[Changes of rat respiratory and locomotory muscles during aerobic exercise training in continuous and interval regimens].

Male Wistar rats were treadmill-trained for 8 weeks using one of the two regimens: with the constant running speed or with alternating high-speed and low-speed intervals. Both training regimens led to an increase of rat aerobic capacities and to a higher citrate synthase activity in the medial head of gastrocnemius muscle. No differences between the effects of two training regimens were observed. However, in contrast to constant-speed training the interval one resulted in myocardium hypertrophy and also in less pronounced changes in diaphragm muscle, such as slow-direction shift of myosin phenotype and reduction of muscle fiber cross-sectional area. Neither of the training regimens had an effect on corticosterone and thyroid hormones levels in rat blood, whereas the interval training resulted in a higher level of testosterone. Anabolic influence of testosterone during interval aerobic training may be favorable for heart hemodynamic capacity and force characteristics of the diaphragm.

[Comparative analysis of gene expression in rat locomotor muscles and diaphragm].

Gene expression profile in diaphragm in comparison to three principally different hindlimb muscles (soleus, red and white gastrocnemius) was studied using quantitative PCR. Expression levels of PGC-1alpha mRNA and myogenin mRNA in diaphragm were in accordance with its myosin phenotype and citrate synthase activity. However, diaphragm was characterised by atypically high content of MyoD mRNA as well as high content of IGF-1 mRNA and low content of myostatin mRNA. The latter two findings suggest high intensity of protein synthesis in diaphragm muscle fibers, although they have smaller cross sectional area than fibers in locomotor muscles.

[Changes in the diaphragm muscle and its feed artery after chronic respiratory airway obstruction in rats].

A chronic respiratory load was produced in Wistar rats by tracheal binding to produce a twofold increase of pleural pressure oscillation amplitude during respiration. Eight weeks after the surgery, a higher proportion of type-I muscle fibers (MFI) in the costal diaphragm along with a greater MFI cross-section area and a higher succinate dehydrogenase activity in MFII in the crural diaphragm were observed. During recording the mechanical activity of ring preparations of diaphragm arteries under isometric conditions, an increase in endothelium-dependent relaxation was found, whereas endothelium-independent relaxation and arterial reactivity to noradrenaline did not change. Tracheal binding did not produce any changes of MF in the gastrocnemius muscle, but endothelium-dependent relaxation of gastrocnemius feed arteries was reduced. We conclude that chronic respiratory load affects the endothelial function in diaphragm arteries in a manner favorable for blood flow control in the diaphragm. Functional alterations in gastrocnemius arteries may be associated with the reduced locomotor activity of operated rats.

[Consequences of the saphenous artery denervation under normal and chronically lowered blood pressure in rats].

We studied constrictor responses of saphenous artery after sympathetic denervation in normotensive rats and rats with chronic regional hypotension. Abdominal aorta was partially occluded in Wistar rats distally to the renal arteries, lowering blood pressure in the hindquarters by about 40%, a week later to denervate saphenous artery the femoral nerve was cut. The density of periarterial nerve plexus and neurogenic responses of the vessel restored partially in 2 weeks and completely in 6 weeks after the surgery; the chronic hypotension did not modify the dynamics of reinnervation. Arteries of both groups of rats demonstrated higher sensitivity to noradrenaline during 6 weeks after denervation, whereas vessel sensitivity to serotonin was enhanced only in normotensive rats. Therefore, chronic hypotension may prevent postdenervation hypersensitivity of vascular smooth muscle to vasoconstrictors.

Frequency characteristics of blood pressure oscillations evoked by sympathetic transmitters, noradrenaline and adenosine triphosphate.

Mean arterial pressure (MAP) was recorded beat-to-beat in chronically instrumented, conscious, unrestrained rats under control conditions and after pharmacological inhibition of vascular sympathetic influences by means of: (1) ganglion blockade with chlorisondamine; (2) alpha-adrenoceptor antagonist phentolamine; (3) P2 receptor blockade with pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS). Angiotensin II was continuously infused to prevent drastic MAP decrease during chlorisondamine and phentolamine administration. Overall MAP variability increased after ganglion blockade and combined blockade of adreno- and purinoceptors. It increased also after inhibition of purinergic influences, but was not significantly changed after vascular adrenergic blockade. Spectral analysis of spontaneous MAP fluctuations in intact rats revealed a peak centered at 0.4-0.5 Hz. Ganglion blockade suppressed MAP fluctuations with frequencies from 0.1 to 0.8 Hz. After blockade of alpha-adrenoceptors, MAP spectral density was suppressed only within the 0.1-0.45-Hz band, but increased in the 0.45-0.8-Hz band. In the latter case, sympathetically-induced peak of MAP spectrum was centered on 0.6 Hz, being evoked, presumably, by adenosine triphosphate (ATP). Blockade of P2 receptors by PPADS enhanced MAP fluctuations in the 0.1-0.45-Hz frequency band, i.e. the noradrenaline-induced peak was centered on 0.2 Hz. No peaks were observed in the 0.1-0.8-Hz frequency band during combined blockade of adreno- and purinoceptors. The present study supports the concept that sympathetic purinergic co-transmission is essential for stabilization of MAP level. MAP fluctuations evoked by noradrenaline and ATP can be distinguished by their frequency characteristics.

The role of purinergic and adrenergic transmitters of the sympathetic system in the control of arterial blood pressure variability.

Variability of mean arterial pressure (MAP) was examined in chronically instrumented, conscious, freely moving rats with pharmacologically altered efferent sympathetic influences on the cardiovascular system. MAP was recorded for 30 min beat-to-beat, using a computer under both control and experimental conditions: after administration of adrenoceptor antagonists (prazosin or phentolamine) or under P2X receptor inactivation produced either by desensitization with alpha, beta-methylene ATP or by PPADS blockade. Inhibition of adrenergic sympathetic effects on the cardiovascular system produced long-lasting and stable decrease in MAP. Prazosin did not modify MAP variability whereas phentolamine enhanced it. Under P2X receptor desensitization MAP decreased, the hypotensive effect being accompanied by a significant increase in MAP variability. A similar increase in MAP variability was observed after PPADS administration, while MAP level was not changed. Administration of PPADS in combination with phentolamine increased MAP variability more significantly than each of the drugs given separately. Changes in MAP variability under the various experimental conditions were not consistently correlated with changes in heart rate variability. We propose that ATP, being a mediator of sympathetic vasoconstriction, participates in baroreceptor-induced stabilization of MAP level.

The role of purinergic neurotransmission in various cardiovascular reflexes.

In urethane-anaesthetized rats the effects of alpha-adrenoceptor antagonists and desensitization of P2-purinoceptors with alpha,beta-methylene ATP on the pressor reflex responses were investigated. Pressor responses were elicited by electrical stimulation of the central end of the sciatic nerve, by asphyxia and by occlusion of the common carotid artery. Responses to sciatic nerve stimulation and to asphyxia, but not those to carotid artery occlusion were entirely suppressed by dihydroergotamine and phentolamine. Under the action of dihydroergotamine the sinocarotid reflex decreased by over 70% in 40% of the experiments. In 60% of experiments the response was only slightly reduced or even augmented, but it was entirely inhibited by subsequent desensitization with alpha,beta-methylene ATP. The magnitude of response to sciatic nerve stimulation was almost unaffected by alpha,beta-methylene ATP, while the response to carotid occlusion was decreased by 40-50%. The recovery of purinoceptor sensitivity to alpha,beta-methylene ATP was accompanied by restoration of the sinocarotid reflex. It is suggested that purinergic neurotransmission plays a considerable role in the pressor sinocarotid reflex, while in the pressor response to stimulation of somatic afferents its role is negligible.