• O Stokland, J Thorvaldson, A Ilebekk, and F Kiil.
• Acta Physiol. Scand. 1983 Apr 1;117(4):481-9.

AbstractTo examine the factors contributing to the rise in systemic blood pressure during alpha- and beta-adrenergic stimulation, phenylephrine, an alpha-adrenergic agonist, and norepinephrine, an alpha- and beta-adrenergic agonist, were infused intravenously to anesthetized dogs until mean aortic blood pressure was raised equally by 40-60 mmHg. Changes in preload were estimated by changes in left ventricular end-diastolic pressure or segment length recorded by an ultrasonic technique. By obstructing the inferior vena cava (IVC), the increase in preload could be reduced to control level during phenylephrine and norepinephrine infusions without altering peripheral resistance (mean aortic blood pressure/cardiac output). Normalization of preload reduced the pressure response by 2/3 during phenylephrine infusion and by 1/4 during norepinephrine infusion. However, after beta-adrenergic blockade by propranolol, normalization of preload reduced the pressure response by 2/3 during both phenylephrine and norepinephrine infusions. Thus, during alpha-adrenergic stimulation, the increase in preload is a more important factor than the increase in peripheral resistance. Norepinephrine raised stroke volume by 24 +/- 5%. When the increase in stroke volume was prevented by IVC obstruction, the pressure response to norepinephrine was halved. Thus, during norepinephrine infusion the rise in stroke volume caused by beta-adrenergic stimulation is as important as alpha-adrenergic stimulation for the pressure response.

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