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Abstract In experiments on rat pups we studied the effect of clonidine on potential-dependent Na+ currents in dorsal root ganglia by the voltage clamp method. Clonidine decreased the amplitude of tetrodotoxin-sensitive and tetrodotoxin-resistant sodium currents. The range of acting concentrations and the absence of modulatory effect of norepinephrine on the efficiency of clonidine-induced blockade of sodium currents suggest that this blockade results from a direct interaction of clonidine with sodium channels.

Acute experiments under chloralose anaesthesia were performed in normotensive (Wistar and Wistar–Kyoto) and hypertensive (SHR) rats for recording of electrical discharge in the upper cervical sympathetic stem in response to stimulation of afferent fibers of the median nerve of the forelimb. These experiments showed that the evoked response was of the same shape in hypertensive rats as in normotensive rats. The latent period, duration of each discharge, and spectral characteristics of the somatosympathetic reflex were identical in animals of all the lines studied, though the amplitude of the reflex was greater in SHR rats than in normotensive animals. It is suggested that the organization of the somatosympathetic reflex is identical in hypertensive and normotensive rats. The reflex excitability of the sympathetic nervous system was increased in SHR rats.

1.The character of baroreceptor reflexes was studied in conscious cats both under resting conditions and during emotional stress.2.During naturally evoked emotional tension 32 cats showed a two-phase change in arterial pressure: an initial hypotension was followed by a rise in arterial pressure. The pressor component was accompanied by a suppression of the baroreceptor reflex evoked by phenylephrine (i.v.).3.Electrical stimulation of the hypothalamic “defence area” also resulted in a raised arterial pressure and a suppression of the baroreceptor reflex.4.3–7 days after bilateral section of the carotid sinus and aortic nerves 5 cats showed a reduction in arterial pressure only when confronted by a dog. When a reflex response to phenylephrine began to return, the depressor responses seemed to diminish and pressor responses reappeared. “Mild” (50–100 µA) stimulation of the hypothalamic “defence area” also caused a reduction of arterial pressure. However, a rise in arterial pressure occurred when the electrical stimulation of the hypothalamic “defence area” was increased.5.In 2 cats the pressor response caused by confrontation with a dog was not accompanied by any noticeable inhibition of the baroreceptor reflex. After cutting the sino-carotid and aortic nerves in these animals, emotional stress produced accentuated pressor responses.6.The results suggest that the presence of baroreceptor reflexes is a prerequisite for the development of hypertensive responses during emotional stress.

In experiments on alert cats shifts of the systemic hemodynamics under emotional stress were studied. The hypertension caused by confrontation with a dog is shown in most cases to be attended by suppression of the baroreceptor reflexes. Hypertension does not develop in these animals after section of the sinocarotid and aortic nerves. In 2 cats the baroreceptor reflexes did not change under emotional stress and deafferentation of the carotid sinuses and arch of the aorta intensified hypertension upon confrontation with a dog. It is concluded that diverse mechanisms lead to hypertension under emotional stress in different animals.

The origin of the period of postactivation depression of spike activity in the renal nerve during stimulation of afferent fibers of cutaneous (cutaneous branch of the peroneal nerve) and visceral (greater splanchnic nerve) nerves was studied in unanesthetized, anesthetized, decerebrate, and spinal cats. This silent period was shown to be considerably prolonged after administration of general anesthetics to unanesthetized animals or after decerebration. Analeptics (strychnine, leptazol, picrotoxin) or division of the spinal cord at the level of the lower cervical segments weaken postactivation depression. The causes of origin of the silent period are discussed and the localization of the structures responsible for its appearance is examined.

Abstract: The relationship between depression of the cardiochronotropic component of the baroreceptor reflex and arterial pressure and heart beat variabilities was investigated in normotensive rats and rats with renal hypertension (one kidney — one clamp). In the hypertensive rats, the arterial pressure and heart rate were both increased and more variable, while the cardiochronotropic component of the baroreceptor reflex was depressed. No cause-effect relationship between baroreceptor reflex attenuation and increased variability of hemodynamic parameters was found in this rat model of arterial hypertension.

Abstract: The effect of anapriline on the blood flow-pressure relationship is assessed for stepwise changes in the rate of perfusion of the vessels in the hind quarter of the cat body. It is demonstrated that when the synthesis of endothelium-relaxing factor is inhibited, the effect of anapriline is changed, and the augmentation of flow-dependent vasodilation is replaced by vasoconstriction, which increases with the increase in the blood flow through the vessel.

Experiments on waking cats showed that electrical stimulation of “protective” zones of the hypothalamus leads to development of hypertension and inhibits baroreceptor reflexes. In animals with divided carotid sinus and aortic nerves, threshold hypothalamic stimulation leads to the appearance of depressor responses, whereas above-threshold stimulation evoked depressor-pressor responses. It is suggested that depression of baroreceptor reflexes is one of the mechanisms of the development of hypertension in response to hypothalamic stimulation.