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- Arner, Anders, et al.
(author)
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Energy turnover and lactate dehydrogenase activity in detrusor smooth muscle from rats with streptozotocin-induced diabetes
- 1993
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In: Acta Physiologica Scandinavica. - 0001-6772. ; 147:4, s. 375-383
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Journal article (peer-reviewed)abstract
- Force generation and tissue glucose metabolism were measured in the urinary bladder smooth muscle from rats with streptozotocin-induced diabetes (7-8 wk duration). Bladder wet wt was almost 4-fold higher in the diabetic animals compared with the untreated controls. Morphological analysis showed that the growth was associated with hypertrophy of the smooth muscle component in the bladder wall. Force generation of isolated bladder strip preparations was measured in vitro at different ambient oxygen tensions. Activation of intramural nerves, with electrical field stimulation, induced contractions that were unaffected by reduction of oxygen tension down to PO2 100 mmHg for both control and diabetic muscle strips. At zero PO2 force was reduced by approximately 10-20%, in both groups. High-K+ solution induced 'tonic' contractions that were slightly more inhibited by lowering PO2. At intermediate PO2 (between 100 and 20 mmHg) the diabetic muscle gave slightly higher force. At zero PO2 no significant difference could be detected between strips from control and diabetic animals. Oxygen consumption and lactate production in the preparations were determined at a PO2 of 290 mmHg and related to the volume of smooth muscle. At zero PO2, lactate formation increased 3- to 4-fold. The metabolic tension cost was lower at zero PO2. No differences in basal and contraction related metabolic rates could be detected between the two groups under normoxic and anoxic conditions. The maximal activity of lactate dehydrogenase (LDH) determined in tissue samples was about 2-fold higher in the diabetic bladder muscle.(ABSTRACT TRUNCATED AT 250 WORDS)
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- Bill, A, et al.
(author)
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Cholecystokinin causes contraction of the pupillary sphincter in monkeys but not in cats, rabbits, rats and guinea-pigs: antagonism by lorglumide
- 1990
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In: Acta Physiologica Scandinavica. - 0001-6772. ; 138:4, s. 479-485
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Journal article (peer-reviewed)abstract
- The effects of intracameral injections of cholecystokinin (CCK) on the pupil size were determined in monkeys, cats, rabbits, rats and guinea-pigs. In animals under muscarinic cholinergic blockade, CCK caused miosis in monkeys but not in the other species investigated. In monkeys CCK-8 was more potent than CCK-33, which was, however, much more potent than non-sulphated CCK-8. These observations indicate that peripheral type A receptors mediated the miotic response. The effect of CCK-8 was not appreciably influenced by pretreatment with indomethacin, 3 mg kg-1 body wt, indicating that prostaglandins were not involved in the response. Nerve blockade with 0.9 micrograms tetrodotoxin intracamerally had no clear effect on the dose-response relationship for CCK-8. The effect of the peptide thus seems to be directly on receptors on the pupillary sphincter muscle. Pretreatment with lorglumide caused a dose-dependent rightward shift of the dose-response curve, indicating competitive antagonism. The results indicate that in monkeys, but not in rabbit, cats, rats and guinea-pigs, CCK is a potent miotic with a direct effect on the pupillary sphincter mediated by type A CCK receptors on the muscle.
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- Bodelsson, Mikael, et al.
(author)
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Cooling enhances alpha 2-adrenoceptor-mediated vasoconstriction in human hand veins
- 1990
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In: Acta Physiologica Scandinavica. - 0001-6772. ; 138:3, s. 283-291
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Journal article (peer-reviewed)abstract
- The contribution of different receptor subtypes in the contractile response during cooling in human hand vessels is of considerable interest in the understanding of cold-induced peripheral vasospasm as it appears in Raynaud's phenomenon. Subcutaneous vein segments from 50 patients undergoing hand operations not related to vascular disorders were examined in vitro. The temperature in the organ bath was initially 37 degrees C and was either continuously lowered to 10 degrees C or kept constant at 37 degrees C, 29 degrees C or 20 degrees C. The characteristics of the alpha-adrenoceptor-mediated motor response were elucidated with the use of the alpha 1-antagonist, prazosin, and the alpha 2-antagonist, yohimbine. A great variability between individuals in the proportions of alpha 1- and alpha 2-adrenoceptors was found. In the majority of the vessels continuous cooling to 25 degrees C augmented a noradrenaline-induced contraction. This augmentation was unaltered in the presence of prazosin but abolished by yohimbine, suggesting that it was mediated via the alpha 2-adrenoceptor. In the remaining vessels with a predominating alpha 1-adrenoceptor-mediated response a cold-induced relaxation was registered. This could be the result of a reduced alpha 1-adrenoceptor-mediated contraction at this low temperature. These varying reactions to cooling were unaffected by the beta-antagonist, propranolol, and by endothelial denudation. The results obtained in corresponding experiments with the alpha 1-agonist methoxamine and alpha 2-agonist, oxymetazoline, were conflicting, probably due to the poor selectivity of these agonists in human tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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- Bodelsson, Mikael, et al.
(author)
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Effect of cooling on smooth muscle response to 5-hydroxytryptamine in human hand veins
- 1990
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In: Acta Physiologica Scandinavica. - 0001-6772. ; 140:3, s. 331-339
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Journal article (peer-reviewed)abstract
- 5-Hydroxytryptamine has been suggested to be a mediator in peripheral cold-induced vasospasm. In order to investigate the contribution of different 5-hydroxytryptamine receptor subtypes in the contractile response during cooling, segments of subcutaneous hand veins obtained from 50 patients undergoing hand surgery were examined in vitro in organ baths. The temperature in the bath was initially 37 degrees C and was either continuously lowered to 10 degrees C or kept constant at 37 degrees C, 29 degrees C. Cooling to 25 degrees C augmented the contractile response to 5-hydroxytryptamine in intact as well as in endothelium-denuded segments. The 5-hydroxytryptamine2 receptor antagonist ketanserin antagonized the contractile response to 5-hydroxytryptamine at 37 degrees C, and in addition abolished the cold-induced enhancement of the response during cooling. This points to a major role of the 5-hydroxytryptamine2 receptor in the cold-induced augmentation of the response to 5-hydroxytryptamine, which was further supported by increased contractions to the 5-hydroxytryptamine2 receptor agonist alpha-methyl-5-hydroxytryptamine during cooling. Contractile responses were also obtained by the selective 5-hydroxytryptamine1-like receptor agonist GR43175 interpreted to indicate the presence of a smaller 5-hydroxytryptamine1-like receptor population. However, the response to GR43175 was unaffected by cooling. These results warrant further investigations of the role of 5-hydroxytryptamine in cold-induced peripheral vasospasm.
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- Carlsson, S, et al.
(author)
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Evidence for an adrenergic innervation of the adrenal cortical blood vessels in rats.
- 1993
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In: Acta physiologica Scandinavica. - 0001-6772. ; 149:1, s. 23-30
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Journal article (peer-reviewed)abstract
- The aim of this study was to investigate the blood flow in the adrenal cortex of the rat. Relative changes in the adrenal cortical blood flow were continuously measured by Laser Doppler flowmetry in 33 chloralose-anaesthetized artificially ventilated rats during electrical stimulation (1 ms, 5 V) of the left great splanchnic nerve (LGSN), which conveys both pre- and post-ganglionic nerve fibres to the adrenal gland. Laser Doppler flux (LDF) was decreased and regional resistance (RR) was increased by augmenting nerve stimulation at increasingly higher frequencies (2, 4, 8, 20 and 40 Hz). The decrease in LDF, when compared to pre-drug stimulations at 4 Hz was partially or totally inhibited by the adrenergic blocking agents trimethaphan (TRIM), guanethidine (GUA) and alpha 1-blockade with prazosin (PRAZ). Furthermore, both the decrease in LDF and the increase in RR were either completely or partially blocked by stimulation at 40 Hz after TRIM-treatment and GUA-treatment. It is concluded that the adrenal cortex in the rat is innervated by post-ganglionic adrenergic nerve fibres, which are involved in the regulation of blood flow in the adrenal cortex.
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7. |
- Cervin, Anders, et al.
(author)
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Sympathetic nerve stimulation influences mucociliary activity in the rabbit maxillary sinus
- 1991
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In: Acta Physiologica Scandinavica. - 0001-6772. ; 143:4, s. 405-411
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Journal article (peer-reviewed)abstract
- The effect of preganglionic sympathetic nerve stimulation on mucociliary activity in the rabbit maxillary sinus was investigated in vivo. Response to nerve stimulation was recorded photoelectrically and expressed as a percentage of the basal mucociliary activity prior to stimulation. Nerve stimulation (15 V, 5 ms) for 60 s at 2, 10 and 20 Hz stimulated mucociliary activity, the maximum increase being 21.1 +/- 1.3% at 20 Hz, an increase that pretreatment with the cholinergic antagonist atropine reduced to 14.5 +/- 2.4%, suggesting that part of the response involves cholinergic mechanisms. Nerve stimulation (10 Hz) of animals pretreated with the beta-adrenoceptor antagonist propranolol reversed the mucociliary response from an increase to a decrease (-10.6 +/- 1.6%), indicating the involvement of beta-receptors in the nerve-evoked increase. Pretreatment with the alpha-adrenoceptor antagonist phentolamine had no effect on response to nerve stimulation. Rabbits given a combined atropine, propranolol and phentolamine blockade manifested decreased mucociliary activity in response to nerve stimulation (-10.6 +/- 2.1%). Guanethidine pretreatment blocked the effect of nerve stimulation on mucociliary activity, including the observed decrease after combined blockade, indicating the effect to be mediated via sympathetic nerve fibres. The decrease in mucociliary activity in response to nerve stimulation after combined cholinergic-, beta-, and alpha-adrenoceptor blockade suggests the presence of a nonadrenergic, non-cholinergic inhibitory mechanism. It is possible that this effect is mediated by release of neuropeptide Y, as intraarterial injections of neuropeptide Y reduce mucociliary activity in the rabbit maxillary sinus, and as neuropeptide Y is released in the upper airways upon sympathetic nerve stimulation.
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