[Nitrogen oxide participation in the mechanism of hemodynamics reactions to tilting].

The NO-dependent mechanism of system hemodynamics reactions comprising increased system blood flow (cardiac output) and blood pressure to head-down tilting at 6, 12 and 18 degrees was studied in anaesthetized rats. Tilting of the rats with inhibited NO synthesis was shown to aggravate hypertension and elevate total peripheral resistance (TPR). Therefore, it can be concluded that NO-dependent vasodilation is involved in regulation of the arterial tone during tilting.

Role of NO in the systemic hemodynamic response to beta2-adrenoceptor stimulation.

Blockade of NO synthesis in most narcotized rats was followed by an increase in depressor effects (by 45%) and decrease in total peripheral resistance (by 63%) upon treatment with isopropyl norepinephrine (isoproterenol). Our results indicate that NO secretion in the endothelium modulates the systemic hemodynamic response to beta(2)-adrenoceptor stimulation.

[Involvement of nitric oxide in the mechanism of adrenergic responses of systemic circulation].

Increased pressor response to the infusion of alpha1-adrenoceptor agonist phenylephrine was observed in conditions of inhibited NO synthesis: the mean blood pressure increased from 33.7 to 41.1% and the total peripheral resistance increased from 6.

NO-dependent mechanism of adrenergic reaction of systemic hemodynamics.

Blockade of NO synthesis in narcotized rats potentiated pressor effects of phenylephrine by 55% and increased total peripheral resistance by 153%. Vasodilation caused by enhanced NO secretion modulated pressor shifts evoked by stimulation of alpha(1)-adrenoceptors with phenylephrine.

[The no-dependent mechanism of the orthostatic reaction of system hemodynamics in rats].

The aim was to describe endothelium-dependent reactions of system hemodynamics to the reduction in system blood circulation (cardiac output) by orthostatic positioning of anesthetized rats. Head rise at 15, 30 and 45 degrees and NO synthesis depression increased the hypotensive reaction to orthostasis by 32, 60 and 71%, respectively, as compared with values prior to the block. This allows the conclusion concerning the recruitment of an NO-dependent vasodilative mechanism in vascular control.

[Mechanisms of responses of systemic circulation: role of endothelial factor in the vascular tone regulation].

Experimental data on the effect of NO synthase inhibition on hemodynamic changes (blood pressure, cardiac output, and peripheral resistance) induced by an increased (polyglucin infusion) or decreased (orthostasis) cardiac output are presented. Under conditions of NO synthase inhibition, the pressor effects of polyglucin and orthostatic hypotension increased by 70 and 72%, respectively. The response of peripheral resistance had a similar trend.

Role of endothelium-dependent mechanism in formation of systemic hemodynamic responses to hypervolemia.

Blockade of NO synthesis in anesthetized rats significantly potentiated pressor responses to Polyglucin (by 70%) and considerably increased total peripheral resistance. It was concluded that vasodilatation induced by increased systemic blood flow (cardiac output) modulates pressor responses under conditions of increased blood volume.

[Endothelium-dependent mechanism of formation of the systemic hemodynamics responses].

In anaesthetised rats, effects of blockade of the NO-synthetase upon hemodynamic shifts were studied (arterial pressure, cardiac output, general peripheral vascular resistance), the shifts being evoked either by increase (infusion of polyglucon) or by decrease (orthostasis) in the cardiac output. Under the blockade of the NO-synthetase, the pressor effects of polyglucon increased by 27% and the orthostatic hypotension by 72%. Responses of general peripheral vascular resistance changed in the same direction.

[Effects of the endothelial relaxing factor on the orthostatic reaction of systemic hemodynamics in rats].

Experiments with unconscious rats showed that blocking of NO secretion intensifies orthostatic hypotension (mean arterial pressure drops by 72%) and reduces proportionally the calculated total peripheral resistance. A supposition has been made concerning involvement of the endothelial relaxing factor in orthostatic hypotension development, since in orthostasis cardiac output (systemic blood circulation) losses its influence on the endothelial NO secretion.

[Vascular factors of the orthostatic responses in systemic haemodynamic].

In anaesthetised rats, bending of the body for 30 degrees and 45 degrees entailed a reverse linear dependence between the systolic and diastolic pressures under conditions of initial blood pressure over 95 mm Hg, whereas in initial blood pressure lower than 95 mm Hg the dependence is direct. In bending of the body for 60 degrees the dependence was direct and only present in initial blood pressure lower than 95 mm Hg. Pressor effects of mesaton in orthostasis directly depended on the level of the initial blood pressure.

Effect of baseline vasodilation on adrenergic reactions of systemic hemodynamics.

Systemic vasodilation produced by sodium nitroprusside in various concentrations and accompanied by a decrease in baseline blood pressure was followed by progressive reduction in pressor responses to alpha-adrenoceptor agonist phenylephrine (mesatone) in rats. In a blood pressure range of below the physiological level (80-100 mm Hg), a positive linear correlation was revealed between the decrease in baseline blood pressure and pressor effect of phenylephrine.

[The mechanisms underlying the formation of systemic hemodynamic reactions: role of initial vessel tone and arterial pressure].

A review of the experimental materials describing the relationships between the initial (background) vascular tone and arterial pressure, on the one hand, and reactivity of the arterial system, on the other. Experiments were carried out on anesthetized rats under arterial hypotension caused by orthostasis or vasoactive agents, such as papaverin and sodium nitroprusside, and arterial hypertension resulting from volume expansion. It has been proposed that these relationships are based on changes in the amplitude of transmural pressure in arterial vessles.

[Effect of hypervolemia on the adrenergic reactivity of the arterial system].

In anaesthetised rats, dependence of haemodynamics upon increase in the blood volume due to infusion of polyglucin in amounts 1.2 and 2.4 ml (8% and 16% of the blood volume in rats, respectively) < was studied.

[Reactivity of the arterial system during vasodilation induced by sodium nitroprusside].

A stepwise decrease in the blood pressure by means of sodium nitroprusside infusion led to progressing diminishing of mesatone pressor effects in anaesthetised rats. Cardiac output changes due to mesatone administration did not depend on the initial blood pressure. The latter being lower than physiological limits, a direct linear correlation occurred between pressor responses and shifts of general peripheral resistance, on one hand, and the degree of the blood pressure initial drop, on the other hand.

[Reactivity of the arterial system to orthostasis].

Reported are data of experiments with unconscious tilted rats (30 degrees, 45 degrees and 60 degrees) in which a dependence of orthostatic hypotensive reactions of systolic (APs) and diastolic (APd) pressure on spontaneous level of baseline mean arterial pressure (APb.mean) was established. Rats tilted at 30 degrees and 45 degrees, APs and APd were in inverse linear dependence with APb.

[Effect of initial (spontaneous) arterial pressure on systemic hemodynamic orthostatic responses].

In anesthetized rats, a reverse linear correlation of arterial pressure (AP) shifts was found within the range of initial AP over 95 mm Hg under the head-up tilts at 30 and 45 degrees. Within the range beneath 95 mm Hg this correlation was transformed into the direct one. Under 60 degrees tilt such correlation only occurred within the range beneath 95 mm Hg.

[Effect of hypotension on the arterial system responsiveness].

The correlation analysis revealed no correlation within the range 110 to 80 mm Hg further transforming into a direct (within the range lower than 80 mm Hg) dependence of the pressure responses to mesatone on the reduction of initial mean arterial pressure under orthostatic hypotension in anaesthetised rats. Under paraverine hypotension a reverse correlation within the range 110-80 mm Hg transforming into a direct dependence (within the range lower than 80 mm Hg) of the responses to mesatone were observed. The dependence of cardiac shifts to mesatone on the initial arterial pressure was not occurred.

[Reactivity of blood vessels: the role of mechanical stimulation and initial tone].

We have studied hemodynamic and some other correlates of the myogenic and endothelium-dependent control of vessel tone and reactivity in experiments with anesthetized cats and rats, as well as in vitro experiments with isolated segments of the mesenteric and tail artery of the rats. We present evidence for the important role of mechanical stimulation of endotheliocytes in the formation of vasodilation in skeletal muscles in response to increased amplitude of the pulse pressure, as well as in response to their active or passive contractions. Interference between mechanical, neurohumoral, and metabolic effects on vascular tone were studied.

[The initial tone of arteries determines the magnitude of depressor responses caused by nitroglycerin].

The correlation analysis revealed a direct (within the range 80 to 120 mm Hg) further transforming into a reverse (within the range 121 to 160 mm Hg) dependence of the blood pressure depressor shifts on the initial mean arterial pressure in anaesthetised rats. Within the physiological range of arterial pressure (70 to 130 mm Hg) there is no difference in responses to nitro-glycerine from their initial values. The mechanisms of dependence of the systemic vascular responses on initial tone of arterial vessels, are discussed.

[The dependence of shifts in arterial pressure and cardiac output during alpha-adrenoreceptor stimulation on the initial (controlled) tonus of arterial vessels in rats].

A significant decrease in arterial pressure and total peripheral resistance occurred following elevation of the initial blood pressure to 160 mm Hg with mesathone in anesthetised rats. The increase in the cardiac output remaining unchanged. Vascular and cardiac mechanisms of the revealed relationships are discussed.

[The effect of the initial (controlled) tonus of the arterial vessels on the correlation of arterial pressure and cardiac output during a pressor reaction to a rapid blood volume increase in rats].

A considerable decrease in pressor responses to polyglykine at an elevated arterial tone and constant increase of cardiac output occurred in anesthetised rats. Vascular and cardiac mechanisms of the interrelationship are discussed.

[Hemodynamic structure of antiorthostatic reactions: relationship of mechanical activity of the heart and arterial pressure].

In acute experiments with antiorthostatic rats tilt-induced changes in the parameters of cardiac activity (left ventricle systolic pressure (LVPs), its first derivative dp/dt, end-diastolic pressure (EDP) were compared in relation to the directionality and extent of systolic (sAP) and diastolic arterial pressure (dAP) shifts. Rise of the tilt angle by 15-45 degrees reduced sAP and dAP, increased LVPs and EDP and did not influence dp/dt. Changes in the cardiac parameters and AP were not unidirectional; sAP and dAP shifts were asynchronous.

[Effects of the tone of arterial vessels on the antiorthostatic response of hemodynamics].

Contribution of the original angiotensin-2 controlled arterial tone to the shifts in systolic and diastolic arterial pressure (AP) was assessed in unconscious rats during tail-suspension. With this technique, values of original mean AP were elevated from 80-110 to 111-140 mm Hg. In the head-down position, rise in the tone was concurrent to a twofold increase in the number of "uncompensated" responses and a similar decrease in the number of test-resistant responses.

[The effect of the initial (controllable) tonus of arterial vessels on the formation of systemic pressor reactions].

A significant decrease of systolic and diastolic effects occurred when initial level of the blood pressure had been elevated from 60 to 200 mm Hg with mesathone and from 70 to 185 mm Hg with polyglukine in anaesthesized rats. A reverse linear correlation was found between the above parameters at a high degree of connection for both agents. "Vascular" and "cardiac" mechanisms of revealed relationships are discussed.

[The correlation of cardiac mechanical activity and arterial pressure in the hemodynamic postural reactions of rats].

In orthostasis, an increase in the body incline angle led to a decrease in the systolic AP, systolic pressure in the left ventricle and a progressive decrease of the final diastolic pressure in rats. The same incline in antiorthostasis decreases the systolic AP, increase the systolic and final diastolic pressure in the left ventricle. These and some other findings show that compensatory responses are mainly manifested in the vascular system both in ortho- and antiorthostasis, whereas shifts in the cardiac activity correspond to the type of blood redistribution.