Cardiovascular System

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between the diaphram left and right lung

heart is covered by fibrous pericardium

innermost layer is endocardioum middle layer is mycardium outer most layer is epicardium

Right atrium Right ventricle

Left atrium Left ventricle

the Receiving Chambers

- Superior vena cava - Inferior vena cava - Coronary sinus

- Right and left pulmonary veins

project into the ventricular cavities

- Pulmonary trunk

- Aorta

Ensure unidirectional blood flow through the heart

Prevent backflow into the atria when ventricles contract When atrial pressure is higher than ventricular pressure, the AV valve opens Tricuspid (right) Mitral valve (left)

anchor Atrioventricular valve cusps to papillary muscles

revent backflow into the ventricles when ventricles relax Aortic semilunar valve (right) Pulmonary semilunar valve (left) When ventricular pressure exceeds the blood pressure in the aorta and pulmonary trunk, the semilunar valves open

pump for the pulmonary circuit Vessels carry blood to and from the lungs

pump for the systemic circuit Vessels carry blood to and from all body tissues

Right atrium -->tricuspid valve -->right ventricle Right ventricle -->pulmonary semilunar valve -->pulmonary trunk -->pulmonary arteries--> lungs

Lungs -->pulmonary veins -->left atrium Left atrium-->bicuspid valve -->left ventricle Left ventricle -->aortic semilunar valve -->aorta Aorta -->systemic circulation

is a short, low-pressure circulation

blood encounters much resistance in the long pathways thick myocardiant to create a greater fource of contraction to pump the blood to the systemic circulation against that higher resistance

striated, short, fat, branched, and interconnected held together by connective tissue (collagen and elastin fibers) T-tubules wide but less numerous; SR is simpler Numerous large mitochondria Microscopic Anatomy of Cardiac Muscle junctions between cells anchor cardiac cells Desmosomes prevent cells from separating during contraction Gap junctions allow ions to pass ensure the heart contracts as a unit

Depolarization is rhythmic and spontaneous AP--> Voltage gates Ca channels open for Ca to enter--> summation of Ca sparks create Ca signal--> Ca ions bind to triponin---> contraction

Ca unbinds with troponin--> pumped back to SR to be stored--> Ca exchanges with Na with antiporter

A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart

The sinoatrial (SA) node (pacemaker) generates impulses about 75 times/minute (sinus rhythm) - Depolarizes faster than any other part of the myocardium

Atrioventricular (AV) node - Smaller diameter fibers; fewer gap junctions - Delays impulses approximately 0.1 second - Depolarizes 50 times per minute in absence of SA node input

Atrioventricular (AV) bundle (bundle of His) - Only electrical connection between the atria and ventricles

Right and left bundle branches - Two pathways in the interventricular septum that carry the impulses toward the apex of the heart

- Complete the pathway into the apex and ventricular walls - AV bundle and Purkinje fibers depolarize only 30 times per minute in absence of AV node input

• Heartbeat is modified by the ANS • Cardiac centers are located in the medulla oblongata - Cardioacceleratory center innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons - Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves

all events associated with blood flow through the heart during one complete heartbeat Flow of blood through the heart is controlled by pressure changes Blood flows from higher to lower pressure through an opening

contraction pressure inside chamber increases and there is emptying of blood

relaxation pressure inside chamber decreases and there is filling of blood

heart rate. During a cardiac cycle of 0.8sec, the ventricles are in systole for 0.3sec and in diastole for 0.5sec.

1. Inflow Phase 2. Isovolumetric Contraction 3. Outflow Phase 4. Isovolumetric Relaxation

inlet valve open, outlet valve closed

both valves closed, no blood flow

outlet valve open, inlet valve closed

all chambers relaxed. atria fill with blood from the veins. AV valves open between atria and ventricles. blood passively flows from atria to ventricles. ventricles expand to accommodate the blood. Semilunar valves are closed

AP fires in the SA node atrial cells depolarize. atria contract (systole) Atrial pressure increases . blood from the atria move into ventricles, remaining blood.

depolarization wave reaches ventricles, contract and pressure in ventricle rises.Ventricular pressure exceeds atrial pressure, AV valves shut- first heart sound ("lub"). ventricles contract, volume of blood in them remains the same (isovolumetric contraction), the atria are repolarizing and relaxing. When atrial pressure falls below the pressure in the veins, the atria fill with blood.

both valves closed, no blood flow

end diastolic volume (EDV).

As ventricles contract, they eventually produce enough pressure to open the semilunar valves and push blood into the arteries. The pressure created by ventricular contraction becomes the driving force for blood flow. The AV valves remain closed and the atria continue to fill.

end systolic volume (ESV).

ventricles begin to repolarize and relax. Ventricular pressure decreases. When ventricular pressure falls below arterial pressure, blood starts to flow backwards in the aorta and pulmonary trunk. This closes the semilunar valves and causes the dicrotic notch (brief rise in aortic pressure). This creates the second heart sound, S2 ("dup"). The ventricles continue to relax, but the volume of blood is not changing (isovolumetric relaxation)

When ventricular pressure falls below atrial pressure, the AV valves open. Blood moves into the ventricles and the cycle has started again.

amount of blood pumped by each ventricle in one minute. CO = heart rate (HR) X stroke volume (SV)

number of beats per minute

volume of blood pumped out of a ventricle with each beat

HR (75 beats/min) × SV (70 ml/beat) = 5.25 L/min

4-5 times resting CO in nonathletic people may reach 35 L/min in trained athletes

difference between resting and maximal CO

-Blood volume before contraction (EDV) - Blood volume after contraction (ESV)

= 135ml - 65ml = 70ml can increase to 100ml during exercise

Venous Return--> Volume of Blood in Ventricle before Contraction (EDV)--> Length of muscle fibers--> Force of Ventricular Contraction--> SV Sympathetic/Parasympathetic Activity--> Contractility (changes in Ca2+ influx)--->Force of Ventricular Contraction-->SV

It states that the heart will pump out whatever volume is delivered to it. If the heart is filled with more blood, the heart is stretched more--> end of the sarcomere to move out--> increase the distant that it will have to travel--> increase contraction force--> more blood leave the heart (high SV) describes the relationship between EDV and SV. If the EDV doubles, then stroke volume will double.

Skeletal muscle pump Respiratory pump Body Position Sympathetic Activity

The skeletal muscle surrounding the veins contracts and increases blood flow back to the heart (increases EDV).

During inhalation, the diaphragm descends and abdominal pressure increases. The increasing pressure squeezes veins and moves blood towards the heart (increases EDV).

Gravity opposes the return of blood from the feet to the heart during sitting or standing. This effect is lost when we lie down.

The veins are innervated by sympathetic nerves. Activation of the SNS will constrict veins and push more blood towards the heart

Parasympathetic nerves innervate the atrial muscle. Sparse innervation to ventricular muscle. They release acetylcholine (ACh) onto muscarinic receptors. This weakens atrial contraction and reduces stroke volume. Parasympathetic nerves innervate the SA and AV nodes.They release acetylcholine (ACh) onto muscarinic receptors. This reduces the frequency of spontaneous depolarization at the SA node and decreases excitability at the AV node. Together, this reduces heart rate.

Sympathetic nerves innervate the atrial and ventricular muscle. They release noradrenaline onto ? receptors on cardiac myocytes. This increases the force of contraction of the atria and ventricles and increases stroke volume. Sympathetic nerves innervate the SA and AV nodes. They release noradrenaline onto ? receptors. This increases the frequency of spontaneous depolarization at the SA node and increases excitability at the AV node. Together, this increases heart rate.

Sympathetic activation causes the release of adrenaline from the adrenal medulla. Adrenaline enters the blood stream and is delivered to the heart where it binds to ? receptors at the SA node to increase heart rate. Thyroxine (thyroid gland hormone) increases heart rate and enhances the effects of noradrenaline and adrenaline

90% water Proteins mostly produced by the liver 60% albumin,36% globulins, 4% fibrinogen Nitrogenous by-products of metabolism Nutrients Electrolytes Respiratory gases Hormones

Plasma Formed elements Erythrocytes (red blood cells, or RBCs), Leukocytes (white blood cells, or WBCs), Platelets

WBC, RBC, platletes (cell fragments)

white blood cells

ratio of red blood cells to plasma as a percentage of the total blood volume

in bone marrow and do not divide

a few days

contact tissue cells and directly serve cellular needs Endothelium with sparse basal lamina

carry blood away from the heart; oxygenated except for pulmonary artery Structure includes Tunica intima, tunica media, and tunica externa

carry blood toward the heart; deoxygenated except for pulmonary vein Structure includes Tunica intima, tunica media, and tunica externa Formed when venules converge Have thinner walls, larger lumens compared with corresponding arteries. Blood pressure is lower than in arteries. Thin tunica media and a thick tunica externa consisting of collagen fibers and elastic networks Called capacitance vessels (blood reservoirs); contain up to 65% of the blood supply

Central blood-containing space

Inner layer Endothelium lines the lumen of all vessels in all blood vessels, larger in vessels with subendothelial connective tissue basement membrane In arteries and arterioles, the outer margin of the tunica intima is delimited by an internal elastic membrane

- Middle layer - Smooth muscle and sheets of elastin - Sympathetic vasomotor nerve fibers control vasoconstriction and vasodilation of vessels

- Outermost layer - Collagen fibers protect and reinforce - In larger muscular arteries, there is frequently an external elastic membrane separating the tunica adventitia from the tunica media - Larger vessels contain vasa vasorum to nourish the external layer

Large thick-walled arteries with elastin in all three tunics Aorta and major branches Conduct blood at high pressure to the medium-sized arteries Large lumen offers low resistance Act as pressure reservoirs—expand when the ventricle pumps blood into them and recoil when the ventricle relaxes Assist with propelling blood forward

Distal to elastic arteries Deliver blood to body organs Have thick tunica media with more smooth muscle and fewer elastic fibers Active in vasoconstriction and vasodilation to adjust rate of blood flow

Smallest arteries Lead to capillary beds Control flow into capillary beds via vasodilation and vasoconstriction Regulate resistance to blood flow Regulate flow into capillaries (when tissue demand for O2 is high, the VSMCs relax and flow to the tissues increases.)

Microscopic exchange blood vessels Walls of thin tunica intima, one cell thick Pericytes within the basal lamina help stabilise their walls and control permeability Size allows only a single RBC to pass at a time In all tissues except for cartilage, epithelia, cornea and lens of eye Exchange gases, nutrients and waste products

1. Continuous capillaries 2. Fenestrated capillaries 3. Sinusoidal capillaries (sinusoids

Abundant in the skin and muscles - Tight junctions connect endothelial cells - Intercellular clefts allow the passage of fluids and small solutes Continuous capillaries of the brain - Tight junctions are complete, forming the blood-brain barrier

Some endothelial cells contain pores (fenestrations) More permeable than continuous capillaries Function in absorption or filtrate formation (small intestines, endocrine glands, and kidneys)

Fewer tight junctions, larger intercellular clefts, large lumens Usually fenestrated Allow large molecules and blood cells to pass between the blood and surrounding tissues Found in the liver, bone marrow, spleen

Interwoven networks of capillaries form the microcirculation between arterioles and venules Consist of two types of vessels 1. Vascular shunt (metarteriole—thoroughfare channel): 2. True capillaries

• Directly connects the terminal arteriole and a postcapillary venule • Contains precapillary sphincters that open or close, thereby allowing different parts of the capillary bed to be perfused Usually only a small part of the capillary bed is perfused, except when a tissue becomes active

• 10 to 100 exchange vessels per capillary bed • Tissues with high metabolic activity have more capillaries • Branch off the metarteriole or terminal arteriole

Formed when capillary beds unite Very porous; allow fluids and WBCs into tissues Postcapillary venules consist of endothelium and a few pericytes Larger venules have one or two layers of smooth muscle cells

Capillaries allow for exchange of substances between the blood and interstitial fluid (extracellular fluid that surrounds the cells of the tissue).

1. Large-diameter lumens offer little resistance 2. Valves prevent backflow of blood • Most abundant in veins of the limbs

flattened veins with extremely thin walls (e.g., coronary sinus of the heart and dural sinuses of the brain)

Plasma membrane invaginates and pinches off to capture large charged molecules (eg. proteins)

Movement of water and solutes is driven by concentration gradient.

Lipid soluble substances diffuse through the membrane (eg O2 and CO2)

Water and solutes can move from the blood in the capillary through fenestrations and clefts between cells. Plasma proteins normally cannot cross capillary walls (except in sinusoid capillaries). Bulk flow is driven by blood pressure and osmotic pressure.

Pinocytosis Diffusion across endothelial cells or via fenestrations Bulk flow

The physical forces that govern the movement of fluid into and out of capillaries are called Starling Forces. These forces come from pressures. Capillary blood pressure drives fluid out of the capillaries. Blood also contains proteins (albumin and globulins) that create an osmotic pressure.

mechanical pressure exerted on a membrane by a fluid. Here, the fluid is causing the pressure. Higher hydrostatic pressure leads to a higher pushing pressure of fluid.

the pulling pressure based on particles within a fluid. Here, the particles are causing the pressure. Higher osmotic pressure leads to a higher pulling pressure of fluid.

1. Hydrostatic pressure (blood pressure) in the capillary (HPc) 2. Osmotic Pressure in the interstitial fluid (OPif) Blood pressure in the capillary decreases along the length of the capillary because blood pressure drops. HPc at the arterial end of the capillary is ~35mmHg HPc at the venous end of the capillary is ~17mmHg Osmotic Pressure in the interstitial space is low due to low protein content (~1mmHg). It remains the same along the length of the capillary.

1. Hydrostatic Pressure in the interstitial fluid (HPif) 2. Osmotic Pressure in the capillary (OPc~26) Hydrostatic pressure in the interstitial fluid is minimal, ranging from slightly negative to slightly positive because fluid is normally removed by the lymphatic system. Most textbooks use 0 mmHg. Osmotic pressure in the capillary is the pressure due to the presence of nondiffusible plasma proteins that draw fluid into the capillary from the interstitial space. The average value of OPc is 26mmHg. Little change occurs along the capillary from the arterial to the venous end.

Comprises all the forces acting on a capillary bed At the arterial end of the capillary bed, hydrostatic forces dominate At the venous end of the capillary bed, osmotic forces dominate Excess fluid is returned to the blood via the lymphatic system results in a net LOSS of fluid from capillary to interstitial fluid: 10mmHg loss from capillary at the arterial end -8mmHg gain to capillary at the venous end 2mmHg net LOSS along the length of the capillary The excess fluid is returned to the blood stream via the lymphatic system.

Forces OUT = HPc + OPif = 35mmHg + 1 = 36mmHg Forces IN = HPif + OPc = 0 + 26mmHg = 26mmHg Net Filtration Pressure = [Forces OUT] - [Forces IN] Net Filtration Pressure = 36mmHg - 26mmHg = 10mmHg (flow OUT of capillary at arterial end)

Forces OUT = HPc + OPif = 17mmHg + 1mmHg = 18mmHg Forces IN = HPif + OPc = 0mmHg + 26mmHg = 26mmHg Net Filtration Pressure = [Forces OUT] - [Forces IN] Net Filtration Pressure = 18mmHg - 26mmHg = -8mmHg (flow INTO capillary at venous end)

Returns interstitial fluid and leaked plasma proteins back to the blood Together with lymphoid organs and tissues, provide the structural basis of the immune system

start as blind-ended tubes and join together to form large lymphatic vessels. They join to the large veins andreturn the fluid to the circulation. This helps to maintain normal blood volume and pressure Lymphatic vessels are structurally similar to veins and capillaries. thin-walled contain one-way valves. holes between endothelial cells to allows movement of fluid and small proteins from interstitial space into the lymph vessels. Once interstitial fluid enters the lymphatic vessels, it is called lymph. only carry fluid away from the tissues no pump movement occurs through skeletal muscles, pressure changes in the thorax in breathing, contraction of smooth muscle in nearby arteries

At steady state, filtration equals reabsorption plus lymph flow. Under certain conditions, more fluid leaks out of capillaries than can be reabsorbed or collected by lymph vessels. The retention of fluid in the interstitial space is called edema. Edema occurs when the rate of filtration exceeds the sum of the rate of fluid reabsorption and lymphatic flow.

The coronary circulation supplies blood to the working heart muscle. The left main coronary artery arises from the aorta, travels behind the pulmonary artery and branches into the circumflex artery and left anterior descending artery (LAD). The circumflex and LAD artery supply blood to the left ventricle. The right main coronary artery arises from the aorta, travels behind the right atrium and ventricle toward the posterior regions of the heart to supply the right ventricle and atrium. These arteries are on the surface of the heart. They divide into smaller branches that dive into the myocardium. These resistance vessels regulate coronary blood flow. Coronary veins are adjacent to the coronary arteries. These veins drain into the coronary sinus which empties into the right atrium. During systole, the contraction of the myocardium compresses the small coronary vessels within the ventricular wall, thereby increasing resistance and decreasing flow. During diastole, the compressive forces are removed and blood flow increases. Coronary blood flow reaches a peak in early diastole and then falls passively as the aortic pressure falls toward its diastolic value. Thus, it is the aortic pressure during diastole that is crucial for perfusing the coronary arteries

Volume of blood flowing through a vessel, an organ or the entire circulation in a given period of time. In the entire circulation, blood flow is equal to the cardiac output (relatively constant at rest). Blood flow through individual organs can vary depending upon need. Blood flow (F) is directly proportional to the blood pressure gradient (P) - If P increases, blood flow speeds up Blood flow is inversely proportional to peripheral resistance (R) - If R increases, blood flow decreases: F = P/R

The distance per unit time with which blood flows through a given segment of the circulation. Varies throughout the vasculature and is inversely proportional to the total cross-sectional area. The velocity of flow is slowest in the capillaries which allows time for exchange of nutrients and wastes.

Force per unit area exerted on the wall of a blood vessel by the blood • Expressed in mm Hg • Measured as systemic arterial BP in large arteries near the heart - The pressure gradient provides the driving force that keeps blood moving from higher to lower pressure areas

Resistance (peripheral resistance) - Opposition to flow - Measure of the amount of friction blood encounters - Generally encountered in the peripheral systemic circulation R is more important in influencing local blood flow because it is easily changed by altering blood vessel diameter If the expression for resistance is combined with the equation describing the relationship between flow, pressure and resistance (Flow = P/R), the following is obtained: Poiseuille's Equation:

- Blood viscosity () - Total blood vessel length (L) - Blood vessel diameter (r)

• The "stickiness" of the blood due to formed elements and plasma proteins

• The longer the vessel, the greater the resistance encountered

• the smaller the radius, the greater the resistance • resistance varies inversely with the fourth power of vessel radiu

Resistance =(n*L)/ r^4

The pumping action of the heart generates blood flow Pressure results when flow is opposed by resistance Systemic pressure - Is highest in the aorta - Declines throughout the pathway - Is 0 mm Hg in the right atrium The steepest drop occurs in arterioles

Flow =(delta G*P * r^4) / 8 n L

Reflects two factors of the arteries close to the heart - Elasticity (compliance or distensibility) - Volume of blood forced into them at any time Blood pressure near the heart is pulsatile Mean arterial pressure (MAP): pressure that propels the blood to the tissues MAP = diastolic pressure + 1/3 pulse pressure Pulse pressure and MAP both decline with increasing distance from the heart

Ranges from 15 to 35 mm Hg Low capillary pressure is desirable - High BP would rupture fragile, thin-walled capillaries - Most are very permeable, so low pressure forces filtrate into interstitial spaces

Changes little during the cardiac cycle Small pressure gradient, about 15 mm Hg Low pressure due to cumulative effects of peripheral resistance

Blood Flow = CO Cardiac Output (CO) is the amount of blood pumped by each ventricle in one minute.

P1 = Parterial P2 = Pvenous In practice, venous pressure is usually small enough to be neglected, therefore ?P ~ Parterial PGradient = P1 - P2 = Parterial - Pvenous ~ MABP

The majority of the resistance in the systemic circulation comes from the resistance in the arterioles. This resistance is called systemic vascular resistance (SVR) or total peripheral resistance (TPR).

An increase in blood volume will increase CVP, EDV and stroke volume (Frank- Starling Law). An increase in stroke volume then increases cardiac output and arterial blood pressure. MABP = SV x HR x SVR MABP = CO x SVR

- Cardiac output (CO) - Total peripheral resistance (TPR) - Blood volume

Short-term neural controls Long-term renal regulation

- Counteract fluctuations in blood pressure by altering peripheral resistance Baroreceptor Chemoreceptors

- Counteracts fluctuations in blood pressure by altering blood volume

located in - Carotid sinuses - Aortic arch - Walls of large arteries of the neck and thorax They relay information back to the brain At rest, arterial baroreceptor activity tonically inhibits sympathetic outflow to the heart and blood vessels and it tonically stimulates vagal outflow to the heart.

located in the - Carotid sinus - Aortic arch - Large arteries of the neck Chemoreceptors respond to rise in CO2, drop in pH or O2 - Increase blood pressure via the vasomotor center and the cardioacceleratory center Are more important in the regulation of respiratory rate

Sympathetic neurons innervate veins, arterioles and the heart (SA node and myocytes). Output from the SNS act on arterioles to change systemic vascular resistance (SVR). Peripheral blood vessels are in a state of partial (rather than full) constriction

Parasympathetic neurons innervate the SA node.

- increased pressure stretches the baroreceptors - increased afferent nerve firing - more activation of PNS ? ?HR - more inhibition of SNS ? ?HR and ?contractility ? ?SV - more inhibition of SNS ? ?constriction of arterioles ? ?SVR - ?MABP since MABP = CO X SVR

- decreased stretching of baroreceptors - decreased afferent nerve firing - less activation of PNS ? ?HR - less inhibition of SNS ? ? HR and ? contractility ? ? SV - less inhibition of SNS ? ? vasoconstriction? ? SVR - ? MABP since MABP = CO X SVR

Adrenaline, released by the adrenal medulla, causes generalised vasoconstriction and increase cardiac output Angiotensin II, generated by kidney release of renin, causes vasoconstriction Antidiuretic hormone (ADH or vasopressin) causes intense vasoconstriction in cases of extremely low BP Atrial natriuretic peptide causes blood volume and blood pressure to decline, causes generalised vasodilation Antidiuretic hormone (ADH or vasopressin) causes intense vasoconstriction in cases of extremely low BP

Baroreceptors quickly adapt to chronic high or low BP Long-term mechanisms step in to control BP by altering blood volume Kidneys act directly and indirectly to regulate arterial blood pressure 1. Direct renal mechanism 2. Indirect renal (renin-angiotensin) mechanism

Alters blood volume independently of hormones - Increased BP or blood volume causes the kidneys to eliminate more urine, thus reducing BP - Decreased BP or blood volume causes the kidneys to conserve water, and BP rises

The renin-angiotensin mechanism - Arterial blood pressure release of renin - Renin production of angiotensin II - Angiotensin II constricts arterioles (? SVR) The renin-angiotensin mechanism - Angiotensin II aldosterone secretion • Aldosterone renal reabsorption of Na+ and urine formation (? blood volume) - Angiotensin II stimulates ADH release leading to water reabsorption by kidneys (? blood volume) - ? MABP

Tissues attempt to adjust blood flow to their own needs by changing the diameter of their resistance vessels. Resistance vessels can be regulated by different mechanisms: Local control - metabolic - myogenic Central control - innervation of the sympathetic nervous system Hormonal control - the release of circulating hormones modulate resistance vessels

Vasodilation of arterioles and relaxation of precapillary sphincters occur in response to - Declining tissue O2 - Substances from metabolically active tissues (H+, K+, adenosine, and prostaglandins) and inflammatory chemicals Effects - Relaxation of vascular smooth muscle - Release of NO from vascular endothelial cells Nitric oxide is the major factor causing vasodilation Vasoconstriction is due to sympathetic stimulation and endothelin

- potent vasodilator - NO mediates the actions of ACh, Substance P, ATP, bradykinin and flow-induced shear stress.

- are synthesized from arachidonic acid - PGE (PGE1, PGE2 and PGE3) and PGI2 (prostacyclin) relax VSMCs - PGF (PGF1, PGF2a, PGF3a) and thromboxane A2 are vasoconstrictors

opens K+ channels on VSMCs - causes hyperpolarization and vasodilation

- are synthesized and released by endothelial cells in response to Ang-II and mechanical trauma - ET1 binds to ETA receptors on VSMCs and causes vasoconstriction

Myogenic responses of vascular smooth muscle keep tissue perfusion constant despite most fluctuations in systemic pressure Passive stretch (increased intravascular pressure) promotes increased tone and vasoconstriction Reduced stretch promotes vasodilation and increases blood flow to the tissue

All resistance vessels (arterioles) are innervated by the sympathetic nervous system. When arterial pressure falls, SNS nerve terminals release noradrenaline onto the VSMCs, causing them to contract. This causes vasoconstriction and a decrease in flow.

Antidiuretic hormone (ADH) Angiotensin II (Ang-II) Adrenaline

released from the posterior pituitary when blood pressure decreases or tissue osmolarity rises. ADH binds to ADH V1 receptors leading to vasoconstriction.

Ang-II appears in the bloodstream when renal artery pressure falls. SNS activity can also trigger Ang-II release. Ang-II is a potent vasoconstrictor

Sympathetic stimulation secretes adrenaline from the adrenal medulla. Adrenaline enters the blood stream. The binding of adrenaline on receptors (on all arterioles) leads to vasoconstriction. The binding of adrenaline on 2 receptors (on arterioles of skeletal muscle and heart) leads to vasodilation.