Contribution of
baroreceptors and chemoreceptors to ventricular hypertrophy produced by sino-aortic denervation in rats.
Larger blood volume and stroke volume in athletes also maintain higher activation of arterial
baroreceptors leading to increased parasympathetic activation (Boushel et al.
For example, pressure on the carotid
baroreceptors from balloon dilation or stent deployment commonly causes sudden bradycardia or transient asystole.
This will be detected by
baroreceptors that stimulate sympathetic nervous responses to maintain circulation, and the renin-angiotensin-aldosterone system (RAAS).
In this position increased central blood volume via arterial
baroreceptors imposes a greater vagal activation than in the supine position and reduces heart rate and cardiac output (Rowell, 1993).
As P waves come earlier and sinus rhythm returns, the appropriately timed atrial systole and the synchronous ventricular contraction resulting from normal depolarization produce an increase in stroke volume that causes the
baroreceptors to increase parasympathetic tone and decrease sympathetic tone.
Baroreceptors (pressure-sensitive receptors found in major vessels such as the aorta) trigger sympathetic activation when blood pressure is decreased and triggers or sympathetic deactivation when blood pressure is increased.
Two afferent pathways, one from
baroreceptors and one from osmoreceptors, control the secretion of AVP in the presence of hypovolemia or hyperosmolality.
The system works by electrically activating
baroreceptors, the body's natural blood pressure sensors that regulate cardiovascular function.
Baroreceptors are stretch receptors found in the aorta and internal carotid arteries that monitor mean arterial pressure.
Changes in blood pressure are signalled to the brain by nerve cells called
baroreceptors.
In doing this, the
baroreceptors, part of the blood pressure regulatory mechanism, send messages to the brain stem, which instigates peripheral vasodilation and hypotension as a compensatory mechanism.
