NO-ERGIC CONTROL OF BLOOD CIRCULATION IN THE MEDULLA OBLONGATA OF RATS WITH EXPERIMENTAL HEMIPARKINSONIZM UNDER EXPOSURE TO CONTINUOUS LIGHT.

The study was conducted on rats with unilateral damage to dopaminergic (DA) neurons in substantia nigra of the midbrain (experimental hemiparkinsonism). Degeneration of dopaminergic (DA) neurons was accompanied by hyperactivity of those neurons that remained intact and responded to apomorphine (Apo) test by rotational movements. Depending on the number of rotations, three groups of animals were defined. In the medulla oblongata of rats with unilateral damage to dopaminergic (DA) neurons, a significant increase in the activity of inducible NO-synthase (iNOS) was observed, while the activity of constitutive NO-synthase (cNOS) tended to decrease compared with that in control rats. An activation of neuronal NO-synthase (nNOS) in those rats by injections of L-arginine in the medullary nuclei was accompanied by weakening of the hemodynamic effects compared to those in control rats. An exposure of animals to continuous light for three weeks was accompanied by increasing the number of damaged DA-ergic neurons in substantia nigra. At that, a significant decrease in cNOS activity in the medulla oblongata was observed, leading to the inhibition of de novo synthesis of nitric oxide (NO). The reduction of NO synthesis in the medulla oblongata neurons of rats with experimental hemiparkinsonism following their exposure to continuous light was also evidenced by the reduction.

[Effect of the Na+, K(+)-ATPase modulation in neurons of the medulla oblongata on hemodynamic effects in spontaneously hypertensive rats].

The study was conducted in normotensive and spontaneously hypertensive rats anesthetized with urethane (1600 mg/kg of animal weight, intraperitoneally). It has been shown that in normotensive rats, injections of a specific inhibitor of Na+, K(+)-ATPase ouabain (10(-8)-10(-5) mol/l) in the populations of the neurons within nucleus of the solitary tract (NTS), paramedian reticular nucleus (PMn) and lateral reticular nucleus (LRN) were accompanied by the development of the hypertensive responses in a dose-dependent fashion. These data suggest that Na+, K(+)-ATPase of the neuron somatic membranes in the medullary cardiovascular nuclei is involved in neural control of the cardiovascular function, and its inhibition by microinjections of ouabain promotes the development of hypertension. In contrast to normotensive rats, ouabain injected in the medullary nuclei of spontaneously hypertensive animals induced either enhanced hypertensive or hypotensive responses. Biochemical analysis revealed that the activity of Na+, K(+)-ATPase in the microsomal fraction of the medulla oblongata of spontaneously hypertensive rats significantly exceeded its activity in the medulla oblongata of normotensive animals. Possible mechanisms of ouabain effects in spontaneously hypertensive rats have being discussed. Activation of Na+, K(+)-ATPase activity of the cardiovascular neurons with asparkam injections in the medullary nuclei resulted in hypotensive responses in both normotensive and spontaneously hypertensive rats.

[Effects of changes in mitochondrial permeability transition of medullary neurons on arterial pressure in rats].

In acute experiments on anaesthetized with urethane normotensive rats we studied effects of modulating the mitochondrial permeability transition (MPT) of the neurons in the medullary cardiovascular nuclei - nucleus of the tractus solitarius (NTS), paramedian reticular nucleus (PMn), n.ambiguus (AMB), and lateral reticular nucleus (LRN) on the systemic arterial pressure level (SAP). An increase in the MPT with injections of an inductor for MPT phenylarsine oxide (10(-12) M - 10(-8) M) into the medullary nuclei under exploration has been shown to induce the lowering in the SAP level in a dose-dependent manner. A decrease in the MPT of the medullary neurons with either cyclosporine A or melatonin (10(-12) M - 10(-10) M) resulted in hypertensive responses of the SAP. Effects of phenylarsine oxide injections into the medullary nuclei were attenuated after preliminary intravenous administration of L-arginine. The data obtained give evidence that functional activity of the medullary cardiovascular neurons and their effects depend to a large extent on the functional state of their mitochondria.

[Role of nitric oxide in effects of intramedullary injected gamma-aminobutyric acid on blood circulation].

In acute experiments on anaesthetized with urethane normotensive rats, we studied the influence of modulation of neuronal NO-synthase (nNOS) activity on the effects of GABA injected in the populations of cardiovascular neurons within the nucleus of tractus solitarius (NTS), n.ambiguus (AMB), paramedian reticular nucleus (PMn) and lateral reticular nucleus (LRN). The data obtained give evidence for nNOS involvement in the effects of intramedullary injected GABA on the cardiovascular system.

[Nitric oxide and reflectory regulation of blood circulation in rats]. / Oksyd azotu i reflektorna rehuliatsiia krovoobihu u shchuriv.

In acute experiments on anaesthetized with urethane normotensive rats we studied the ways of participation of nitric oxide (NO) in reflector control of the cardiovascular system by the medullary neurons within n.tractus solitarii (NTS), dorsal nucleus of the vagus nerve (DNV), n. ambiguus (AMB), and the lateral reticular nucleus (LRN). Modulations of the activities of neuronal NO-synthase (nNOS) in the populations of the cardiovascular neurons within the medullary nuclei which are involved in the reflector cardiovascular control were induced by intramedullary injections of sodium nitroprusside as NO donor, L-arginine as NO precursor, L-NNA as an inhibitor of NOS, as well as by intraperetoneal injections of 7-nitroindazol (nNOS inhibitor). We have determined that stimulation of nNOS activity in the populations of the medullary neurons resulted in both remarkable shifts in the SAP level and in inhibiting the chemoreceptor reflector responses. After preliminary inhibiting nNOS chemoreceptor reflexes induced by epinephrine were found to be enhanced in most experiments.

[The role of the endothelium and of biologically active substances of endothelial origin in regulating blood circulation and cardiac activity]. / Rol' endoteliiu ta biolohichno aktyvnykh rechovyn endotelial'noho pokhodzhennia v rehuliatsiï krovoobihu i diial'nosti sertsia.

The role of endothelium and its biologically active derivatives in the central and local control of circulation is under consideration. Molecular and cellular mechanisms of the activation of the endothelium-dependent responses of different functional significance are being discussed, as well as the state of endothelial responses in the development and compensation of pathological processes in the cardiovascular system.