[Role of mechanosensitivity of the endothelium in weakening of the vascular bed vasoconstriction]. / Rol' mekhanochuvstvitel'nosti éndoteliia v oslablenii konstriktornykh reaktsii sosudistogo éndoteliia.

The effect of control of arterial diameter by the shear stress at the endothelium on noradrenaline-induced constriction of femoral vascular bed was investigated in anaesthetised cats. We compared noradrenaline-induced responses during the perfusion of the hindlimb at a constant blood flow and at a constant pressure as vasoconstriction is accompanied by an increase in wall shear stress only in the former case. We found that the same concentration of noradrenaline at a constant flow caused an augmentation of vascular resistance that was considerably smaller than at a constant pressure perfusion. This difference was almost eliminated after either removal of the endothelium or selective impairment of the endothelial sensitivity to the shear stress. These findings demonstrate that the control of arterial smooth muscle tone at a constant blood flow by shear stress at the endothelium does weaken noradrenaline-induced vasoconstriction.

[The role of endothelial mechanosensitivity in vessel bed responses to changes in blood pressure in cats]. / Rol' mekhanochuvstvitel'nosi éndoteliia v reaktsiiakh sosudistogo rusla na izmeneniia davleniia u koshek.

In 19 anaesthetised cats, the response of vascular bed to increasing perfusion pressure at a constant blood flow perfusion consisted of two phases: a myogenic constriction and a subsequent arterial dilatation. The latter depended on ability of the endothelium to relax the smooth muscle under stress. The findings suggest that the control of the smooth muscle tone by a stress has to fight against the myogenic constriction and thus determines the changes in vascular resistance induced by an increased arterial pressure.

[The anticonstrictor effect of endothelial sensitivity to shear stress]. / Antikonstriktornyi éffekt chuvstvitel'nosti énodeliia k napriazheniiu sdviga.

Responses of the femoral artery to drops in transmural pressure and to norepinephrine revealed the anticonstrictor effect of the endothelium sensitivity upon a stress action. The effect was less obvious at high flow rate. The data obtained suggests that the endothelium sensitivity to stress inhibits the arterial constrictor responses irrespective of the nature of the constrictor stimuli.

Anticonstrictor effect of endothelium sensitivity to shear stress.

The lumen of arterial vessels is controlled by shear stress at the endothelium; increased shear stress relaxes the smooth muscle thus evoking arterial dilatation. Since shear stress relates directly to flow rate and inversely to the third power of the internal diameter, a decrease in diameter at a constant arterial blood flow augments the shear stress which should result in smooth muscle relaxation counteracting the constriction. This anticonstrictor effect must be stronger the higher the arterial blood flow. To demonstrate the effect of endothelium sensitivity to shear stress on arterial constriction we compared constrictions of endothelium-intact femoral arteries of anaesthetized cats at different blood flow rates. An abrupt decrease in transmural pressure from 120 to 90 or 70 mm Hg at almost zero blood flow rate (where the shear stress mechanism is practically inactive) evoked a fast passive decrease in diameter with further progressive constriction. On the other hand, at flow rates of 8-15 ml/min, after passive constriction the artery began to dilate and the resultant constrictor effect appeared to be considerably smaller than in the virtual absence of flow. Analogously, responses to norepinephrine (3 x 10(-7) or 10(-6) M) were smaller the higher the blood flow. The difference in the magnitudes of the responses at different flow rates was precisely equal to the value calculated using the experimental data characterizing the diameter/flow rate relation. Endothelium removal abolished the dependence of the magnitude of the constrictor responses on blood flow. These data suggest that the endothelium sensitivity to shear stress provides considerable inhibition of arterial constrictor responses, whatever the nature of constrictor stimulus.

[Nitrogen oxide is not an agent of endothelium-mediated arterial dilatation to an increase in the blood flow rate]. / Oksid azota ne iavliaetsia mediatorom oposreduemoi éndoteliem dilatatsii arterii na povyshenie skorosti krovotoka.

I. v. administration of inhibitors of endothelium-mediated synthesis of the oxide of nitrogen raised the arterial blood pressure, constricted the femoral artery and decreased the acetylcholine- and ATP-induced vaso-dilatation in anesthetized cats. However, the dilatation induced by an increased blood flow velocity, was not affected. The data obtained suggest that the endothelium-dependent arterial dilatation is not mediated by oxide of nitrogen formed from L-arginine.

Nitric oxide does not mediate flow induced endothelium dependent arterial dilatation in the cat.

OBJECTIVE: The aim was to determine whether the endothelium derived nitric oxide formed from L-arginine is the factor which mediates flow induced dilatation of conduit arteries. METHODS: Changes in diameter of feline femoral artery caused by blood flow rate increases, acetylcholine, and ATP were recorded during perfusion with blood in situ before and after the inhibition of endothelium derived nitric oxide synthesis by NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine. Fourteen anaesthetised cats of either sex, weight 2.6-3.9 kg, were used for the studies. RESULTS: Intravenous administration of NG-nitro-L-arginine methyl ester and NG-monoethyl-L-arginine in doses 10 and 30 mg.kg-1 evoked a rise in mean systemic arterial pressure, constriction of the femoral artery, and considerable decrease in acetylcholine and ATP induced dilatation. However, it did not affect the dilator response induced by increased blood flow rate. CONCLUSIONS: Flow induced endothelium dependent arterial dilatation is not mediated by nitric oxide or, if nitric oxide is still released in response to flow rate increase, it has a source distinct from L-arginine.