pressure is decreased. Under this condition,
increased firing by the AV receptors opposes
the decreased firing by arterial baroreceptors.
During hemorrhage, cardiac chamber pres-
sures and arterial pressures are both reduced.
This causes the atrioventricular receptors and
the arterial baroreceptors to decrease their fir-
ing rates and therefore reinforce each other.
How do the carotid sinus baroreceptors
respond to occlusion of both common
carotid arteries? What are the cardio-
vascular responses to bilateral carotid
occlusion? How would these responses
be altered by bilateral vagotomy?
How would these responses be altered
by the pharmacologic blockade of
Chemoreceptors are specialized cells located
on arteries (peripheral chemoreceptors) and
within the medulla (central chemoreceptors)
that monitor blood P02 (partial pressure of
oxygen), PC02 (partial pressure of carbon
dioxide), or pH (log H+
concentration). Their
primary function is to regulate respiratory
activity to maintain arterial blood P02, PC02,
and pH within a narrow physiologic range.
cardiovascular function either directly by
influencing medullary cardiovascular cent-
ers or indirectly through altered pulmonary
stretch receptor activity. Impaired respiratory
gas exchange, hypoxic environments, cerebral
ischemia, and circulatory shock, for example,
increase chemoreceptor activity, leading to
enhanced sympathetic outflow to the heart
and vasculature by activating neurons in the
found in two locations. Small carotid bod-
ies are associated with the external carotid
arteries near their bifurcation with the inter-
nal carotids. Afferent nerve fibers from the
carotid body receptors join with the sinus
nerve before entering the glossopharyngeal
nerve to synapse in the RTS in the medulla.
The carotid bodies increase their firing in
response to a fall in arterial P02 (hypoxemia)
or to an increase in arterial PC02 (hypercap-
nia) and hydrogen ion concentration (acido-
sis). The threshold P02 for activation is about
80 mm Hg (normal arterial P02 is about
mm Hg). Any elevation of PC02 above its
normal value of 40 mm Hg, or a decrease in
pH below 7.4, also increases receptor firing.
In addition, carotid body firing can be stimu-
lated by reduced carotid body perfusion, as
occurs during hypotension associated with
circulatory shock. This response to reduced
perfusion can occur without changes in arte-
rial P02, PC02, and pH. The mechanism may
involve cellular hypoxia resulting from inad-
equate oxygen delivery to the carotid bod-
ies (i.e., “stagnant hypoxia”). Another set of
peripheral chemoreceptors, the aortic bodies,
are located on the aortic arch, and they func-
tion similarly to the carotid bodies. Their
afferent connections to the NTS travel with
vagal afferent fibers.
medullary regions that control cardiovascu-
lar and respiratory activity. These receptors
increase their firing in response to hypercap-
nia and acidosis but not directly in response
to hypoxia. Carbon dioxide diffusing from
the blood into the cerebrospinal fluid forms
hydrogen ion by the bicarbonate buffer sys-
tem, and it is the hydrogen ion rather than the
carbon dioxide that stimulates receptor firing.
If a subject breathes a gas mixture contain-
ing 10% instead of 21% oxygen, chemorecep-
tor activation (primarily peripheral) increases
respiratory activity and stimulates sympathetic
activity to the heart and systemic vasculature,
causing arterial blood pressure to increase. If,
however, respiratory rate and depth are not
allowed to change, the sympathetic-mediated
pressor response is accompanied by brady-
cardia resulting from vagal activation of the
heart. This demonstrates that the tachycardia
normally found during hypoxemia is second-
ary to respiratory stimulation and activation
of pulmonary stretch receptors. Cardiovas-
cular responses to hypercapnia and acido-
sis likewise depend in part upon respiratory
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