Central regulatory mechanisms of blood flow


Reduction of high blood pressure by centrally acting agents can be successful only when they are able to effect on tonic activity of sympathetic vasomotor neurons, according to concept developed by researchers of the Division of Experimental Physiology and Pharmacology. Mechanisms of increase in blood pressure induced by aversive emotiogenic stimuli have been demonstrated for the first time. Researchers of the Division have proved that the mechanism of increase in blood pressure in both negative and positive emotions is mediated by activation of different types of central regulatory mechanisms. Questions of neurochemical organization of central regulatory mechanisms have a significant place in research activities. It has been proved that functional activities of imidazoline systems are higher in animal models of arterial hypertension than in normotensive animals. Studies have revealed that imidazoline systems are also involved in the functioning of central pathway of baroreceptor reflex. Imidazoline receptors are involved not only in activation of baroreceptor reflex arc at the bulbar level, but also in suprabulbar modulation processes of the reflex mediated by emotional stress.

Attempts to influence the development of target organ damage processes in the spontaneously hypertensive rats during the early postnatal period as an adequate model of human hypertension were made in experiments performed in the Division of Experimental Physiology and Pharmacology. It has been proved that reduction of the sympathetic activity in the prenatal and early postnatal periods inhibits the development of hypertension and prevents vascular remodeling of resistance vessels in an animal model. Studies of recent years were designed to explore the role of arterial baroreceptor reflex in the long-term control of blood pressure. Researchers of the Division of Experimental Physiology and Pharmacology have demonstrated that arterial baroreceptor reflex is involved in the long-term regulation of blood pressure and inhibited its long-term increase in response to a stimulus.