摘要:

The disynaptic pathway from muscle spindle la afferents to motoneurones of the antagonist muscle is one of the best studied pathways in the spinal cord. Early animal studies ‐ mainly in the cat ‐ have provided a detailed knowledge of the pathway itself and of the integration of segmental and supraspinal convergence at the interneuronal level. Although this knowledge was used to formulate hypotheses on the function of the pathway during natural movements, the reduced animal preparation limited the possibilities of testing these ideas. However, such information has more recently been obtained from human subjects by using indirect electrophysiological techniques. In most of these experiments the disynaptic la inhibition was demonstrated as a short‐latency depression of a monosynaptic test reflex (H‐reflex) following a conditioning stimulation of the antagonist nerve. Changes in the size of this depression during voluntary tasks were then taken as evidence of a central regulation of the pathway. It has for example been demonstrated in this way that the brain regulates the la inhibitory interneurones in parallel with their corresponding motoneurones during extension‐flexion movements, but not during co‐contraction of antagonistic muscles. The importance of the central control of the pathway has also been emphasized by the finding of a disordered regulation of its activity in patients with lesions of the brain. This may possibly contribute to the inappropriate co‐contraction of antagonistic muscles observed in some of these patients. It seems reasonable to expect that this kind of experiment in the future may contribute significantly to the knowledge of the central control of spinal mot

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09817.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

In skeletal muscle, the excitation induced influx of Na+and efflux of K+may be sufficient to exceed the activity or even the capacity of the available Na+, K+‐pumps. This leads to a rise in intracellular Na+and extracellular K+Both events interfere with excitability and may present important limitations for the continuation of contractile activity. Furthermore, inhibition of the Na+, K+‐pump or reduction of the concentration of functional Na+, K+‐pumps decrease excitability and the maintenance of force during continued stimulation. Conversely, in muscles where contractile force is inhibited by exposure to high extracellular K+, acute stimulation of the Na+, K+‐pump with catecholamines, CGRP or insulin leads to a rapid recovery of force. The large passive fluxes of Na+and K+associated with excitation constitute the major drive on the activity of the Na+, K+‐pump, giving rise to up to 20‐fold stimulation of the transport rate. In keeping with this, training induces an upregulation of the total concentration of Na+, K+‐pumps in skeletal muscle. The activity and the capacity of the Na+, K+‐pump are important limiting factors determining the maintenance of excitability and contract

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09818.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

The rat hepatic artery responds to acetylcholine (ACh) with an endothelium‐dependent relaxation, which is unaffected by nitric oxide (NO) synthase and cyclooxygenase inhibition. The purpose of this study was to investigate whether the NO‐independent relaxation is caused by hyperpolarization of the smooth muscle cells. In vessels with endothelium ACh induced a hyperpolarization in the presence of 0.3 mMNw‐nitro‐l‐arginine (l‐NOARG) and 10μm indomethacin. The hyperpolarization, which slowly decayed after an initial maximum, generally lasted for at least 20 min. ACh in contrast to levcromakalim failed to hyperpolarize the smooth muscle cells in endothelium‐denuded vessels. In vessels contracted by phenylephrine (PhE) ACh caused a concentration‐dependent hyperpolarization and relaxation, and both events occurred over the same concentration interval. Curve fitting using the Hill equation showed a close correlation between the hyperpolarization and the relaxation. Exposure to a 30 mM K+solution abolished the hyperpolarization and suppressed the relaxation induced by ACh. Nimodipine did not affect the ACh‐induced hyperpolarization, whereas the relaxation induced by ACh and levcromakalim, but not that evoked by the NO donor 3‐morpholino‐sydnonimin, were attenuated. Glibenclamide had no effect on the ACh‐induced hyperpolarization and relaxation, but abolished the corresponding responses to levcromakalim. The results demonstrate a NO‐independent hyperpolarization and relaxation in the rat hepatic artery. The hyperpolarization and relaxation were endothelium‐dependent, and apparently causally related to each other, since interference with the hyperpolarization or the subsequent effector path

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09819.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

l‐Arginine is the biological precursor for nitric oxide (NO). NO is formed continuously in endothelial cells and maintains a certain degree of vasodilator tone under physiological conditions. Although the formation of NO is not primarily controlled by precursor availability, the extent to which extra supplementation withl‐arginine may affect endothelial NO formation, and hence, vasodilator tone and systemic blood pressure, is not entirely clear. To address this issue, we infusedl‐arginine i.v. in anaesthetized normotensive rats pretreated withNG‐nitro‐l‐arginine methyl ester (l‐NAME, 50 or 200 mg‐1) and in untreated controls, under continued recording of mean arterial pressure (MAP). In control animalsl‐arginine (25 or 100 mg kg‐1min‐1) had no effect on systemic MAP (111 ± 3 mm Hg), whilel‐arginine (200 mg kg‐1min‐1) lowered MAP (to 70 ± 6mmHg). D‐Arginine (200 mg kg‐1min‐1) also induced hypotension; during infusion of D‐arginine MAP fell from 106 ± 4 to 64 ± 4 mm Hg. Pretreatment withl‐NAME (50 and 200mgkg‐1) elevated MAP to 140 ± 2 and 147 ± 3 mm Hg, respectively, but failed to affect the hypotensive response tol‐arginine; during infusion ofl‐arginine (200 mg kg‐1min‐1) in rats pretreated withl‐NAME (50 and 200 mg kg‐1) MAP fell to 86 ± 9 and 104 ± 6 mm Hg, respectively. Plasma levels of the NO metabolite, nitrate, were 18 ± 4 and 17 ± 3μmol l‐1, respectively, before and after infusion ofl‐arginine (200 mg kg‐1min‐1). Trapping of NO to haemoglobin (HbNO) could not be detected, either before or after infusion ofl‐arginine (200 mg kg‐1min‐1). We conclude that a high dose ofl‐arginine may act hypotensive in normotensive rats. T

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09820.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

The relaxant effect of hypercapnia (15% CO2) was studied in isolated circular segments of rat basilar arteries with intact endothelium. The nitric oxide synthase inhibitor nitro‐l‐arginine (l‐NOARG) and the cytosolic guanylate cyclase inhibitor methylene blue (MB), significantly reduced this relaxation by 54% and 70%, respectively. The effect ofl‐NOARG was completely reversed byl‐arginine. Blockade of nerve excitation with tetrodotoxin (TTX) had no affect on the 15% CO2elicited vasodilatation. Measurements of cGMP in vessel segments showed no significant increase in cGMP content in response to hypercapnia.l‐NOARG and MB, but not TTX, significantly reduced the basal cGMP content in cerebral vessels. Adding 1.5% halothane to the incubation medium did not result in a significant increase in cGMP content. Lowering the pH by cumulative application of 0.12 m HCl resulted in relaxation identical to that obtained by lowering the pH with 15% CO2. In vessel segments in which the endothelium had been removed beforehand 15% CO2induced relaxation that was not different from that seen in vessels with intact endothelium.l‐NOARG had no affect in endothelium denuded vessels. The results suggest that high CO2elicits vasodilatation of isolated rat basilar arteries by a mechanism independent of nitric oxide synthase (NOS) activity. The markedly reduced basal cGMP levels in cerebral vessels byl‐NOARG and MB suggest that there exists a basal NO formation in the cereb

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09821.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

TRH has pronounced vascular effects. The final transmitter mechnisms of these effects are not fully understood. The present study was conducted in order to elucidate whether these effects are mediated by prostaglandic or muscarinic mechanisms. Muscarinic blockade augmented the vasoconstricting‐ and pressor effect of TRH; vasodilation in the brain was attenuated only in the caudate nucleus. Indomethacin provoked a decrease in regional cerebral blood flow and in the gastric mucosal blood flow. No effect of indomethacin was observed on the vascular effects of TRH. It is concluded that the cerebral vasodilating and peripheral vasoconstricting effects of TRH are not mediated by prostaglandins. Muscarinic mechanisms are involved in the vasodilating effect of TRH only in the caudate nucleu

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09822.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

The influence of the cranial sympathetic nerves on the architecture of pial arteries in normo‐ and hypertension was examined. For this purpose the effect of bilateral superior cervical ganglionectomy was evaluated in normotensive rats (WKY) and stroke‐prone spontaneously hypertensive rats (SHRSP). The operations were performed at the age of 1 wk, which is just prior to the onset of ganglionic transmission. The length of the inner media contour was measured and the media cross‐sectional area was determined planimetrically, with computerized digitalization of projected photographic images of transversely sectioned pial arteries. Four wk after sympathectomy there was a 20% reduction in media cross‐sectional area and a consequent reduction in the ratio between media area and calculated luminal radius in the major pial arteries at the base of the brain in WKY but not in SHRSP. Conversely, in small pial arteries linear regression analysis showed that in WKY subjected to ganglionectomy the relationship between media cross‐sectional area and luminal radius was significantly larger in arteries with a radius less than 21 μm compared to untreated WKY. No such effect was seen in the corresponding SHRSP vessels. In addition, the cross‐sectional area of the internal elastic membrane (IEM) in the basilar arteries of WKY was measured by means of a computerized image‐analysing system. Mean cross‐sectional area of the IEM was approximately 45% larger following SE than in control animals. The present findings propose a ‘trophic’ role for the sympathetic perivascular nerves in large pial arteries of the rat. The increased media‐radius ratio in the small pial arteries of the WKY following sympathectomy might reflect a compensatory hypertrophy due to reduced protection from the larger arteries against the pressure load. The inability to detect any morphometrically measurable effect of the sympathectomy in the cerebral arteries of SHRSP is probably explained by a marked growth‐stimulating effect of the high pressu

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09823.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Effects of the dihydropyridine calcium antagonist felodipine and of calcium reduction were studied on osmotically induced contractile responses in the vascular smooth muscle of the rat isolated portal vein. Previous studies have shown that changes in osmolarity that cause cell swelling are accompanied by increased contractile activity in this smooth muscle (Johansson&Jonsson 1968). A transient enhancement of the contractile activity developed in the portal vein on return to standard Krebs solution after exposure to 60 mM urea. This osmotic response was dependent on extracellular Ca2+(abolished in Ca2+free solution+ 0.1 mM EGTA) and was reduced in proportion to the decrease in spontaneous phasic contractile activity when Ca2+was lowered from the standard 2.5 mM concentration. Felodipine, 3 nM, reduced the spontaneous activity to approximately 50% but showed an even more pronounced inhibitory effect on the osmotic responses which were reduced to less than 20% of control. Other calcium antagonists such as verapamil, 60 nM and diltiazem, 300 nM, were also more effective in inhibiting the osmotic responses than the spontaneous activity. In contrast, the K+channel opener, pinacidil, 100–200 nM, reduced the spontaneous activity to 50% but had only minor inhibitory effect on the osmotic responses, about 75% still persisting.It is suggested that stretch of the cell membrane in response to variations in osmolarity induces contractile activity in vascular smooth muscle by mechano‐electrical coupling involving dihydropyridine‐sensitive pat

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09824.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09825.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09826.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY