Structurally based resistance and vascular reactivity of the posterior body to noradrenaline were studied in normotensive rats and rats with DOCA-salt hypertension. The hypertension was induced in rats with intact sympathetic nervous system and in rats subjected to neonatal sympathectomy with guanethidine. During the prehypertensive stage, vascular sensitivity of the smooth muscles to noradrenaline was enhanced, with structural lesions being observed only in steady hypertension. Elevation of arterial pressure was accompanied by an increased vascular response to the stimulation of the sympathetic nerves. Sympathectomy prevented arterial pressure elevation and structural alterations in the vessels.

Guanethidine (30 mg/kg daily for first 15 days of life) decreased by 85% the amount of cells in the rat upper cervical sympathetic ganglion for 4 months. In ageing, the volume of the ganglion's cells, the density of adrenergic fibers and the noradrenaline content in the heart, intestine and ductus deferens increased in the desympathized animals. The neural cells remaining after desympathization seem to develop a growth of axons and to restore to some extent the density of sympathetic innervation of the periphery. The firing rate of single preganglionic fibers of the cervical sympathetic nerve is increased in the desympathized animals. The increased firing rate seems to be the cause of changes in the surviving neurons.

This study showed that arterial blood pressure of chemically sympathectomized rats (SR) was decreased, whereas heart rate was increased relative to controls. The cardiac output in SR was higher than that in intact animals (by 36% under urethane anaesthesia and by 80% without anaesthesia). The total peripheral resistance of SR was 1.7 times less than normal, although the magnitude of the structural component of resistance was increased. The half-time clearance of133Xe from skeletal muscle during motor nerve stimulation was greater in SR than in intact rats by a factor of 2. It is concluded that the number of small resistance vessels in SR is low, while the lumen of individual vessles is greater than in controls, thus giving rise to an insufficient “vasodilator reserve”.

Desympathized rats developed a lower arterial pressure, a higher heart rate and a greater one--minute blood volume heart output as compared to intact rats. The total peripheral resistance in the major circulation of desympathized rats is by 1.7 times lesser although their structural component of the resistance is higher. The latter finding seems to be due to a reduce density of vessels per unit of tissue volume. The time of half--washing of Xe33 out of intramuscular depot in working hyperemia during motor nerve stimulation is nearly twofold in desympathized rats. The humber of small resistance vessels seems to be lessened per unit of tissue volume in desympathized animals whereas the lumen of separate vessels in them is larger than in normal animals. This accounts for considerable reduction of the range of vasomotor vascular regulation in desympathized animals.

Partial sympathectomy of neonatal rats was produced by treatment with guanethidine. The number of neurons of the superior cervical ganglion decreased to 15% of control values and remained constant throughout the subsequent observation period of 4 months. The volume of the remaining neuronal perikarya increased faster than that of control animals during the observation period, and the density of adrenergic innervation of the iris and the noradrenaline content of the heart were found to partially recover after the initial decrease produced by the guanethidine treatment, reaching 33% and 30% of control values, respectively, after 4 months. The noradrenaline content of the duct of the vas deferens was greatly reduced by guanethidine treatment, but almost recovered after 4 months. The frequency of sympathetic preganglionic impulses was elevated throughout the 4 months observation period, and it is suggested that this increase is responsible for the compensatory changes in cell volume, terminal density and terminal noradrenaline content of the remaining neurons.

In 3--week guanetidine--desympathized rats, the noradrenaline (NA) concentration in myocardium, small intestine and ductus deferens constituted 1, 6 and 3% of the control, resp., whereas release of the NA from the ductus deferens on transmural stimulation dropped to 3%. From 4 to 16--week age the NA content in myocardium and small intestine reached 30 and 23%, resp., and its release was equal to control. The diminishing of NA content was followed by augmented adrenaline--sensitivity and diminished cholinosensitivity of the organs under study. Significance of local adaptive mechanisms for normalizing of activity of the adrenergic nervous system under conditions of desympathization, is considered.

In the heart of intact rats aged 6 and 10 weeks the activity of nonenzymatic fibrinolysis was found to be maximum in the auricular tissue. In partly sympathectomized (destruction of 75% of neurons in the ganglia) 10-week-old rats fibrinolytic activity was sharply reduced in the auricular tissue, and in the atrial and ventricular myocardium. The content of the plasminogen activator in all parts of the heart decreased to zero value. In stress situations 50% of the rats die from thrombi in the atrial cavity. In partly sympathectomized 10-week-old rats (characterized by restoration of peripheral sympathetic innervation) the studied parameteres were normalized. The fibrinolytic potential of the heart tissue was markedly decreased in totally sympathectomized rats (destruction of more than 99.5% of the neurons); under the effect of stress 80% of these animals died.

The rats desympathised with guanetidine developed a 58% decrease of the noradrenaline content in the myocardium, 37% - in the deferent duct, and 82% - in the small intestine. No significant changes of the catecholamines content occurred either in adrenal glands or in the hypothalamus. Sensitivity of the deferent duct's adrenoreceptors increased by 9 times. Sensitivity of the small intestine to noradrenaline increased by 3.4 times whereas the sensitivity to the antagonistic transmitter acetylcholine decreased by 2.4 times. Local adaptation mechanisms maintaining functioning of the organism in chronic desympathisation, are regarded.

It is shown that the ability of blood platelets to aggregate in partially and completely sympathectomized rats is significantly lower than in intact animals. The blood clotting system of sympathectomized rats is hyperactive. The sympathectomy-provoked changes may be due to the increased content of adrenaline in the blood.

This discusses a study to examine the restoration of functional activity of adrenergic system in partially sympathectomized rats. After two-week administration of guanethidine to newborn rats, about 15% of neurons were left in the superior cervical ganglion. In 2-week-old sympathectomized rats, NA content in the myocardium, small intestine and vas deferens fell, respectively, to 3%, 11%, and 2% of control; no sympathetic nerve terminals were found. After partial sypathectomy in rats, there occurs an increase in the density of sympathetic nerve terminals and that in NA content in the tissues. At the same time, the adrenoceptor sensitivity to NA returns to the control level.