Abstract

Control of arterial blood pressure is normally effected by altering the key parameters of heart rate and stroke volume (which influence cardiac output), arteriolar vascular resistance (peripheral resistance) and venous capacitance (to modulate venous return). Both divisions of the autonomic nervous system are involved in control of blood pressure. The parasympathetic system plays a relatively minor part by altering heart rate only (increased vagal activity causing a bradycardia) while the sympathetic system influences the heart (increased activity increasing heart rate and stroke volume) and vasculature. Increased sympathetic nervous activity generally increases vascular tone via an effect of noradrenaline on vascular α-adrenoreceptors. Circulating adrenaline can activate both vascular ?2- and α-adrenoreceptors to cause respectively a vasodilatation or vasoconstriction. The predominant effect of adrenaline in any particular vascular bed depends on the concentration of adrenaline and the relative proportions of ?2- and α-adrenoreceptors on the smooth muscle. Under resting conditions arterial blood pressure is controlled by the arterial baroreceptor reflex, which serves as a negative feedback mechanism. However, the baroreceptor reflex can be over-ridden by other reflexes and responses, for example the visceral alerting response of the defence reaction or the depressor response to severe haemorrhage.Control of arterial blood pressure is normally effected by altering the key parameters of heart rate and stroke volume (which influence cardiac output), arteriolar vascular resistance (peripheral resistance) and venous capacitance (to modulate venous return). Both divisions of the autonomic nervous system are involved in control of blood pressure. The parasympathetic system plays a relatively minor part by altering heart rate only (increased vagal activity causing a bradycardia) while the sympathetic system influences the heart (increased activity increasing heart rate and stroke volume) and vasculature. Increased sympathetic nervous activity generally increases vascular tone via an effect of noradrenaline on vascular α-adrenoreceptors. Circulating adrenaline can activate both vascular ?2- and α-adrenoreceptors to cause respectively a vasodilatation or vasoconstriction. The predominant effect of adrenaline in any particular vascular bed depends on the concentration of adrenaline and the relative proportions of ?2- and α-adrenoreceptors on the smooth muscle. Under resting conditions arterial blood pressure is controlled by the arterial baroreceptor reflex, which serves as a negative feedback mechanism. However, the baroreceptor reflex can be over-ridden by other reflexes and responses, for example the visceral alerting response of the defence reaction or the depressor response to severe haemorrhage.