• Carotid Sinus. At the very begining of the Internal Corticoid Artery branch. In the neck. Its afferent nerves run in the glossopharyngeal
• Aortic Arch. Its afferent nerves are the vagus nerves.

• Baroreceptor reflex: short-term regulation. ANS
• Renin-angiotensin II-aldosterone system: Hormonal. Long-term regulation.

MAP=CO x TPR

Intergrating center: Has the set point that constitutes the desired level of what is being regulated. Takes information from receptor. Controls effector.

A receptor: to sense variable.

Afferent pathway: info from receptor to center.

Efferent pathway: center uses info to regulate effector.

Effector: muscle, organ.. ect

• Blow all the air out of your lungs while holding your nose closed.
• Should increase sympathetic activity.
• Test Baroreceptor reflex.

High blood pressure NOT corrected due to:

-Increased set point blood pressure in brain stem.

-Decreased sensitivity of the receptors to high blood pressure.

Carotid Massage: fools medulla into thinking there is high blood pressure.

Volume Load:

No gravity(in space): Pooling blood goes into circulation and increases venous return.

• ↑Afferent Activity
• ↑Parasympathetic
• ↓Sympathetic
• ↓Blood Pressure
• ↓Heart Rate

Orthostatic hypotension: Happens with older people. They stand up fast and feel light headed. Blood goes to legs and less venous return.

IX Nerve Cut:

Hemorrhage(bleeding):

Carotic occlusion(blockage):

• ↓Afferent Activity
• ↓Parasympathetic
• ↑Sympathetic
• ↑Blood Pressure
• ↑Heart Rate

1. Increased renal sympathetic tone
2. Decreased renal perfusion pressure
3. Decreased NaCl in distal tubule

Location: Carotid bodies and Aortic bodies

Causes: Decrease arterial PO₂, Increase PCO₂ and decrease in pH

Effects:

-Increased sympathetic outflow→ arteriolar vasoconstriction in skeletal muscle, renal and splanchnic vascular beds.

-Increase parasympathetic outflow→ decrease heart rate.

-Increase ventilation→ increase heart rate (lung inflation reflex)

Location: medulla of the brain

Causes: Change in Arterial PCO₂ and pH (brain ischemia), Less sensitive to O₂ changes.

Effects: Increase sympathetic outflow→ arteriolar vasocontriction (to redirect blood flow to the brain), however increase peripheral resistance→ increase arterial pressure.

Maintain cerebral blood flow via cerebral chemoreceptors.

Causes: increase intracranial pressure (e.g. brain tumors)→ compression of cerebral arteries→ decrease blood perfusion to brain→ increase PCO₂ and decrease pH.

Effects: increase sympathetic outflow to blood vessels→ vasoconstriction (redirect blood to the brain) and increase in arterial pressure.

• Atrial A and B type receptors.
• Minimize arterial pressure changes as a result of changes in blood volume.
• ↑stretch: VD, ↓BP
• ↓stretch: VC, ↑BP

Also called Vasopressin

Causes: Increase serum osmolarity, Decrease in blood pressure (e.g. hemorrahage).

Effects:

-V1 receptors→ vascular smooth muscle constriction

-V2 receptors(renal collecting duct)→ ↑water absorption

Causes: Increase in extra cellular fluid (ECF) volume and atrial pressure.

Effects:

-Vasodilation→ ↓total peripheral resistance

-Increase Na and water excretion from the kidney.

• Ensures that blood volume does not back upon the venous side. (observed only when HR is low)
• Overall net effect: increase pressureat venous side  (volume) → increase HR.

• Combination of several reflexes
• Overall net effect: inspiration→ increase venous return→ increase HR (tachycardia)