Increases heart rate contractility peripheral

Increases heart rate, contractility, peripheral vascular resistance
(PVR)

Parasympathetic signals are transmitted to the heart via the
vagus nerve

Decreases heart rate

ANS control is mediated via intrinsic and extrinsic reflexes

Neural Mechanisms
 Pre-synaptic in the CNS

Stimulation of α
2
receptors

Inhibits norepinephrine release

Positive feedback mechanism

Stimulation of β receptors

Causes norepinephrine release

Post-synaptic

Stimulation of β
1
receptors in heart

 HR

Stimulation of β
2
receptors in arterioles & venules

Vasodilation

Stimulation of α
1
receptors in arterioles & venules

Vasoconstriction

Neural Mechanisms
 Intrinsic control of ANS
1.
Baroreceptors

Pressure sensitive
receptors located in the
walls of blood vessels and
the heart

Respond to changes in the
stretch of the vessel wall

Example: juxtoglomerular
cells of the kidney
1.
Chemoreceptors

Monitor oxygen, carbon
dioxide and hydrogen
contents of blood

Hypoxemia due to a chronic
lung disease could trigger
HTN

Neural Mechanisms
 Extrinsic control of the ANS

Found outside circulation

Very diffuse

Responses are inconsistent

Associated with factors like pain, cold, and
emotion

Humoral Mechanisms:
RAAS System

Most influential in the control of homeostatic BP
 Regulates

Sodium, potassium, and fluid balance

Vascular tone and sympathetic activity

Influenced by

Intrarenal factors: renal perfusion, catecholamines, angiotensin II

Extra renal factors: sodium, chloride, potassium

Juxtoglomerular cells sense decreased renal artery pressure and kidney blood
flow

Release renin
 Macula densa and/or juxtoglomerular cells sense a decrease in sodium and
chloride

Releases renin

Humoral Mechanisms
Renin-angiotensin-aldosterone system (RAAS)

Extracellular Fluid Volume
 Elevates BP directly and indirectly

Direct

Higher volumes directly increase CO

SV x HR x PVR

Indirect

Higher blood flow to organs causes
vasoconstriction (increase in PVR)

Stimulates a tissue-regulation response

Tissue Auto-regulation

Purpose is to maintain adequate tissue perfusion and
oxygenation
 Kidney’s

volume-pressure balance/adaptation
 Tissues have auto-regulatory mechanisms

Normal

With low-normal metabolism  vasocontriction

High metabolism  vasodilation
 Defects in renal 

 volume & blood flow to tissues 

Vasoconstriction 

 PVR

Different types of HTN

Primary Vs. Secondary Hypertension
 Primary

90% of HTN cases

Chronic elevations in blood pressure

No evidence of other disease

Secondary

Minority of cases

HTN that results from another disorder

Mechanisms of Pathogenesis:
Primary Hypertension
 Increased cardiac output

Increased fluid volume from excess sodium intake or renal sodium retention

Excess stimulation of the RAAS

Sympathetic over activity
 Increased peripheral resistance