Physiology II
Cardiovascular Physiology
Pathophysiology Of Hypertension

Learning Objectives 4

Describe LOCALLY PRODUCED factors arising from the tissues or from the endothelium which might influence the force of of contraction of vascular smooth muscle for the purpose of matching TISSUE BLOOD FLOW WITH TISSUE METABOLISM.

The specific needs of the tissue nutrition/metabolism are met through DELIVERY ( o2/substrates), REMOVAL ( CO2/H), MAINTENANCE ( proper conc of ions), and TRANSPORTATION ( hormones and other substances)of . Guyton describes a tissue unit – as related to the oxygen demand theory – the unit consists of a metarteriole, a single capillary, and its surrounding tissue. The metabolic/ nutritional needs are met through the cyclic opening and closing of the pre cap sphinc, and metarterioles (vasomotion). Vasomotion is thought to be caused by locally produced vaso-active substances diffusing to the pre capillary sphincter/metarterioles in the tissue unit areas, - thus causing either vaso dilation or vasoconstriction.

Locally produced vasodilator factors are thought to diffuse back to pre capillary sphincters, metarterioles, and arterioles to cause dilation. The number of pre capillary sphincters and that open, and the vasc sm musc around arterioles open and close proprtional to metabolic/nutritional needs of the local tissue.

• adenosine - released from the ht muscle cells when coronary bld flow is too little – causes vaso dilation and returns blood flow through coronaries to nl. (degredation of ATP) this mech occurs in response to DECREASED O2.
• inc co2 -
• inc adenosine po4 -
• dec amino acids -
• lack of vitiman B(thiamine, niacin, riboflavin – in Beriberi)
• histamine – in response to inflammation/allergy/ injury to tissue – endothelial tissue, derived from mast cells in tissues, & basophils in blood. Histamine is rel which reacts with the H2 receptor which causes inc cAMP which reacts with the H1 receptor which initiates a vasodilation response (class notes – ?????)
• Prostaglandins – almost every tissue has it. Most important prostaglandins cause vaso diltion but some cause vaso constriction( Guyton)
• inc potassium ions – inhibits smooth muscle contraction
• inc Mg - inhibits smooth muscle contraction
• inc Na – causes mild arteriolar dilation mostly due to an inc osmolality from the fluids rather than from the Na itself . Inc GLUCOSE has same effect
• lactic acid
• inc hydrogen ions
• NO – dilates large upstream arteries when microvascular blood flow increases. When blood flow through the small arteries and arterioles causes Increased shear stress occurs on the endothelial cells because of viscous drag of the blood against the vasc walls. This stress contorts the endothelial cells in the direction of flow and à rel NO from the arterioles and small arteries) (t ½ = 6 secs) – this prevents damage to the microcirculation.
• Bradykinin – produced in blood and in tissue fluids of some organs. It causes vaso dilation and inc cap perm. It is believed that kinins play special roles in regulating blood flow and cap leakage of fluids in inflamed tissues.
• Serotonin – acts as a vasodilator and vasoconstrictor. Not thought to play a widespread general role in circ regulation according to Guyton
• H+ - an INC causes vasodilation and an intense DEC causes dilation also

VASO CONSTRICTORS –

• thromboxane – from platelet, once cyclooxyginase is rendered inactive the platelets can not regenerate more thromboxane(plavix)
• Serotonin – produced at site of injury from endothelial cells.
• Endothelin – functional vasoconstriction for acute problems – narrow radius of vs to inc pressure(responds to resistance. Structural causes hypertrophy through increasing amt of elastin, collagen, and cell growth, angiogenesis. Its released from the endothelial tissue in response to pressures encountered and its goal is to protect the vessels and tissue at all costs. Think of profs fathers surgery explanation. It is present in the endothelial cells of most blood vessels, and is released in response to bleeding
• Ca- a vasoconstrictor due to the general effect of calcium to stimulate smooth muscle contraction(chap 8)
• H – a slight decrease causes vaso C
• Decreased serum osmolality causes vaso constriction

Learning objective - 5

PHYSICAL PROPERTIES

Veins – are thin walled tubes with less muscle and elastic tissue

composed of from inside to out –

• endothelium with valves
• areolar and internal elastic tissue
• smooth muscle cells
• areolar and external elastic tissue
• fibrous connective tissue

Arteries – are thick walled vessels (high pressure) the smooth muscle acts in regulating blood distribution. Arteries are composed of the same tissue as veins only each layer is thicker. The arterial endothelial tissue lack valves.

Capillaries are simple endothelial tubes in which nutrients and gasses can diffuse into or out of tissues in close proximity, in response to simple diffusion and osmotic pressures.

FUNCTIONAL PROPERTIES

Veins provide a low pressure storage system (resevoir) for blood. Veins (smooth muscle) respond to changes in pressure to by dilating or constricting. The venous system is considered the low pressure system.

Venous return is mediated by the pressure gradient (MSAP – CVP), by pumping of skeletal muscle, and by the respiratory pump. Venous pressure is effected by hydrostatic, pgh, ht function, and the effectiveness of the valves.

Arteries – the arterial walls expand as blood enters them, which decreases the pressure with in them. The arterial walls also recoil to propel blood forward toward the capillaries. Arteries keep pressure changes with in a range to minimize fluctuations, rather than expanding so much to allow pressure to fall near zero, thus the expanding and recoiling. Hydrostatic pressure and pgh affect arterial pressure also.

Transmural pressure can be defined as – the pressure exerted against and through the thickness of the wall of, in this case a vessel.

Velocity of flow can be defined as – speed /sec of movement of, in this case blood, through a vessel in relation to the pressure exerted on the vessel as a result of the velocity of the flow.

Discussion of flow – flow is a motion through a constraint, which is accompanied by deformation of the fluid. In this case we discuss the flow of fluid thru a tube, (diameter is less than its length). Velocity is greatest when the diameter is least, and pressure is at its least at the points of greatest constriction (BERNOULLI). When fluid flows through a tube of varying cross sectional diameters, the velocities of the various segments of fluid, as postulated by the laws of continuity, are greatest where the diameters are least, and the speed is greatest at this point as well. At the point of widest diameter the pressure is the greatest and the speed is the least.

Blood flows from arteries thru caps to veins because pressure is higher in the arteries than in the veins. The blood in the arteries pushes harder than the blood in the veins. It is the difference in pressure that constitutes the driving force for the fluid. The greatest fall in pressure occurs across the arterioles that enter the capillaries. ( in blood circulation the arterioles offer the greatest resistance to flow) this is frictional resistance which is quantified by using the formula (flow = pr diff/resistance). Resistance is determined mainly, by the radius of a tube, and somewhat by the length of the tube. Being that the greatest fall in pressure falls across the arterioles, they serve as a rate limiting area in circulation, and therefore regulate and blood pressure and flow to specific tissues. Arterioles have bands of smooth muscle which are innervated and controlled by nerves, hormones and other mediators, as mentioned in LO4. Through controlling the radius of the arterioles, the body exercises tight control over the flows and pressures in its own circulation.

Factors controlling VASCULAR REMODELING in response to changes in transmural pressure and the velocity of flow. The greater the metabolism in an organ the greater the blood flow ????????(what does this do to pressure in the vessel) ????????. In pathologic conditions, the flow to tissue/organ can be less than is needed in lite of its metabolism. In an effort for the tissue to survive, REMODELING of the tissue occurs so as to bring adequate blood flow to meet metabolic demands. Remodeling ( a structural change) occurs as a result of long term control of blood flow and is accomplished by the release of endothelin, and or angiotension II(vaso constrictors) and NO a vaso dilator. These vaso active substances counter each other to keep each other in check. If a patient developes hypertension the capillaries will undergo changes to maintain a normal perfusion pressure. If a tissue becomes chronically overactive and therefore requires chronically increased amounts of nutrients, the blood supply usually increases with in a few weeks to match the needs of the tissue – that is, unless the circ system has become pathological or too old to respond. REMODELING can be physiologic or pathophysiologic. Angiotensin II causes pathophysiologic changes (to heart and blood vessels) in response to increases in arterial blood pressure.

After Fem Pop arterial bypass graft( vein used in graft) the vein arterializes in response to long term regulated change in vascular tissue, through endothelin ( increases elastin, collagen, and cell growth – hypertrophy), and modified prn by NO.

References are GUYTON, ADRAINI, PHYSIOLOGY COLORING BOOK AND ANATOMY COLORING BOOK. Direct quotes were taken out of these references.

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