Dr. Edmee Y. Martinez

• thin-walled lined with a single layer of endothelial cells, which are surrounded by a basal lamina 1. Lipid soluble substances (O2 & CO2) cross the capillary wall by dissolving in & diffusing across the endothelial cells 2. H2O soluble substances (ions) cross the capillary either a. Through water-filled clefts (spaces) between the endothelial cells or b) Through large pores in the wall of some capillaries (ex. Fenestrated caps)

 Not all capillaries are perfused with blood at all times. Instead, there is selective perfusion of capillary beds – depending on the metabolic needs of the tissues. – This selective perfusion is determined by the degree of dilation or constriction of the arterioles & pre-capillary sphincters (smooth muscle bands that lie before the capillary)

controlled by the: 1. by Vasoactive metabolites produced in the tissues .– The degree of dilation or constriction is in turn. sympathetic innervation of the vessel smooth muscle 2.

5 micrometer • diameter = 4 to 9 micrometers .STRUCTURE OF CAPILLARY WALL • lined by single layer of endothelial cells • surrounded by very thin basement membrane • total thickness = 0.

intercellular cleft and and pericytes  Total area exceeds 6300 m2 and 1 µm thick . fenestrations (pores). basement membrane  (-) smooth muscle and (-) elastic tissue  tight junctions.CAPILLARIES  endothelial cells.



000 Type of Endothelium Brain (except CVO Skin Skeletal muscle Lungs Heart GIT (intestinal mucosae) Kidney (glomerulus) Liver Bone marrow Endocrine glands Lymphoid tissue Continuous Fenestrated Sinusoidal (Marieb. Human Anatomy and Physiology) . Medical Physiology 2001) Organ Conductivity 3 100 250 340 860 13.Hydraulic conductivity of capillaries in various parts of the body (Ganong.

.Capillary Fluid Shift  the rate of filtration at any point along the capillary depends upon the balance of forces called Starling’s Forces across the capillary wall.

Starling’ Forces • Total Filtration Pressure – Capillary Hydrostatic Pressure – Tissue Colloid Osmotic Pressure Total Absorption Pressure – Plasma Colloid Osmotic Pressure – Tissue Hydrostatic Pressure • .

(∏ p .FILTRATION = Kf ( Pc – Pif) .∏if) = Kf (Pc + ∏if) – (Pif + ∏ p) = Kf X NFP .

THP Subatmospheric or negative  subcutaneous tissue Positive  kidney. liver and brain Factors that affect THP  solute in the interstitium Factors that affect CHP  arterial blood pressure  arteriolar resistance  venular resistance  venous pressure .

PCOP  28 mmHg  19 mmHg (proteins) 9 mmHg (Donnan Effect) Factors that affect PCOP  proteins in the plasma (80% albumin) Factors that affect TCOP (8mmHg)  protiens in the interstitium  other solutes in the interstitium Factors that affect Kf  capillary membrane permeability  total surface area for diffusion .

Arteriolar end ( Filtration) Venular end ( Reabsorption ) CHP TCOP TFP THP PCOP -------------TRP 35 mmHg 8 mmHg ------------43 mmHg 1 mmHg 25 mmHg 26 mmHg CHP TCOP TFP 15 mmHg 8 mmHg ------------23 mmHg THP 1mmHg PCOP 25 mmHg ------------TRP 26 mmHg Total reabsorption pressure Total filtration pressure > ARTERIOLAR END Total reabsorption pressure > Total filtration pressure VENULAR END .


Plasmalemmal vesicles – which coalesce to form vesicular channels all the way through the endothelial cells . Intercellular cleft – a thin-slit channel between adjacent endothelial cells called “slit-pores” 2.• Pores 1.

• most pores permit only molecules with radius less than 3 – 6 mm to pass through vessel wall • allowed to pass through small pores – water – inorganic ions – glucose – amino-acids – water-soluble solutes .

• not allowed to pass through – serum albumin – globular proteins – blood cell components • lipid soluble molecules (O2 & CO2) pass through lipid components of endothelial cell membrane .

Liver – the clefts between endothelial cells wide open. Thus only the smallest water-soluble molecules pass through (H2O. O2 & CO2) 2. Capillaries in cardiac & skeletal muscles – have low porosity to water and small water-soluble substances 3.• Porosity of capillaries NOT the same in all organs 1. So.have continuous tight junctions between endothelial cells. almost all dissolved substances of plasma (plasma proteins) can pass from blood to liver tissues . Brain & Spinal Cord .

Spleen & Bone Marrow Capillaries – large pores . GIT – midway between liver and muscles 5.4. Glomerular tuft of kidneys – numerous small oval windows (fenestrae) penetrate all the way through endothelial cells. Only plasma protein cannot pass. 6.

CAPILLARY HYDROSTATIC PRESSURE (CHP) • main determinant of transcapillary exchange • force exerted by the blood against the walls of capillaries • pushing pressure – pushes fluid from capillary to interstitium .

. 25 mm Hg .. 15 mm Hg average CHP ……….• normal CHP: arteriolar end ………. 35 mm Hg venular end ……….

TISSUE (INTERSTITIAL) HYDROSTATIC PRESSURE (THP) • normal THP: -7 to 1 mm Hg • pushing pressure – pushes fluid from interstitium back to the capillaries and veins through the lymphatic system .

PLASMA COLLOID OSMOTIC PRESSURE (PCOP) • normal PCOP: 25 mmHg • also known as Osmotic Pressure of Plasma Proteins (OPPP) & Oncotic pressure • exerted by the plasma proteins (particularly albumin) • pulling pressure – pulls fluid from interstitium to capillaries .

TISSUE (INTERSTITIAL) COLLOID OSMOTIC PRESSURE (TCOP) • normal TCOP: 7 – 8 mm Hg • exerted by plasma proteins that leaked through the capillary wall & go into the interstitium • pulling pressure – pulls fluid from capillaries to interstitium .


Systemic regulation of circulation and Arterial Blood Pressure .

Circulatory Adjustments are effected by: 1. Changing the diameter of the resistance vessels – TPR 3. Altering the output of the heart – CO 2. Altering the amount of blood pooled in the capacitance vessels .

Vasoconstriction Vasodilation changes in caliber of Arterioles Venoconstriction Venodilation changes in caliber of Veins .

the nerves that innervate the arterioles (Neural) . 3. autoregulation locally produced Vasodilator Metabolites subs secreted by Endothelium systematically produced by circulating vasoactive subs (Hormones) 5. 4.Caliber of Arterioles adjusted or effected by: 1. 2.

Vasomotor Nerves .Caliber of Veins adjusted by: 1. the circulating Vasoactive subs 2.

AUTOREGULATION • Capacity of tissues to regulate their own blood flow oDue to the intrinsic contractile response of smooth muscle to stretch (Myogenic Theory of Autoregulation) oDue to vasodilator metabolites that accumulate in active tissues (Metabolic Theory of Autoregulation) • Well developed in the Kidneys .1.


increased magnesium f.d. increased potassium --.vasodilation in skeletal muscles e. Lactate .

Histamine • derived from basophils in the blood • released from mast cells in damaged tissue • vasodilation • increased cap. Permeability → swelling in areas of inflame. .g.

NOT in skeletal muscles – inhibits release of NE . Adenosine – vasodilator in Cardiac muscles.h.

decrease H† conc. Sl. 4. increased calcium conc. Serotonin 2. . drop in temperature – localized vasoconstriction 3.VASOCONSTRICTORS (Local) 1.

3. PROSTACYCLIN – inhibits platelet aggregation & promotes vasodilation THROMBOXANE A2 – produced by platelets .promotes platelet aggregation & vasoconstriction . Substances secreted by Endothelium a.

EDRF (Endothelium Derived Relaxing Factors) now called NITRIC OXIDE (NO) –Vasodilator c.b. ENDOTHELIN 1 – potent vasoconstrictor .

4.may cause vasodilation in coronary arteries during increased heart activity Angiotensin II Vasopressin – more powerful than Angiotensin II as a Vasoconstrictor . Systemic Regulation by Hormones Vasoconstrictor Hormones: NE – powerful vasoconstrictor E – less powerful than NE .

Vasodilator Hormones: • KININS .Antagonizes the action of vasoconstrictor agents & lowers BP .bradykinin • VIP • ANP – Atrial Natriuretic Peptide .

5. Neural Factor – (Rapid control of ABP) • All blood vessels except capillaries & venules contain smooth muscle and receive innervation from sympathetic nervous system – The fibers to the arterioles regulate tissue blood flow and arterial pressure .

– The fibers to the capacitance vessels vary the volume of blood stored in the veins Ex. Venoconstriction »decreased venous capacity »increased venous return .

NORADRENERGIC FIBERS to blood vessel – vasoconstriction – contain NEUROPEPTIDE Y – which is a vasoconstrictor – vasoconstrictor fiber exhibit tonic activity (S tone to blood vessel) Cut S to b.v. spleen. powerful in the kidneys. → b. dilates o S vasoconstrictor effects esp.v. skin. less in brain & skeletal muscles .

SYMPA CHOLINERGIC to b. skeletal muscles – Vasodilator – called Sympathetic Vasodilator System – Contain VIP which prod. Vasodilation • NO tonic activity .v.


continues with the sustaining characteristics of the intermediate mechanisms 3. is stabilized at the long term mechanism by the renal – body fluid mechanism .ARTERIAL PRESSURE CONTROL 1. finally. begins with life saving measures of the nervous control mechanism 2.

CONTROL MECHANISM divided into 3 groups Arterial pressure is regulated by several inter-related systems each of which performs a specific function • Rapidly Acting Pressure Control Mechanism – begins to act within seconds or minutes but cannot maintain ABP because they adapt to prolonged change in pressure – attempts to restore BP rapidly toward normal .

– Involves participation baroreceptors & chemoreceptors located in the peripheral circulation
– begin to act within seconds or minutes – Powerful control mechanism – most nervous control of BP is achieved by reflexes that originate in the baroreceptors & chemoreceptors located in the peripheral circulation outside the brain

o Includes:

A. Baroreceptor Feedback Mechanism –Activated instantly by any BP change –Attempts to restore BP rapidly toward normal –Cannot maintain BP b/c they adapt to prolonged change in pressure. Thus, Short – term Regulator of ABP –Involves participation of baroreceptors in arch of aorta & carotid sinus

B. CNS ISCHEMIC MECHANISM – Ex. Cushing Reaction

Chemoreceptors in the Carotid and Aortic bodies

II. Stress – Relaxation of the Vasculature . Intermediate Time Period Control Mechanism A. Capillary Fluid Shift Mechanism C. RAAS B.

III. Long Term Mechanism
• The major factor for long term regulation is blood volume The Renal Body Fluid Pressure Control Mechanism or Renal-Blood Volume Pressure Control Mechanism – It takes a few hours to show significant response – This mechanism can eventually return the arterial pressure all the way back to normal pressure that will provide normal output of salt & water by the kidneys – Has multiple interactions with the RAAS and the Nervous System

Baroreceptor Reflex / Sino-aortic Reflex / Marey’s Law of the Heart
• Reflex Arc Components • Vasomotor Area or VMC – groups of neurons in the Medulla Oblongata responsible for the main control of ABP • Afferent fibers end in the Nucleus of Tractus Solitarius (NTS)

• After the baroreceptor signals have entered the NTS of Medulla, secondary signals inhibit the VMC (Gaba) & excite the CIC (Glutamate) • VMC transmits sympathetic impulses to blood vessels • Lateral portion of VMC transmit excitatory impulses through S to heart • Medial portion of VMC transmits PS signals to dorsal motor nucleus of CN X to heart

• Practical application of baroreceptor reflex – Changes in body posture – Direct pressure on the carotid sinus – ↓ HR This maneuver is used to treat paroxysmal tachycardia .


Increased baroreceptors discharge decreases ABP How? 1. Venodilation . inhibits the tonic discharge of the vasoconstrictor nerves →vasodilation → decreases PR 2. excites the vagal innervation of the heart →decreases HR and CO 3.

Carotid Sinus Baroreceptors – Not stimulated by pressure between 0mmHg and 50 to 60 mmHg – Responds rapidly above this level and reach a maximum of 180 mmHg .

Aortic Baroreceptors • Operate at pressure levels above 30mmHg oMost nervous control of BP is achieved by reflexes that originate in the baroreceptors and chemoreceptors located in the peripheral circulation outside the brain .

Factors that affect the VMC: A. Excitatory inputs from: 1. Excitatory inputs from the higher centers like hypothalamus and cortex Ex. Emotions like anger and sexual excitement → Increased HR and vasoconstriction → Increased ABP .

Excitatory inputs pain pathways and muscles Ex.2. Acute pain → increased BP via afferent impulses in the reticular formation converging on the VMA Exception: Prolonged severe pain →Vasodilation → decreased BP → fainting .

Cortex via hypothalamus Ex. Inhibitory Inputs from 1.B. Fear & grief → bradycardia & vasodilation → decreased BP → Syncope 2. Lungs Inflation of lungs → inhibit vasomotor discharge through CN X → Vasodilation and decreased BP .

CNS ISCHEMIC MECHANISM ABP also controlled by the VMC in the brain in response to diminished blood flow to the brain Cerebral Ischemia → increased ABP → decreased HR .


Example: CUSHING REACTION • is an example of the response to cerebral ischemia • is a special type of the CNS ischemic response that results from an increased pressure in the cranial vault .

• happens when CSF pressure rises to equal ABP – compresses arteries in the brain – cuts off blood supply to brain – cerebral ischemia – increases ABP to a level higher than CSF pressure – blood flows once again to brain vessels – relieve the cerebral ischemia .

• SIG: helps protect the vital centers of the brain from loss of nutrition when the CSF pressure rises at a level high enough to compress the Cerebral arteries .


Called the “LAST DITCH STAND” pressure control mechanism .CNS ISCHEMIC RESPONSE: • operates primarily as an emergency arterial control system that acts rapidly and powerfully to prevent further decrease in ABP when blood flow to brain decreases.

Kidneys almost entirely stop production of urine because of arteriolar constriction . – Ex.• is one of the most powerful of all the activators of the Sympathetic vasoconstrictor system because can elevate MAP to as high as 250 mmHg. to a point that some peripheral vessels become almost totally occluded.

• Powerful so that ABP rise high enough to correct brain ischemia before it causes nutritional depression and death of neuronal cells .

ATRIAL STRETCH REFLEXES • elicits reflexes parallel to baroreceptor reflex BAINBRIDGE REFLEX Rise in CVP as in increased blood volume → distend right atrium → (+) atrial stretch receptors → afferent signals to medulla through CN X → efferent signals to heart through S → increased HR and contractility .

in atria.• this reflex help prevent damming of blood in veins. sino – atrial reflex predominates over Bainbridge reflex . and in pulmonary circulation • under conditions of HYPERVOLEMIA. Bainbridge reflex predominates over sino – aortic reflex • under conditions of HYPOVOLEMIA.

but not in minute to minute regulation of normal BP • synthesized mainly by the supra-optic nuclei of hypothalamus and to a lesser extent by the paraventricular nuclei • stored and released by posterior pituitary gland .VASOPRESSIN (ADH) • involved in the regulation of BP in response to hemorrhage.

• adequate stimulus for its release : decreased blood volume ADH is released when atrial receptors detect a decrease in blood volume o it’s secretion is inhibited by: • A stretch in atrial wall caused by increased VR due to increased blood volume • Target organs: oSmooth muscles of arterioles oKidneys (DCT & CD) .

increased TPR – Increased permeability of DCT & CD to water • ↑ Water reabsorption • ↑ Plasma volume • ↑ CO .• Effects: – Vasoconstriction --.

CHEMORECEPTOR MECHANISMS CHEMORECEPTORS in the CAROTID and AORTIC BODIES – Located along aortic arch and near the bifurcation of common carotid arteries – Important at BP below 80 mmHg – Have very high rates of oxygen consumption .

carbon dioxide and hydrogen excess .– Sensitive to oxygen lack.


RENIN • an enzyme that catalyzes the conversion of Angiotensinogen (liver) to Angiotensin I • secretion increased when ABP falls or ECF volume reduced ACE (Angiotensin Converting Enzyme) • catalyzes conversion of Angiotensin I to II primarily in the lungs .

Captopril) • block conversion of Angiotensin I to II. thus lowers ABP • act on β receptors to produce the cough that is an annoying side effect in 20% of patients treated with ACE inhibitors .ACE INHIBITORS (Ex.

increase SP or DP • 4 to 8 times as active as NE • its pressor activity is decreased in Na† depleted individual and in patients with Cirrhosis • acts directly on adrenal cortex (ZONA Glomerulosa) to increase sec. of aldosterone .ANGIOTENSIN II (Hypertensin or Angiotonin) • vasoconstrictor.

• acts on the brain to decrease the sensitivity of he baroreceptor reflex • acts on the brain to increase water intake and increase sec. of vasopressin and ACTH .

ANGIOTENSIN III • has about 40% of the pressor activity of Angiotensin II. but 100% of the aldosterone stimulating activity • is the natural aldosterone – stimulating peptide while Angiotensin II is the natural BP – regulating Peptide .

ALDOSTERONE • increases Na† reabsorption by the Renal distal convoluted tubule • increases water reabsorption – Thus. increasing ECF volume (plasma volume) – Increase total blood volume – Increase cardiac output Without the RAAS. the effect of excessive salt intake on arterial pressure is 10 times as great .



Renal Body Fluid Pressure Control Mechanism .

Renal Body Fluid Pressure Control Mechanism .