Fig. 9-3, p.361

Plasma = 55% of whole blood

Packed cellvolume, orhematocrit

Red blood cells =45% of whole blood

White blood cells

“Buffy coat”<1%

Platelets

Vessellumen

Vesselwall Collagen

Normal endothelium

Prostacyclinand nitric acid

Adenosinediphosphate(ADP)

Normal endothelium

Aggregatingplatelet plug Exposed collagen

at site ofvessel injury

Platelet

Prostacyclinand nitric acid

Inhibits plateletaggregation

Fig. 9-9, p.368

Fig. 9-11, p.369

Goals• To describe the general structure of blood vessel walls.• To compare and contrast the types of blood vessels.• To relate the blood pressure in the various parts of the vascular system to differences in blood vessel structure.

• Role is to direct the flow of blood from the heart to the capillaries, and back to the heart.

Peripheral Circulation

• Arteries

• Arterioles

• Capillaries

• Veins

Arteries• Elastic arteries:

– Walls of smooth muscle and elastin.– Expand when the pressure of the blood rises.– Acts as recoil system when ventricles relax.

• Muscular arteries:– Are less elastic and have a thicker layer of

smooth muscle.• Arterioles:

-Contain highest % smooth muscle. -Greatest pressure drop. -Greatest resistance to flow.

Capillaries• Capillaries consist of only a thin tunica intima or endothelium.• Most capillaries are arranged in capillary beds.• Thinness allows exchange of materials between blood and tissues.

Capillaries

• Smallest blood vessels.

• 1 endothelial cell thick.

• Provide direct access to cells.

• Permits exchange of nutrients and wastes.

The velocity of flow at any point in the circulation is not related to the proximity of the heart, but to the total cross-sectional area of that part of the circulation.

Venules

Veins

• Venules:– Formed when capillaries unite.– Very porous.

• Veins: – Little smooth muscle or elastin.– Capacitance vessels (blood reservoirs).– Contain 1-way valves ensure blood flow to the

heart.

Summary

1. Of the three types of vessels, arteries have the thickest tunica media (allowing stretch/recoil and vasoconstriction), veins have relatively thick tunica adventitia, and capillaries are the thinnest (allowing exchange of materials.)

2. Blood pressure varies in different parts of the vascular system. At least part of this variation reflects vessel structure. Structural adaptations of veins assist in returning blood to the heart.

Sources of Peripheral Resistance

• Three main sources of peripheral resistance:1. blood vessel diameter2. blood viscosity3. total vessel length

Factors Affecting Blood Pressure

Vessel Elasticity Blood Volume Cardiac Output

Blood Vessel Diameter

Blood Viscosity

Total Vessel Length

Peripheral Resistance

Total Blood Vessel Length Affects Peripheral Resistance

•Increased fatty tissue requires more blood vessels to service it and adds to the total vessel length in the body.•The longer the total vessel length, the greater the resistance encountered, and the greater the blood pressure.

1. short-term mechanisms, which regulate blood vessel diameter, heart rate and contractility

2. long-term mechanisms, which regulate blood volume

Blood Pressure Regulation

Long-Term Regulation of Low Blood Pressure

• Long-term regulation of blood pressure is primarily accomplished by altering blood volume.• The loss of blood through hemorrhage, accident, or donating a pint of blood will lower blood pressure and trigger processes to restore blood volume and therefore blood pressure back to normal.• Long-term regulatory processes promote the conservation of body fluids via renal mechanisms and stimulate intake of water to normalize blood volume and blood pressures.

Kidney Juxtaglomerular Cells• Juxtaglomerular cells in the kidney monitor alterations in the blood pressure. If blood pressure falls too low, these specialized cells release the enzyme renin into the bloodstream.

reninangiotensinogen

angiotensin I

Step 1: Renin-Angiotensin Mechanism:

As renin travels through the bloodstream, it binds to an inactive plasma protein, angiotensinogen, activating it into angiotensin I.

Step 2: Conversion of Angiotensin I

angiotensin IIangiotensin I enzyme

Converting Angiotensin I to Angiotensin II: As angiotensin I passes through the lung capillaries, an enzyme in the lungs converts angiotensin I to angiotensin II.

Step 3: Angiotensin II Stimulates Aldosterone Release: Angiotensin II continues through the bloodstream until it reaches the adrenal gland. Here it stimulates the cells of the adrenal cortex to release the hormone aldosterone.

Angiotensin II as a Vasoconstrictor• A secondary effect is that angiotensin II is a vasoconstrictor and therefore raises blood pressure in the body's arterioles

Aldosterone Mechanism• Long-Term Regulation: The target organ for aldosterone is the kidney. Here aldosterone promotes increased reabsorption of sodium from the kidney tubules.• As sodium moves into the bloodstream, water follows. The reabsorbed water increases the blood volume and therefore the blood pressure.

antidiuretic hormone (ADH).

Long-Term Effect of Osmolarity on BP

ADH

Distal Tubule

Long-Term Effect of Osmolarity on BP• the posterior pituitary to release antidiuretic hormone (ADH). Short-Term Effect of Osmolarity on BP• excitation of the thirst center in the hypothalamus, stimulates the individual to drink more water.

• Increased blood osmolarity stimulates release of antidiuretic hormone (ADH), which promotes reabsorption of water, and excites the thirst center, resulting in increased blood volume and blood pressure.

Summary• In the short-term, rising blood pressure stimulates increased parasympathetic activity, which leads to reduced heart rate, vasodilation and lower blood pressure.• Falling blood pressure stimulates increased sympathetic activity, which leads to increased heart rate, contractility, vasoconstriction, and blood pressure.

• Long-term blood pressure regulation involves renal regulation of blood volume via the renin-angiotensin mechanism and aldosterone mechanism.