How the Nervous System and Local Controls Work to Regulate Blood Pressure and Blood Flow in Tissues - Essay Example

?Regulation of Blood Pressure and Blood Flow by Nervous System and Local Controls The regulation of oxygen supply to tissues is largely dependent on the regulation of blood flow. Blood flow to the organs is maintained by the cardiovascular system by two main mechanisms: One, through the maintenance of input pressure to all organs within specific limits with the help of arterial pressure regulation, and second, through the adjustment of vascular resistance (R) to blood flow of each organ within a specific optimal value. These functions of the cardiovascular system are regulated by three main mechanisms, namely – local, neural and humoral (Pittman 2011). These three mechanisms, although independent of each other, also interact with one another. While the local mechanisms are tissue intrinsic, the neural mechanisms employ the central nervous system, which primarily depends on the release of the catecholamine neurotransmitter and hormone – norepinephrine, released from the autonomic nervous system’s (ANS) sympathetic nerve endings (Pittman 2011). The humoral mechanisms are dependent on vasoactive hormones epinephrine and angiotensin II. Blood flow to tissues is dependent on mechanisms that function at a local level. Blood flow in the body is autoregulated, because of which the blood flow is constant, irrespective of changes occurring in arterial perfusion pressure (Johnson 1986). The blood pressure, which is the force responsible for flow of blood through arteries and capillaries, is closely regulated by the three physiological mechanisms described above. The blood pressure depends on the cardiac output, which is the rate of blood flow produced by the heart, and the resistance to blood flow exhibited by the blood vessels (Sharma 1992). The resistance is mainly seen in the arterioles and is called peripheral vascular resistance (PVR) or systemic vascular resistance (SVR). The blood pressure is equal to the product of cardiac output and SVR. Neural Regulation The heart rate is modulated by neural influences that affect the myocardial rhythm. The neural influences involve sympathetic and parasympathetic components of the ANS. These two operate distinctly through different structural pathways, yet in parallel (McArdle, Katch, and Katch 2010). Pressure sensitive receptors called baroreceptors are present on the carotid sinus and aortic arch. These receptors stimulate the sympathetic and parasympathetic autonomic nervous system. The information (upon increase or decrease of blood pressure) is relayed to the vasomotor center for stimulation of sympathetic and parasympathetic systems (Sharma 1992). In the sympathetic influence, chronotropic effect and tachycardia occur. When epinephrine and norepinephrine is released by sympathetic cardioaccelerator nerves, they accelerate SA node depolarization. This, through the chronotropic effect, induces the heart to beat faster (tachycardia). The heart beat rates increase to more than 100 beats per minute at rest (McArdle, Katch, and Katch 2010). Epinephrine and norepinephrine also cause the inotropic effect by increasing the myocardial contractility. When the sympathetic nervous system is stimulated to the maximum, the ventricular contraction almost doubles. When epinephrine is released by the adrenal glands during sympathetic activation, a slow but similar tachycardial effect occurs. Vasoconstriction also occurs due to the effect of sympathetic stimulation on blood flow. In case of parasympathetic influence, acetylcholine is released by parasympathetic neurons upon stimulation. It slows down heart rate by retarding the rate of sinus discharge. The heart rate is thus reduced (called bradycardia) because of the stimulation of the vagus nerves in the medulla. Local Regulation The local mechanisms for control of blood flow are tissue intrinsic and act independently of the humoral or neural influences. These mechanisms offer each tissue to possess some degree of autonomy, so that it can satisfy its specific requirements of blood flow. The cardiac output among tissues is redistributed on the basis of relative need. This is achieved by altering the resistance to blood flow (Pittman 2011). Microcirculation is the name given to the site of local regulation. This is composed of arterioles, venules and capillaries. The function of these blood vessel networks is to regulate the exchange of substances between tissues blood, in addition to tissue perfusion. Blood flow is redistributed from region to region within the tissue. Two major mechanisms are involved in local regulation of blood flow in tissues. These include myogenic and metabolic mechanisms (Pittman 2011). The myogenic mechanism states – Vascular smooth muscle actively contracts in response to stretch, in an attempt to maintain circumferential wall tension, T, relatively constant in the resistance vessels. The relationship among wall tension (T), intravascular pressure (P), internal radius (a) and vessel wall thickness (w) is given by the law of Laplace (1805) for a cylindrical elastic tube: T = Pa/w (Pittman 2011). Therefore, blood vessels when subjected to increase in intravascular pressure, become passively distended, leading to active contraction in the vessel wall’s smooth muscle. The active contraction leads to vasoconstriction that strives to bring the wall tension to the baseline values. It also tends to lessen the vascular caliber from its original value. The modulation of blood flow by myogenic mechanism is thus influenced by pressure. The metabolic mechanism is more complex. According to this mechanism, a close relationship exists between tissue metabolism and blood flow. More specifically, it depends on the link between amount of oxygen required and supplied. Oxygen linked metabolites like adenosine, hydrogen and lactate ions are the chemical mediators involved in the metabolic regulation of blood flow. Reduction in oxygen supply in tissues increases the levels of these metabolites, leading to hypoxia. Increased carbon dioxide results in vasodilation because of increase in hydrogen ions because of its dissociation into hydrogen and bicarbonate ions. This is accompanied by increased levels of potassium ions and higher interstitial fluid osmolarity. Under these conditions, vasodilation occurs, thus modulating the blood flow. This lowers the resistance to blood flow, causing increased blood flow and higher oxygen supply. Several other mechanisms for regulation of blood flow have been investigated. These mechanisms are oxygen linked and thus influence the modulation of tissue oxygenation. As is seen, local and neural influences regulate blood pressure and blood flow in tissues. In the context of blood flow in tissues, local regulation is more relevant, while the neural control is more relevant in case of blood pressure and blood flow throughout the body. References Johnson, PC 1986, ‘Autoregulation of Blood Flow’, Circulation Research, vol. 59, no. 5, pp. 483-495. McArdle, WD, Katch, FI& Katch, VL 2010, Exercise Physiology: Nutrition, Energy, and Human Performance, Lippincott Williams & Wilkins, n.d. Pittman RN 2011, Regulation of Tissue Oxygenation, Morgan & Claypool Life Sciences, San Rafael, viewed 25 February 2013, . Sharma, S 1992, Control of Arterial Blood Pressure, Update in Anaesthesia, viewed 25 February 2013, . Read More