摘要:

The main purpose of the present study was to test the hypothesis that adrenergic stimulation of muscle fibres during exercise is a major stimulus for the training‐induced enhancement of skeletal muscle respiratory capacity. Therefore, Sprague‐Dawley rats either underwent bilateral surgical ablation of the adrenal medulla or were sham‐operated. Furthermore, unilateral surgical extirpation of the lumbar sympathetic chain was performed. Half of the rats were then trained for 12 weeks by swimming (up to 5.5 h‐day‐1, 4 days‐week‐1) and the remaining rats were sedentary controls. In the gastrocnemius muscle, training significantly increased the mitochondrial enzymes citrate synthase, succinate dehydrogenase, cytochromecoxidase, and 3‐hydroxyacyl‐CoA dehydrogenase. In sham‐operated rats, the increases were 40%, 43%, 66%, and 25%, respectively, in legs with intact sympathetic innervation. The training‐induced enzyme adaptation after adrenodemedullation and/or sympathectomy was not significantly lower than these control values. In sham‐operated rats, training decreased resting plasma insulin and glucagon levels and increased liver glycogen content. Similar changes were induced by adrenodemedullation, but training did not augment these changes in adrenodemedullated rats. In conclusion, the data suggest that neither adrenomedullary hormones nor local sympathetic nerves are prerequisites for the training‐induced increase in muscle mitochondrial enzymes. The training‐induced decline in resting plasma insulin and glucagon levels in intact rats may be mediated

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1985.tb07569.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

In rats of the Milan hypertensive strain (MHS) the disease can be transplanted with the kidney to rats of the Milan normotensive strain (MNS). It has been found that GFR, salt and volume regulation differ between MHS and MNS rats. Tubuloglomerular feedback control mechanism (TGF) is important for body volume regulation and we therefore wanted to study the TGF control in MHS and MNS rats. Whole kidney and micropuncture experiments were done before and during saline volume expansion (5% of body weight). In an initial series of experiments measurements were madeoftotal kidney GFR, urine excretion rate of sodium and potassium and subcapsular interstitial hydrostatic pressure (psc); interstitial oncotic pressure (ρint) was estimated from hilar lymph protein concentration. In a second series, proximal tubular stop‐flow pressure (Psf) was determined upstream from a wax block while the distal nephron was being perfused with Ringer solution at a flow rate varying from 0 to 40 nl min‐. In this way the maximal drop in stop‐flow pressure (ΔPst) and also the turning point (TP), the tubular flow rate at which 50% of this response was achieved, could be determined after saline volume expansion and after 2 h of complete ureteral occlusion. The results showed that GFR was similar in MHS and MNS rats in the control situation, but that during volume expansion it was significantly lower in the MHS group. Interstitialscand 7tintand net interstitial pressure (psc–πint) were similar in MHS and MNS rats both under control conditions and during volume expansion. The TGF investigation showed a slightly increased Δpst(8.5vs.5.2 mmHg) in the MHS animals while pstand TP were normal in the control state (38 mmHg and 21 nl‐min‐1). During volume expansion, however, the TGF sensitivity was significantly higher in the MHS animals than in the normotensive controls, showing a TP of 25 nl‐min‐1(MNS 39 nl‐min‐1) and a Δsfof 5.6 mmHg, (MNS 1.3 mmHg). During ureteral occlusion the resetting to a low TGF sensitivity that occurs in control animals did not take place in the hypertensive animals. Thus, the feedback sensitivity was reset to a low level in the MNS animals during volume expansion and ureteral occlusion, while the MHS animals were unable to reset this sensitivity in the normal way. This inability might be expected to lead to overloading of the extracellular fluid volume, which may participate in the development and maintenance of

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1985.tb07570.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

After 12 weeks of treadmill training 10 Sprague‐Dawley rats got a significant bradycardia at exercise of submaximal intensities compared to 10 sedentary controls. Twenty rats were subjected to the same training programme during oral treatment with the cardioselective beta receptor blocker metroprolol (10 rats) or proprnolol (non‐selective, 10 rats). Both treated groups developed a training‐induced bradycardia at submaximal exercise of the same magnitude as the trained untreated group. It is concluded that the stimulation of cardiac beta receptors or the heart rate increase during exercise are not critical for the development of training bradycardia and that in this respect the effects of cardioselective and non‐selective beta receptor blockade were not significantly di

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1985.tb07571.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

Experiments were performed to study the regulation of the single‐nephron glomerular filtration rate (SNGFR) in superficial and juxtamedullary nephrons, as the left kidney of Sprague Dawley rats was submitted to a reduced arterial pressure of 70 mmHg by means of an aortic clamp. The SNGFR at different cortical levels was measured 0.5, 1, 5, 20 or 45 min after the reduction, in order to ascertain whether the effects of the regulatory mechanisms are modified with time. A Hanssen technique was used, which allows one determination of filtration rates per animal. At a renal arterial pressure (RAP) of 100 mmHg (= control animals) the SNGFR amounted to 20±1.2 and 23± 0.8 nlmin‐1–g‐1kidney weight in the outer and inner cortical (OC, IC) nephrons. When RAP was further reduced to 70 mmHg, the autoregulation of SNGFR, determined after 0.5 min, was highly efficient for both OC and IC nephrons (19 ± 2.0, 23 ± 2.6). A prolonged reduction in RAP caused a gradual decline in SNGFR. The filtration rate measured after 5 min was 15 ±1.4 for OC and 20 ± 1.8 for IC nephrons. The decline was most pronounced for OC nephrons, which led to a fractional redistribution in favour of IC nephrons. Thus, SNGFRIC/SNGFRocwas 1.16± 0.065 when RAP was 100 mmHg and 1.41 ± 0.126 after 5 min with an RAP of 70 mmHg. It is well documented that suprarenal aortic occlusion is a powerful stimulus for the release of renin. This was manifested as an increase in the arterial pressure proximal to the aortic clamp. The fractional redistribution to IC nephrons and the loss of autoregulation, when the renal hypotension was sustained, may be an expression of the intrarenal mechanisms attempting to restore RAP. It is likely that the renin/angiotensin system is involved in

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1985.tb07572.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

Normotensive (WKY) and hypertensive rats (SHR) were, from 5 to 12 weeks of age, given ‘low’ (LNa), ‘control’ and ‘high’ (HNa) Na diets (0.5, 5 and 50 mmol‐100 g‐1food, respectively, during weekly recordings of body weight, conscious indirect systolic blood pressure (SBP) and heart rate (HR). During the last week, mean arterial pressure (MAP) and HR responses to standardized stress stimuli (air jet) were recorded before and after sequential cardiac nerve blockade. While resting, SBP was about equal in all WKY groups, but it was significantly reduced in SHR‐LNa (152 mmHg versus 174 and 178 mmHg in SHR controls and HNa;P<0.05). In both LNa groups HR was elevated nearly 25% compared with controls, being in SHR 513 versus 419 bpm (P<0.01) and in WKY 489 versus 393 bpm (P<0.01). Cardiac nerve blockade indicated that this HR elevation was about equally due to elevations of sympathetic activity and ‘intrinsic’ pacemaker activity. SHR‐LNa also showed attenuated MAP elevations to acute mental stress. There were, however, no significant differences between groups concerning haematocrit or plasma Na‐K levels. The results suggest that SHR have a greater salt requirement than WKY, as Na restriction to one‐tenth of normal led to a considerable MAP reduction in SHR despite compensatory sympathetic activation, and also to attenuated pressor responses to mental stress. Further, the cardiovascular effects in SHR were much more extensive when on a low‐Na diet than when Na intake was i

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1985.tb07573.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

The aim of the study was to determine the fibre size distribution within the human m tibialis anterior. Ten‐micron thick cross‐sections of the whole muscle were enzyme histochemically stained for myofibrillar ATPase at pH 9.4. The cross‐sectional area of 100 fibres with low (type 1) ATPase and high (type 2) ATPase activity was measured in three different regions (superficial, central and deep). Both the type 1 and type 2 fibres were found to be larger in the deep region than in the central or superficial regions. The variation in fibre size could not be explained by the cryofixation or cryo‐embedding techniques used. The data suggest that muscle adaptation to physical demands may not only occur by means of variation in types and number of muscle fibres, but also by variation in fibre size over the muscle cross

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1985.tb07574.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

A methodological study was performed on single myelinated dorsal root fibres of rats. The recovery of excitability following a conditioning electrical stimulus delivered through the same electrode as the test stimulus and following a conditioning propagated nerve impulse were compared. Using low test stimulus strength, the recovery time permitting a propagated test impulse was 2.31 ± 0.72 ms (mean ± SD) after a conditioning electrical stimulus and 1.96 ± 0.78 ms after a conditioning propagated impulse (P<0.001). The difference and its significance for clinical refractory period measurements are discuss

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1985.tb07575.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

Enprofylline is a novel xanthine with a low adenosine antagonistic potency, but with a good bronchodilator activity. In order to further elucidate its central nervous actions we have studied its effects in the rat hippocampus, both electrophysiologically and biochemically. Adenosine was found to depress evoked field excitatory post‐synaptic potentials (EPSPs) in the rat hippocampus. The effect of adenosine was antagonized by theophylline but not by enprofylline. Both xanthines caused a slight increaseper seof the field EPSP amplitude. Cyclic AMP accumulation in the rat hippocampus was stimulated by the adenosine analogue NECA, by isoprenaline and by noradrenaline in the presence of propranolol. The cyclic AMP accumulation induced by these agents was not significantly altered by omitting calcium. Enprofylline antagonized the effect of NECA and noradrenaline (after beta‐blockade) but not that of isoprenaline. The IC50of enprofylline against NECA was about 20μmol I‐1. The inhibitory effect of enprofylline against NECA induced cyclic AMP accumulation was not affected by omitting calcium or by the calcium channel antagonist felodipine, but was decreased by the calmodulin inhibitor stelazine and the intracellular calcium chelator Quin‐2. The results show that enprofylline is much more potent as an inhibitor of adenosine A2‐receptor‐mediated cyclic AMP accumulation than against adenosine A1‐receptor‐mediated inhibition of field EPSP. The difference may depend on a role of a special pool of calcium in the

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1985.tb07576.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

The effects of oestrogen and of oestrogen combined with progesterone were examined on the fractional distribution of cardiac output (blood flow) in the genitourinary tissues of the female rabbit. Oestradiol treatment significantly increased blood perfusion in the uterus, vagina and urethra but caused no change in the perfusion of the urinary bladder or the kidneys. The wet weight of the uterus and vagina increased significantly and in the urethra there was a tendency to weight gain following oestradiol treatment. Progesterone treatment following oestrogen appeared to reduce the effect of oestrogen on both perfusion and weight gain.

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1985.tb07577.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

The receptors involved in adenosine‐induced modulation of cholinergic neuroeffector transmission in guinea‐pig ileum were explored by means of the non‐selective stable analogue, 2‐chloroadenosine and analogues with preference for A, receptors, L‐N6‐phenylisopropyladenosine (L‐PIA), AND A2receptors, 5′‐N‐ethylcarboxamideadenosine (NECA) and D‐N6‐phenylisopropyladenosine (D‐PIA). 2‐chloroadenosine, L‐PIA AND NECA were equipotent in inhibiting contractile responses to nerve stimulation, whereas D‐PIA exerted a similar activity only in high concentrations. The release of acetylcholine induced by nerve stimulation was inhibited to a similar degree by NECA, L‐PIA AND D‐PIA. The phosphodiesterase inhibitor, ZK 62.711, and the activator of adenylate cyclase, forskolin, enhanced the inhibitory effect of NECA, but not that of L‐PIA, on contractile responses to nerve stimulation. Only NECA inhibited contractions induced by direct muscle stimulation and ZK 62.711 enhanced this inhibition. It is concluded that adenosine inhibits the neuroeffector transmission in guinea‐pig ileum mainly by a prejunctional, cAMP‐independent, mechanism, involving A, receptors and a supplementary activation of post‐junctional A2receptors. In addition there may be a prejunctional inhibitory effect of high agonist concentrations, exerted via A2receptors and

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1985.tb07578.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY