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What are the short-term cardiovascular regulatory responses to a sudden decrease in peripheral conductance in healthy humans?
What are the short-term cardiovascular regulatory responses to a sudden decrease in peripheral conductance in healthy humans?
The regulatory correction of a sudden increase in arterial pressure in humans involves an immediate transient parasympathetic bradycardia followed by a more gradual sympathetic peripheral vasodilation.
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Elucidates rapid autonomic buffering of acute pressure rises in healthy humans; extends baroreflex models but leaves clinical translation open.
A step decrease in total peripheral conductance (TPC) was introduced in 10 healthy volunteers by rapid inflation to suprasystolic pressure of bilateral thigh cuffs. This provoked a sudden statistically significant increase in mean arterial blood pressure (MAP) of 5 mmHg during supine rest and of 8 mmHg during moderate supine exercise by the quadriceps muscles. Central venous pressure was not changed by cuff inflation. The increase in MAP was blunted by a rapid but transient decrease in both heart rate (HR) and cardiac stroke volume. At rest, a gradual increase in TPC, starting after 4 s, nearly fully restored MAP to its original value at 10 s. During exercise, MAP was halfway corrected at 10 s but then started to increase again, probably as a result of an ischaemic muscle pressor response. After cholinergic blockade by atropine, the immediate HR response was eliminated, but HR decreased gradually after a delay of 3 s. The time development of the slow increase in TPC was not changed by atropine. In conclusion, the regulatory correction of a sudden increase in arterial pressure in supine unanesthetized healthy humans is achieved through an immediate transient parasympathetic bradycardia during the first few seconds and a more gradual sympathetic peripheral vasodilation after 4 s. After cholinergic blockade, a slow presumably sympathetic HR response was observed.
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Toska et al. (1994) studied this question.
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