

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1988.tb08292.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

The plasma concentrations of the gastrointestinal regulatory peptides vasoactive intestinal polypeptide (VIP), insulin, secretin, somatostatin, motilin, pancreatic polypeptide (PP) and gastric inhibitory polypeptide (GIP), as well as blood glucose, were measured in eight healthy women before, during and after oxytocin infusion in post‐term pregnancies. Plasma VIP increased significantly (P<0.01) during oxytocin infusion. Plasma secretin showed a significant (P<0.05) decrease during oxytocin infusion. Plasma somatostatin remained unchanged during oxytocin infusion, but thereafter a significant (P<0.05) increase occurred. Both plasma motilin and plasma PP showed a non‐significant increase during oxytocin infusion with sustained levels thereafter. No changes were found for plasma insulin, GIP and blood gluc

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1988.tb08293.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

This study was performed in order to investigate whether activation of sensory fibres within the sciatic and vagal nerves might influence the release of oxytocin. In anaesthetized rats the sciatic and vagal nerves were stimulated electrically in an afferent direction with a variety of stimuli. Rats were also stroked on their backs or nociception was inflicted by pinching a foot. Plasma oxytocin levels were measured with a highly sensitive radioimmunoassay in samples drawn from the carotid artery. Afferent electrical stimulations of both sciatic and vagal nerves at 5 V, 0.2‐2 ms and 3–10 Hz caused immediate significant elevations of oxytocin levels. Thus, basal levels increased by 30–184%. Furthermore, in response to touch and nociceptive stimuli, oxytocin levels rose by 181 % and 206%, respectively. These data indicate that oxytocin can be released by stimulation of peripheral nerves originating in the skin and/or muscle and in the gastrointestinal tract and thus these organs may be involved in the control of oxytocin secr

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1988.tb08294.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

Hind legs of adult rats were exposed to vibrations (81 Hz; amplitude 0.50 mm peak to peak) for 4 h during two consecutive days. The sciatic, tibial and plantar nerves were isolated and processed for immunohistochemical demonstration of IGF‐I (insulin‐like growth factor I; somatomedin C) immunoreactivity at different time intervals after the vibration exposure.In sham‐exposed rats the axons in peripheral nerves showed no or faint IGF‐I immunoreactivity while most Schwann cells were negative. Exposure of the hind legs to vibrations induced increased IGF‐I immunoreactivity in the Schwann cells, demonstrable at the end of the exposure period and reaching maximal intensity 2–3 days after vibration exposure. Several distended axons similarly showed increased staining. The IGF‐I immunoreactivity decreased after 7–10 days to almost the level in the control nerves. The most extensive changes were observed in the plantar nerves. The tibial nerves similarly expressed strongly increased IGF‐I immunoreactivity in their Schwann cells. The sciatic nerve showed, however, only slightly to moderately increased staining. Cells in the epineurium of the plantar and, to a limited extent, of the tibial nerves expressed concomitantly increased IGF‐I immunoreactivity. We conclude that the transiently increased IGF‐I immunoreactivity in peripheral nerves reflects reactive changes caused by vibrations and most prominently expressed

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1988.tb08295.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

Sympathetic nerve stimulation (2 min, 2 and 10 Hz) increased perfusion pressure in the blood perfused canine gracilis musclein situafter pretreatment with atropine, desipramine and beta‐adrenoceptor antagonists. This vasoconstriction was accompanied by clear‐cut increases in the overflow of endogenous noradrenaline (NA) at both frequencies and, at 10 Hz but not at 2 Hz, also of neuropeptide Y‐like immunoreactivity (NPY‐LI). The irreversible alpha‐adrenoceptor antagonist phenoxybenzamine enhanced the nerve stimulation induced overflows of NA and NPY‐LI five‐ to eightfold and threefold, respectively. The fractional overflows of NA and NPY‐LI per nerve impulse were similar in response to the high‐frequency stimulation, indicating equimolar release in relation to the tissue contents of the respective neurotransmitter. The maximal vasoconstrictor response elicited by 10 Hz was reduced by about 50% following a dose of phenoxybenzamine which abolished the effect of exogenous NA and the remaining response was more long‐lasting. Local i.a. infusion of NPY evoked long‐lasting vasoconstriction in the presence of phenoxybenzamine, while the stable adenosine 5′‐triphosphate (ATP) analogue α‐β‐methylene ATP was without vascular effects. Locally infused NPY reduced the nerve stimulation evoked NA overflow by 31% (P<0.01) at 1μMin arterial plasma, suggesting prejunctional inhibition of NA release. In conclusion, NPY‐LI is released from the canine gracilis muscle upon sympathetic nerve stimulation at high frequencies. There is nerve stimulation evoked vasoconstriction, which is resistant to alpha‐adrenoceptor blockade. This may in part be mediated by NPY released together with NA

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1988.tb08296.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

NPY, a peptide with 36 amino acid residues, is co‐stored together with noradrenaline (NA) in cardiac and sympathetic perivascular nerves as well as with adrenalin (A) in adrenal chromaffin cells. NPY is released together with NA from sympathetic nerves and with A from the adrenal glands and appears to be involved in the control of sympathetic neurotransmission.The aim of the present study was to analyse the effect of NPY on the preganglionic nerve stimulation (PNS) evoked increases in plasma A and NA concentrations in pithed rats. In the first part of the study (I) only one PSN period (2 Hz for 45 s) was performed in each rat and the control group was compared to the NPY treated group. In the second part of the study (II) two PNS periods (1 Hz for 45 s) were performed in each rat, which either received saline or NPY before the second PNS. Thus, interindividual changes between the responses to the first and second PNS in control and NPY rats could be compared.In both study I and II, systemic infusion of NPY (2 μg kg‐1min1i.v.) significantly reduced the PNS‐induced increase in plasma A by 26% and 42%, respectively (P<0.05). However, the increase in plasma NA elicited by PNS was significantly reduced only in study II by 23% (P<0.05). Infusion of NPY did not affect basal heart rate in either of the studies, but significantly increased basal blood pressure by about 10 mmHg. The blood pressure responses to PNS were significantly greater in NPY treated rats.It is concluded that PNS‐evoked release of A and NA is under inhibitory control of NPY. The inhibition of NA release from the sympathetic nerve terminals is most probably due to a prejunctional site of action, whereas the reduced secretion of A could be due to a local effect of NPY in the adrenal medulla,. The negative influence of NPY on A and NA release appears to be compensated for by the additional facilitatory action of NPY on the postjunctioned responses to these catech

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1988.tb08297.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

Microsurgical renal denervation of the rat has been reported to increase blood loss and bleeding time after a standardized kidney resection. To investigate the vascular effects of denervation, isolated intrarenal arteries were studied using sensitive ‘isometric’ recording equipment. Four pieces of evidence were obtained to indicate an effective functional denervation 1 week after renal nerve transection: (i) Phentolamine reduced the K+‐induced contraction in controls but not in denervated arteries, (ii) The K+‐induced contraction was significantly smaller in denervated than in control arteries, (iii) Noradrenaline (NA) was a significantly more potent vasoconstrictor (4 x) in denervated than in control arteries, (iv) Cocaine increased the NA sensitivity in control arteries (3 x), whereas it failed to do so in denervated vessels. Vasopressin, 5‐hydroxytryptamine (5‐HT), NA (in the presence of cocaine), prostaglandin F2α(PGF2:α) and dopamine (DA) produced concentration‐dependent contractions in the mentioned order of potency. Denervated arteries were found to be about two to three times more sensitive to the vasoconstrictors than control arteries. Angiotensin I and II had no contractile effect in any of the vessel segments examined. Indomethacin‐pretreated arteries also failed to respond to angiotensin II. Neuropeptide Y produced only weak contractions and failed to influence the NA concentration‐response relationship in either control or denervated arteries. In conclusion, renal denervation caused a general supersensitivity of the vascular smooth muscle cells to both circulating and non‐circulating vasoconstrictors. Our results cannot explain the increased blood loss and bleeding time seen after denervation, but rather support the view that the enhanced bleeding was caused by an interrupted vasoconstrictor influence of t

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1988.tb08298.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

In five goats water deprivation for 26 h increased plasma osmolality, total plasma protein concentration, and plasma vasopressin (AVP) concentration to higher levels during lactation compared to nonlactation. At the end of the dehydration period intraruminal loads of saline or water (corresponding to 50% of the body weight loss) were given to lactating goats. The saline load decreased the plasma protein concentration below control levels, while plasma osmolality, Na concentration and AVP did not change. After the water load the plasma protein concentration stayed elevated. Plasma osmolality, Na concentration and AVP fell, but remained significantly above control levels. Both plasma renin activity (PRA) and aldosterone (PA) concentration increased after water, but decreased after saline administration. Three hours after the fluid loads the goats were offered water to drink. AVP decreased at the sight of water. After drinking, plasma osmolality, Na and AVP continued to decrease in water loaded animals, and fell also in saline loaded goats. PRA remained elevated, and PA increased in water loaded goats, while these hormones still were depressed in saline loaded goats. Mean renal ‘free water clearance’ became positive after drinking in both groups. It is concluded that the water losses with the milk cause lactating goats to become dehydrated more rapidly than non‐lactating goats during water deprivation. Lowering of the plasma osmolality and Na concentration are more important than restoration of the plasma volume in suppressing the high plasma AVP concentration in the dehydrated lactating goat. The water diuresis, which occurred after voluntary drinking, indicates that the goats had not been able to anticipate their water deficit accurately. In goats, water deprivation causes no stimulation of PRA, but PRA increases in response to both a load of water and to voluntary drinking. The cause of these effects is un

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1988.tb08299.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

The effect of furosemide on carbohydrate metabolism was studied in mice. Single‐dose administration (200 mg kg‐1body weight) resulted in transient hyperglycaemia and a rise in the glucose/insulin ratio within 60 min. The glucose tolerance was impaired with elevated serum glucose and reduced insulin response 2 h after the furosemide injection, but had recovered within 24 h. In mice made hypoglycaemic by prior injection of insulin, the basal serum glucose and the glucose tolerance were impaired 22 h after the injection of furosemide. It is suggested that furosemide has both acute and long‐term effects on carbohydrate metabolism in mice and that, at least in part, this is due to reduced insulin secretion. Glucose may protect against the diabetogenic action of furos

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1988.tb08300.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY