MAP = CO * TPR

1. Baroreceptor reflex: short-term regulation

2. renin-angiotensin II-aldosterone system: long-term regulation

*An integrating center - this has a set point that constitutes the desired level for the variable being regulated. The set point is compared to a signal received from a receptor and if the regulated variable is not at the set point level, an error signal is generated to bring the variable back to the set point level.

*A receptor - to sense the variable.

*An afferent pathway - taking information from the receptor to the center.

*An efferent pathway - taking any error signal information from the center to the effector than controls the regulated variable.

*An effector - such as a muscle, endocrine cell, etc. responsible for the variable in question.

*The controlled variable is the arterial blood pressure - measured at two points shortly after blood leaves the heart, the carotid sinus and the aortic arch, with afferents running in the glossopharyngeal (cranial IX) and vagus (cranial X) nerves respectively.

*The set point for MAP is usually about 100 mm Hg.

*When the arterial pressure falls below the set point there is sympathetic activation and reduced parasympathetic stimulation - increasing HR and contractility and increasing vascular resistance to increase arterial pressure.

*When arterial pressure rises above the set point there is a reduction in sympathetic stimulation and an increase in parasympathetic stimulation - decreasing HR and contractility and decreasing vascular resistance to decrease arterial pressure.

*Carotid sinus and aortic arch baroreceptors send afferent info about low BP through the glossopharyngeal and vagus nerves to the medulla

*This info is integrated in the nucleus tractus solitarius

*The cardiac accelerator center (sympathetic system) is inhbited so there is less stimulation of the SA node and a decrease in contractility

*The vasoconstrictor center (sympathetic system) is inhibited which leads to less constriction (or more dilation) of arterioles and veins

*The cardiac decelerator (parasympathetic system) is activated which causes inhibiton of the SA node

*Sympathetic system is more dominat

* Decreased stretch on carotid sinus baroreceptors leads to decreased firing of the glossopharyngeal (cranial IX) nerve

*This causes increased sympathetic activity to the heart and blood vessels causing increased HR, increased contractility, constriciton of arterioles (increase in TPR), constriction of veins (decrease in unstressed volume and increase in venous return)

 *Decreased firing also causes decreased parasympathetic activty to the heart which leads to increased HR

*expiring against a closed glottis as during coughing, defecation, or heavy lifting

*this causes an increase in intrathoracic pressure which decreases venous return to the heart

*this decrease in venous return produces a decrease in cardiac output and a consequent decrease in arterial pressure

*baroreceptor reflex detects low blood pressure and causes an increase in HR

High blood pressure is not corrected due to:

1) increased set point of blood pressure in the brain stem

2) decreased sensitivity of the receptors to the high blood pressure

* carotid massage

*volume load

*no gravity (in space)

The high BP causes an increase in afferent activity which cause increased para, decreased symp, decreased HR, and decreased BP (to return back to normal)

*orthostatic hypotension

*IX nerve cut

*hemorrhage

*carotid occlusion

The low BP cause a decrease in afferent activity which causes decreased para, increased symp, increased HR to increase BP back to normal levels 

Major causes of increased renin secretion by the kidney (Juxtaglomerular cells):

1- Increased renal sympathetic tone

2- Decreased renal perfusion pressure (renal baroreceptor)

3- Decreased NaCl in the distal tubule

*Low blood pressure leads to low renal perfusion pressure which leads to increased renin secretion

*Renin catalyzes the conversion of angiotensinogen to angiotensin I

*angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE)

*increased angiotensin II leads to: 

1) increased aldosterone leading to increased Na+ reabsorption

2) increased Na+-H+ exchange leading to increased Na+ absorption

3) stimulation of thirst (increased water intake) and release of antidiuretic hormone to increase water reabsorption

4) vasoconstriction leading to increased TPR

Location: carotid bodies and aortic bodies

Causes:

a) Decrease arterial PO2

b) Increase PCO2 and decrease in pH

Effects:

a) Increase sympathetic outflow -> arteriolar vasoconstriction in skeletal muscle, renal and splanchnic vascular beds.

b) Increase parasympathetic outflow -> decrease heart rate

c) Increase ventilation -> increase heart rate (lung inflation reflex) - this is independent of the first two effects and is in response to the decreased arterial PO2

Location: medulla of the brain

Causes:

a) Change in arterial PCO2 and pH (brain ischemia)

b) Less sensitive to O2 changes

Effects: Increase sympathetic outflow -> arteriolar vasoconstriction (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 -> increase PCO2 and decrease pH

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

*Located in the veins, atria, and pulmonary arteries

*They are located in the venous side of the circulation so that they can easily sense changes in blood volume

ADH (anti-diuretic hormone) or vasopressin

Release caused by:

1)Increased serum osmolarity

2)Decreased in blood pressure (e.g. hemorrhage)

Effects

V1 receptors -> vascular smooth mucle constriction V2 receptors (renal collecting ducts) -> ↑ water reabsorption

ANP (atrial natriuretic peptide)

Secretion by the atria caused by:

Increase in ECF volume and atrial pressure

Effects:

1)Vasodilation -> decreased total peripheral resistance

2)Increase Na+ and water excretion from the kidney

This is a reflex that appears to ensure that blood volume does not back up on the venous side (observed only when HR is low).

Overall net effect: increase pressure at venous side (volume) -> increase HR

*Increasing venous return and arterial pressure stimulates atrial stretch receptors and this results in an increased heart rate. The afferents for this reflex appear to run in the vagus nerves and the centers are located in the medulla.

*It compete with high-pressure baroreceptor-mediated decrease in HR to lower high blood pressure

*The physiological significant of this reflex is not yet known

* decreased ADH secretion -> increased urine output and decreased blood volume

*increased ANP secretion -> vasodilation

*decrease renin secretion -> decreased activity of the renin-angiotensin II-aldosterone system -> decreased BP

*increased HR (due to bainbridge reflex) - reaction to decreased HR used to lower BP

*increased ADH secretion leading to decreased urine output

*decreased ANP secretion -> vasoconstriction

*increased renin secretion -> increased activity of the renin-angiotensin II-aldosterone system -> increased BP

*Combination of several reflexes

Overall net effect:

inspiration -> increase venous return -> increase HR (tachycardia)

*Complicated by many reflexes and physical effects of respiration on venous return to both the right and left atrium.

*Involves lung stretch receptors, Bainbridge reflex receptors (inspiration increases atrial filling), arterial baroreceptor stimulation as increased venous return increases preload and SV, direct cross-talk between respiratory centers and cardiovascular centers in the medulla.