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.
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 effect of the elevated arterial tone on pressure responses to stimulation of arterial alpha-adrenoreceptors by phenylephrine hydrochloride was studied in anesthetized Wistar rats. Different levels of the arterial tone and, hence of the mean arterial pressure, were established by means of angiotensin II infusion in the range from 101 to 160 mmHg. An elevation of the arterial tone led to a significant reduction of the arterial pressure and peripheral resistance rise produced by phenylephrine. The degree of relative reduction of the increase in the diastolic pressure exceeded 1.3 times that in the systolic pressure. The shifts of cardiac outputs remained unchanged. After cessation of angiotensin II infusion the restoration of the arterial pressure took place almost till the initial level. At this time the pressure effects of phenylephrine were tended to recovery. It is suggested that the elevated arterial tone attenuates the systemic pressure response to stimulation of arterial alpha-adrenoreceptors by a vascular mechanism based on a transmural pressure changes evoked by the constriction of the arterial vessels.
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