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At least 343 records · Page 19Linked to original sources
PubMed1991

Capsaicin-sensitive nerves modulate resting blood flow and vascular tone in rat gut.

Acute and chronic treatments with capsaicin were used to evaluate the role of afferent neurons in the regulation of intestinal blood flow. Experiments were performed on anesthetized rats, in which mean intestinal blood flow was determined with a pulsed Doppler flowmeter, mean systemic arterial pressure was determined with a transducer, and intestinal vascular conductance (C) was calculated from these measurements. Acute administration of periarterial capsaicin (0.5 mg) induced biphasic intestinal vascular responses. An early hyperemic response occurred with a maximal increase in blood flow of 31% at 5 min, followed by a decrease in blood flow of 17% at 30 min. Arterial pressure was decreased by the application of capsaicin, initially by 10%. There was an early increase of 49% in conductance, followed by a 15% decrease, compared with control values. When 1 or 4 mg capsaicin was instilled into the lumen of the jejunum there was a response pattern similar to that observed after periarterial application of capsaicin. Intrajejunal capsaicin (4 mg) increased blood flow by 51%, followed by a decrease of 16%. Mean mesenteric artery conductance was increased by 32% initially and subsequently was decreased by 21%, in response to acute intrajejunal administration of capsaicin. Both mean blood flow and conductance were increased (44% and 76%, respectively) in adult rats chronically pretreated with capsaicin (170 mg total dose) when compared with vehicle-treated controls. However, in rats pretreated neonatally with capsaicin (50 mg/kg) and allowed to mature, basal flood flow was lower than in control animals but C was not different from control littermates.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Phorbol 12,13-dibutyrate increases vascular tone but has a dual action on intracellular calcium levels in porcine coronary arteries.

The effects of phorbol 12,13-dibutyrate (PDBu). a protein kinase C activator, on the tone and intracellular calcium level (Cai2+) of vascular smooth muscles were simultaneously measured by use of a force-displacement transducer and the fura-2 microscopic fluorometric technique in porcine coronary arteries. Cumulatively applied PDBu produced a slowly developing and concentration-dependent contraction in the concentration range of 10(-8)-10(-6) mol/l. Contractions induced by PDBu were sustained after removal of PDBu. Changes in Cai2+ produced by PDBu were very slight, although Cai2+ was increased at lower concentrations (3 x 10(-8) and 10(-7) mol/l) and decreased at higher concentrations (3 x 10(-7) and 10(-6) mol/l). Verapamil 10(-6) mol/l partially inhibited the contractions throughout the concentration range of PDBu and the increase in Cai2+ induced by lower concentrations of PDBu. When the effects of PDBu were compared with those of the 90 mmol/l KCl medium, the force of contraction induced by a single concentration of 10(-7) mol/l PDBu was about 50% and the increase in Cai2+ was about 10%. Removal of extracellular calcium by 1 mmol/l EGTA decreased Cai2+ by about 20% but vascular tone did not change. PDbu (10(-7) mol/l) produced a small contraction without an increase in Cai2+ in the Ca2+-free medium. Depolarization by the 20 mmol/l KCl medium increased Cai2+ by about 20%, whereas vascular tone did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Functional relation between nitric oxide and noradrenaline for the modulation of vascular tone in rat mesenteric vasculature.

As previously reported, N omega-nitro-L-arginine (L-NNA), an inhibitor of nitric oxide (NO) synthesis, decreased transmural field stimulation (TFS)-induced noradrenaline overflow from the isolated perfused rat mesenteric vasculature attached to the intestine. The decrease was attenuated by L-arginine. This suggests that NO may increase noradrenaline release (Yamamoto et al. 1993). The present experiments with this preparation were done in order to monitor changes in vascular perfusion pressure caused by TFS or by noradrenaline infusion in parallel with those in the noradrenaline outflow caused by TFS in the presence of atropine (0.1 mumol/l) (to block acetylcholine-induced release of endothelial NO) and of indomethacin (3 mumol/l) (to inhibit L-NNA-induced production of vasoconstrictor prostanoids). (1) TFS (2-10 Hz) caused a frequency-dependent increase in noradrenaline overflow and perfusion pressure. (2) L-NNA (10 and 30 mumol/l) caused a concentration-dependent inhibition of TFS-induced noradrenaline overflow, whereas the TFS-induced pressure increase was augmented by L-NNA in a concentration-dependent manner. At any given concentration of L-NNA, the potentiation of vasoconstriction by L-NNA became greater in magnitude as the frequency of the TFS was raised. (3) Infusion of noradrenaline (0.38-6 nmol) caused a dose-dependent increase in perfusion pressure up to a value comparable with that caused by TFS. The pressure increase in response to noradrenaline infusion was also enhanced by L-NNA, relatively, to a greater extent than the enhancement, by L-NNA, of the pressure response to TFS.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Octopamine relaxes rabbit jejunal smooth muscle by selective activation of dopamine D1 receptors.

The effect of octopamine on intestinal smooth muscle of rabbit isolated jejunum has been studied. Octopamine induced a dose-dependent decrease of muscle tone and this reproducible relaxation was not modified by tetrodotoxin or by agents that acted on adrenergic nerve terminals. Adrenoceptor antagonists, at concentrations sufficient to block each adrenoceptor type, did not reduce the actions of octopamine. On the other hand, octopamine-induced relaxations were affected by agents that have the ability to change cyclic AMP (cAMP) content; such as alloxan (an adenylate cyclase inhibitor), imidazole (a stimulator of phosphodiesterase), and isobutyl methylxanthine (an inhibitor of phosphodiesterase). Direct stimulation of adenylate cyclase by octopamine was demonstrated using radioimmunoassay of cAMP. Furthermore, haloperidol and perphenazine at concentration required to block dopamine receptor sites attenuated both smooth muscle relaxation and the formation of cAMP induced by octopamine. The effect of octopamine was totally blocked by SCH 23390, an antagonist of dopamine D-1 receptors. The lack of effect of domperidone and sulpiride, antagonists of dopamine D-2 receptors, on the actions of octopamine excludes the involvement of dopamine D-2 receptors. These results suggest that octopamine acts on intestinal dopamine D-1 receptor sites to produce relaxation of rabbit jejunum through an increase of cAMP.

Adenylyl Cyclases↗
PubMed1994

Regulation of tone in penile cavernous smooth muscle. Established concepts and new findings.

Since Benson, in 1983, reported on a potent nonadrenergic, noncholinergic (NANC) transmitter postulated to relax penile vessels and the corpus cavernosum, much new information on the mechanisms of contraction and relaxation of corporeal smooth muscle and penile vasculature has been obtained. The information currently available suggests that NANC transmitters may be involved in both contractile and relaxant responses of penile erectile tissues. There is good experimental evidence to allow the assumption that neurogenic nitric oxide (NO) is a mediator of penile erection, but even if NO probably is the most important factor for relaxation of penile vessels and the corpus cavernosum, this does not exclude the possibility that other agents released from nerves may have a modulatory function in this process. However, the roles of, for example, vasoactive intestinal polypeptide and related peptides as neurotransmitters and/or neuromodulators in the nervous control of penile erection have yet to be established. The restricted availability of human penile erectile tissues has led to the use of cavernous tissue and penile vessels from animals, both for screening and for detailed analysis of mechanisms previously demonstrated to exist also in human tissues. When interpreting the results obtained, it is important to stress that there may be important differences between human and animal tissues, that each of the tissues only gives a piece of information on the complex process of penile erection, and that the physiological and clinical importance of results from such experiments may be limited. The differing responses in different parts of the vasculature within the penis and the multiplicity of putative transmitters present in the corpus cavernosum and in perivascular nerves make further investigations necessary, as do the interactions between transmitters and neuromodulators at the neuromuscular junction, and between the neural and endothelial control of vascular tone.

Adenosine Triphosphate↗
PubMed1994

Characterization of cyclic nucleotide phosphodiesterase isoenzymes in the human ureter and their functional role in vitro.

An increase in cyclic nucleotide monophosphate levels is suggested to play a prominent role in mediating smooth-muscle relaxation. Cyclic nucleotide phosphodiesterase (PDE) influences smooth-muscle tone by decreasing the level of cyclic nucleotides. At present, five different families of isoenzymes of PDE exist that show a distinct species- and organ-specific distribution. Our study was done to evaluate the existence of specific PDE isoenzymes and its functional role in human ureteral tissue. Normal ureteral tissue was homogenized and centrifuged and the supernatant fraction was separated using anioin-exchange diethylaminoethyl (DEAE)-Sephacel chromatography. A PDE assay was then performed and the peak fractions were added to different specific PDE activators and inhibitors. In vitro, longitudinal ureteral strips were precontracted and different selective and non-selective PDE inhibitors were added incremently. Three different PDE isoenzymes were characterized: PDE I (calmodulin-sensitive), PDE II (cGMP-stimulated), and PDE IV (cAMP-specific). All PDE inhibitors relaxed the strips dose-dependently, with the 50% effective concentrations (EC50) being 30 microM for papaverine, 40 microM for zaprinast, 25 microM for quazinone, and 0.1 microM for rolipram. The ureter-relaxing effect of the PDE IV inhibitor at low concentrations, combined with its low-level effect on the systemic circulatory parameters, may open the possibility of using selective PDE IV-inhibitors in the treatment of ureteral colics or for ureteral stone passage.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMedDate not supplied

Intra- and extraluminally-applied acetylcholine on the vascular tone or the response to transmural stimulation in dog isolated mesenteric arteries.

Acetylcholine applied extraluminally to isolated, perfused dog mesenteric artery segments produced an endothelium-dependent depressor response when the perfusion pressure was raised by continuous infusion of noradrenaline; the potency was 1/30 to 1/60 that of intraluminal acetylcholine. Contractions induced by transmural electrical stimulation were attenuated by treatment with intra- and extraluminal acetylcholine; the inhibitory effect of intraluminal acetylcholine was greater than that of extraluminal acetylcholine. Removal of endothelium did not significantly alter the inhibitory effect. In mesenteric artery strips with endothelium, treatment with oxyhaemoglobin suppressed the relaxant response to acetylcholine but did not influence the inhibitory effect of acetylcholine on stimulation-evoked contractions. Acetylcholine reduced the 3H-overflow and contraction of superfused mesenteric artery strips, preloaded with 3H-noradrenaline, response to transmural stimulation. By the use of bioassay (dog femoral artery segment with endothelium/coronary artery strip without endothelium), the release of EDRF was first determined in the perfusate, which was introduced to dog mesenteric artery strips loaded with 3H-noradrenaline. The 3H-overflow and contraction caused by the stimulation were not attenuated by EDRF and were also observed following treatment with superoxide dismutase. Inability of the perfusate to reduce the stimulation-evoked 3H-overflow was also observed when the donor and assay tissues were treated with superoxide dismutase. It may be concluded that the inhibition by acetylcholine of the release of neuronal noradrenaline is not dependent on endothelium. Extraluminally applied acetylcholine would reach the endothelium and release EDRF, and intraluminal acetylcholine is presumed to act directly on prejunctional muscarinic receptors; however, acetylcholine appears to cross the medial layer more efficiently from intima to adventitia than in the reverse direction.

Acetylcholine↗
PubMed1975

Functional states and fine structure of the contractile apparatus of the penis retractor muscle (PRM) of Helix pomatia L.

The ultrastructure of the isolated glycerinated penis retractor muscle (PRM) of Helix pomatia was investigated. The diameter distributions of thick myofilaments from birbre cross sections in the relaxed, phasic contracted, tonic contracted, and in the catch state.s show that a characteristic filament spectrum is formed in the catch state and its preceding active state. The significant structural differences are discussed in relation to earlier hypotheses related to the catch state

Animals↗
PubMedDate not supplied

Paracrine functions of the coronary vascular endothelium.

Coronary vascular endothelial cells control vascular tone by modulating the local concentration of circulating vasoactive substances (e.g. adenine nucleotides, biogenic amines and bradykinin) and by synthesising and releasing the vasoactive autacoids nitric oxide (NO) and prostacyclin (PGI2). The fluid shear stress exerted by the streaming blood is the physiologically most important stimulus for a continuous endothelial NO production, which counteracts neuro- and myogenic constriction. This shear stress-dependent NO release represents a highly effective local system for maintaining adequate blood flow to the myocardial tissue. At the transcriptional level endothelium-derived NO modulates the regulation of a number of genes (e.g. monocyte chemoattractant protein-1, P-selectin and vascular cell adhesion molecule-1) most probably by direct and/or indirect interaction with transcription factors. In addition to NO and PGI2, the coronary vascular endothelium is also able to release a factor which causes hyperpolarisation of the underlying smooth muscle. This so-called endothelium-derived hyperpolarising factor (EDHF) displays the characteristics of a cytochrome P450-derived arachidonic acid metabolite. However, since NO is able to attenuate production of this factor, EDHF may contribute to the regulation of vascular tone essentially in situations associated with an apparent dysfunction of the endothelium.

Acetylcholine↗
PubMed1991

Wrist muscle activation patterns and stiffness associated with stable and unstable mechanical loads.

The objectives of this study were to examine the effects of load mechanical characteristics and agonist-antagonist muscle cocontraction, on the stretch reflex response of wrist flexor muscles, and to measure the associated wrist stiffness. Subjects were required to maintain a constant wrist angle while operating against flexor loads with different stability characteristics (constant, elastic or unstable). We measured the stretch reflex responses and joint stiffness by applying step displacements of 3 degrees and 10 degrees. Subjects used very little cocontraction of wrist flexor and extensor muscles when the load was constant or elastic, but increased cocontraction dramatically when the load was unstable, in order to increase the wrist stiffness. Although the magnitude of stretch reflex responses also increased with cocontraction, this simply reflected the level of tonic flexor muscle activity. We found no evidence to suggest that phasic stretch reflexes contributed significantly to the joint stiffness in this task. Clear differences in flexor muscle synergy were observed in the presence and absence of cocontraction, particularly when comparing the FCR and FCU muscles.

Adult↗
PubMed1991

Patterns of reinnervation of denervated cerebral arteries by sympathetic nerve fibers after unilateral ganglionectomy in rats.

In order to clarify the manner in which previously denervated cerebral arteries become reinnervated after unilateral excision of the superior cervical ganglion (SCG), we observed directly the reinnervating sympathetic nerve fibers originating in the contralateral SCG by using anterograde labeling with wheat germ aggulutinin-horseradish peroxidase in rats. The nerve fibers sprouted from the nerve fibers in the contralateral anterior cerebral artery and reinnervated the arterial wall of the anterior cerebral artery of the denervated side as early as one week after ganglionectomy. In addition to this sprouting route, three other reinnervating nerve fiber routes were observed in the circle of Willis of the denervated side two weeks after ganglionectomy: the proximal portion of the internal carotid artery, the route passing between bilateral ethmodial arteries, and the posterior communicating artery. Eight weeks after ganglionectomy, these reinnervating nerve fibers formed a fairly dense plexus in a circular pattern in the circle of Willis. However, the reinnervation could not be observed in the arterial branches derived from the circle of Willis (middle cerebral artery and posterior cerebral artery) even 16 weeks after ganglionectomy. The present results clearly demonstrated the time course, distribution pattern and limitation of the reinnervation from the contralateral SCG following unilateral ganglionectomy. The fact that reinnervation could be observed only in the main cerebral arteries of the circle of Willis, in which the nerve plexus appeared to have a circular pattern, suggests a difference between the qualities of sympathetic innervation controlling the cerebral circulation in these arteries and the other arterial branches related to these differences in reinnervation capacity.

Animals↗
PubMed1975

Recurrent inhibition of individual Ia inhibitory interneurones and disinhibition of their target alpha-motoneurones during muscle stretches.

The effects of ramp stretches applied to triceps surae muscle on the discharge patterns of single Ia inhibitory interneurones, monosynaptically invaded from various nerves, were studied in either decerebrate or anesthetized cats. Interneurones which received direct excitatory Ia input from the stretched muscle exhibited augmented activity both during the dynamic and static phase of stretch, which was, however, interrupted by a transient inhibitory influence during the dynamic phase of stretch. The influences on Ia inhibitory interneurones, monosynaptically invaded from hamstring or tibial nerve, were exclusively inhibitory. These stretch-induced inhibitions were better demonstrable in decerebrate than in anesthetized preparations. The timing of the discharge patterns of additionally recorded Renshaw cells during stretch, and the disappearance or reduction of the above described inhibitory effects after administration of DHE, strongly support the idea that these inhibitory actions are caused by Renshaw inhibition. In Ia inhibitory interneurones, monosynaptically activated from the antagonistic peroneal nerve, stretch induced also pronounced inhibitory effects, which were most probably caused by mutual inhibition between Ia inhibitory interneurones. The suppression of agonistic Ia inhibitory interneurone activity below the tonic resting activity corresponded to an enhancement of the monosynaptic reflex amplitude of the antagonistic motoneurone pool. The findings suggest that normal orthodromic activation of Renshaw cells, and consequently the recurrent inhibition of the Ia inhibitory interneurones, is predominantly linked with rapid phasic, rather than slow tonic, motoneuronal firing. The functional role of this mechanism for the performance of rapidly alternating movements and the damping of ballistic agonist contractions is discussed.

Animals↗
PubMed1975

Urodynamics.

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Biomechanical Phenomena↗
PubMed1989

Selective posterior rhizotomy: a long-term follow-up study.

Fifty-one spastic children who had undergone selective posterior lumbar rhizotomy between 1981 and 1984 were re-examined to determine whether the gains achieved had persisted and to look at other aspects that had not previously been explored in detail. The reduction of tone was maintained in all cases, while motor function continued to improve in 42 cases. Functional gains were greatest in children operated on under the age of 8, but pleasing results were also achieved in older children. Forty-five children continued to receive physiotherapy, particular attention being paid to building up muscle strength. Sensory disturbances were minimal, and there was no evidence of spinal instability. Post-rhizotomy orthopaedic surgery for fixed-joint contractures generally brought further improvement. Parents and older children were also questioned and almost all were enthusiastic about the outcome. Rhizotomy can be of considerable benefit to spastic children, but great care must be taken in the selection of suitable cases.

Adolescent↗