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Lecture 8 Control of Resistance Vessels 1. What is meant by resistance vessels?

- Arteries or arterioles that contribute most substantially to TPR -

VESSEL TYPE Aorta Large Arteries Small Arteries Arterioles Capillaries Venules Veins Vena Cava -

DIAMETER (mm) FUNCTION 25 Pulse dampening and distribution 1.0 - 4.0 Distribution of arterial blood 0.2 - 1.0 Distribution and resistance 0.01 - 0.20 Resistance (pressure & flow regulation) 0.006 - 0.010 Exchange 0.01 - 0.20 Exchange, collection, and capacitance 0.2 - 5.0 Capacitance function (blood volume) 35 Collection of venous blood

Large arteries branching off the aorta (e.g., carotid, mesenteric, renal arteries) distribute the blood flow to specific organs. These large arteries, although capable of constricting and dilating, serve virtually no role in the regulation of pressure and blood flow under normal physiological conditions. Once the distributing artery reaches the organ to which it supplies blood, it branches into smaller arteries that distribute blood flow within the organ. These vessels continue to branch and become arterioles. Together, the small arteries and arterioles represent the primary vessels that are involved in the regulation of arterial blood pressure as well as blood flow within the organ 2. Flow Principles

Blood flow is the volume of blood flowing through a vessel, organ, or the entire circulation in a given period and may be expressed as ml/min (blood flow of the entire circulation is equal to cardiac output) Blood pressure is the force per unit area exerted by the blood against a vessel wall and is expressed in millimeters of mercury (mm Hg) Resistance is a measure of the friction between blood and the vessel wall, and arises from three sources: blood viscosity, blood vessel length, and blood vessel diameter. The variable with the greatest effect on resistance is the diameter (or radius, 1/2 the diameter) of a particular vessel - resistance drops exponentially as the radius increases. TPR is total peripheral resistance - resistance throughout the entire systemic circulation.

3. Control of Resistance

Blood pressure varies with changes in blood volume, TPR, and cardiac output, which are determined primarily by venous return and neural and hormonal controls Autonomic Factor Vessels are highly innervated by autonomic nerves Both sympathetic and parasympathetic division of autonomic nervous system control the tone of resistance vessels by opposing actions Almost all blood vessels receive efferent nerve fibres from sympathetic nerve system to their smooth muscles. Even though only a small portion of smooth muscle is innervated by the nerves, once the upper part of smooth cells are fired, the electrical impulse will be transmitted to the neighbouring cells via the gap junctions.

Receptors for norepinephrine on heart muscle are mainly beta-adrenergic

Other neurotransmitters for sympathetic nerves such as noradrenaline (aka norepinephrine) co-transmitters ATP, Neuropeptide Y(NPY) Sympathetic nerves are tonically active (continuously firing) Parasympathetic nerves- acetylcholine, vasoactive intestinal polypeptide (VIP), nitric oxide (NO) They are all responsible for vasodilation and only affect limited number of tissues and plays no significant role in TPR Parasympathetic nerves are not tonicaly active

Humoral Modulation

Autoregulation : a nearly constant flow in the face of changing pressure Autoregulation is the automatic adjustment of blood flow to each tissue in proportion to its needs, and is controlled intrinsically by modifying the diameter of local arterioles. (Extrinsic influences control MAP.)

Metabolic controls of autoregulation are most strongly stimulated by a shortage of oxygen at the tissues There are two mechanisms that control autoregulation. One comprises same metabolic factors described for active hyperemia. When arterial pressure reduction lowers blood flow to organ, the supply of oxygen to the organ diminishes Extracellular concentrations of CO2, H+ ions, and metabolites all increase because blood cannot remove them as fast they are produced. Unlike hypermia, flow autoregulation is not limited to circumstances in which arterial pressure decreases. Initial increase in flow due to increased pressure removes the local vasodilator chemical factors faster than they are produced and also increases the local concentration of oxygen This causes arterioles to constrict, thereby maintaining relatively constant local flow in the face of increased pressure. Another mechanism that involve in autoregulation is myogenic response Its a direct response caused by changes in calcium movement into the smooth muscle cells through stretch-sensitive calcium channels in the plasma membrane.

Myogenic response in independent of endothelium and nerves.

the effects of suddenly reducing perfusion pressure from 100 to 70 mmHg

In a passive vascular bed, that is, one that does not show autoregulation, this will result in a rapid and sustained fall in blood flow. In fact, the flow will fall more than the 30% fall in perfusion pressure because of passive constriction as the intravascular pressure falls, which is represented by a slight increase in resistance in the passive vascular bed. If a vascular bed is capable of undergoing autoregulatory behavior, then after the initial fall in perfusion pressure and flow, the flow will gradually increase (red line) over the next few minutes as the vasculature dilates (resistance decreases After a few minutes, the flow will achieve a new steady-state level If a vascular bed has a high degree of autoregulation (e.g., brain and coronary circulations), then the new steady-state flow may be very close to normal despite the reduced perfusion pressure.

If an organ is subjected to an experimental study in which perfusion pressure is both increased and decreased over a wide range of pressures, and the steadystate autoregulatory flow response measured, then the relationship between steady-state flow and perfusion pressure can be plotted as shown in the figure If a vasodilator drug is infused into an organ so that it is maximally dilated and incapable of autoregulatory behavior, the curve labeled "Dilated" is generated as perfusion pressure is changed. It is non-linear because blood vessels passively dilate with increasing pressures, thereby reducing resistance to flow The "Constricted" curve represents the pressure-flow relationship when the vasculature is maximally constricted and when autoregulation is not present. This figure also shows that there is a pressure below which an organ is incapable of autoregulating its flow because it is maximally dilated. This perfusion pressure, depending upon the organ, may be between 50-70 mmHg. Below this perfusion pressure, blood flow decreases passively in response to further reductions in perfusion pressure. This has clinical implications in coronary, cerebral, and peripheral arterial disease, where proximal narrowing (stenosis) of vessels may reduce distal pressures below the autoregulatory range; hence, the distal vessels will be maximally dilated and further reductions in pressure will lead to reductions in flow.

4. . Hypermia - Active hypermia : increased blood flow subsequent ton an increased metabolism - Mechanism used : metabolic vasodilation - Functional hyperaemia is an increase in blood flow to a tissue due to the presence of metabolites and a change in general conditions. When a tissue increases activity there is a well-characterized fall in the partial pressure of oxygen and pH, an increase in partial pressure of carbon dioxide, and a rise in temperature and the concentration of potassium ions (same situation as reduction arterial pressure in autoregulation) - When cells within the body are active in one way or another, they use more oxygen and fuel, such as glucose or fatty acids, than when they are not. Increased metabolic processes create more metabolic waste. The byproducts of metabolism are vasodilators. (Vasodilating metabolites: CO2, H+, K+, lactate, adenosine) Local arterioles respond to metabolism by dilatating, allowing more blood to reach the tissue - Since most of the common nutrients in the body are converted to carbon dioxide when they are metabolized, smooth muscle around blood vessels relax in response to increased concentrations of carbon dioxide within the blood and surrounding interstitial fluid. The relaxation of this smooth muscle results in vascular dilation and increased blood flow. - Mostly developed in skeletal muscle, cardiac muscle and glands. - Reactive hypermia : the increased blood flow subsequent to release of an obstruction - Mechanism used : metabolic and myogenic vasodilation 5. Endothelial mechanisms regulating blood flow

The three most important endothelial-derived substances are: nitric oxide (NO), endothelin (ET-1), and prostacyclin (PGI2). NO and PGI2 act as vasodilators, whereas ET-1 serves as a vasoconstrictor. Damage to the vascular endothelium due to atherosclerotic processes or following ischemia and reperfusion alters the formation and release of endothelial factors. When endothelial damage occurs, the endothelium produces less nitric oxide and prostacyclin, which causes the adrenergic vasoconstrictor tone to be unopposed This can lead to increased vascular tone and vasospasm. Furthermore, decreased production of both of these endothelial factors can lead to increased platelet adhesion and aggregation, and therefore enhanced thrombogenesis.