Ikhlas Muhammad Jenie, Refleks Cardiovascular ......

Cardiovascular reflex

Refleks Cardiovascular

Ikhlas Muhammad Jenie Bagian Fisiologi Fakultas Kedokteran Universitas Muhammadiyah Yogyakarta

Abstrak Tekanan darah dan frekuensi denyut jantung merupakan parameter kardiovaskular. Pengukurannya dalam praktek kedokteran klinis telah menjadi suatu hal yang wajar dilakukan, sedangkan kepentingannya telah banyak diketahui. Pada dasarnya, parameter kardiovaskular tersebut merupakan hasil dari refleks. Tulisan ini memaparkan dasar refleks kardiovaskular ditinjau dari pengaturan melalui saraf, tidak ditinjau dari pengaturan oleh secara mekanis dan maupun faktor lokal. Refleks kardiovaskular yang dibahas meliputi barorefleks, refleks kardiopulmonar, khemorefleks, refleks kardiovaskular yang disebabkan oleh stimulasi eksteroreseptor, serta interaksi antarrefleks kardiovaskular tersebut.

Kata kunci : refleks kardiovaskular, barorefleks, tekanan darah, frekuensi denyut jantung

Abstract It is familiar to measure cardiovascular parameters, such as pressure and rate, in health care practice. The importance of such measure in clinical practice is out of question. Those cardiovascular parameters, basically, are products of reflex. In this paper, we would like to describe the basic tenets of cardiovascular reflex limited to that governed by autonomic , but not to that exerted by mechanical and local factors. The cardiovascular reflexes to be discussed are arterial , cardiopulmonary baroreflex, cardiovascular reflex of stimulation of peripheral chemoreceptors, cardiovascular reflex associated to stimulation of exteroceptors, and interaction among those reflexes.

Keywords: cardiovascular reflex, baroreflex, , rate

Introduction excitation, b) an afferent neuron transmitting Reflex implies all process develops impulses from the receptor to the central in an organism in response to stimulation of nervous system, c) a nerve centre with an the receptors with indispensable participation efferent neuron, d) an efferent nerve fibres 1 of the central nervous system1. Reflex is extending to certain working organs . produced by the activity of certain structures Endocrinal glands can involve either of the nervous system called reflex arc, as intermediary link or the effector organ. which can be represented as follows: The role of endocrinal gland as the receptor Æ afferent nerve fibres Æ central intermediary link in the reflex arc can be shown as follows: receptor Æ afferent nerve nervous system Æ efferent nerve fibres Æ effector. Thus, reflex arc of any reflex must fibres Æ central nervous system Æ efferent include: a) a receptor, a nervous structure nerve fibres Æ endocrinal gland that able to transform energy coming from discharges the into the blood Æ specific stimulus into a process of nervous effector. Thus, stimulation of any receptors

43 Mutiara Medika Vol. 7 No. 1: 43-50, Januari 2007 may produce a reflex excitation of the nerves entrance of the superior and inferior vena that innervates a certain endocrinal gland, cava and pulmonary veins (veno-atrial which can alter the passage of the hormone stretch receptors), on the wall of left of the given gland into the blood. The ventricles, and in the pulmonary circulation hormone released by the endocrinal gland (together known as cardiopulmonary will modify the activity of certain effector ), are sensitive to changes in organs1. the blood volume that represented by The nature of the reflex depends on changes in the , the two aspects: 1) the state of any structure intra-ventricular pressure, and the along the reflex arc, 2) the nature and pressure, respectively3. strength of the stimulus over the receptor1. There are also numerous baroreceptors in Cardiovascular parameters, such as the vessels of tissues and organs, which blood pressure, , , continuously maintain tone of blood vessels, total peripheral resistance, basically, are responsible for redistribution of the blood products of reflex. Those parameters are among different organs1. Baroreceptors in actually cardiovascular responses to stimuli. blood vessels of skeletal muscle are Here, we would like to describe the stimulated by local pressure and active basic tenets of cardiovascular reflex limited muscle tension2. to that governed by autonomic nervous Peripheral chemoreceptors, which system, but not to that exerted by mechanical located in the carotid bodies and aortic and local factors. bodies3, and in small vessels of tissues and organs1, are sensitive to a rise of the partial + Discussion pressure of CO2, concentration of H ions The reflex arc in the cardiovascular and K--+ ions in the arterial blood, and a system decline in the partial pressure of arterial O2. 1. Receptors In the blood vessels of skeletal muscle, they There are two kinds of receptors: are known as metaboloreceptors that + interoceptors and exteroceptors. activated by an increase in K ions, H2PO4 Interoceptors are receptors located within ions and H+ ions during hard muscular works the effector organs, which can be stimulated or exercise2. by agents arising within the organism itself, Exteroceptors are located outside although some time can be stimulated also the cardiovascular system, such as: a) by external agents. In the cardiovascular receptors of the skin and mucous system, interoceptors lie in the heart and membranes of the mouth cavity, upper blood vessels. Two kinds of interoceptors respiratory tracts, cornea (tactile, thermal, here are mechanoreceptors and and pain receptors), b) receptors receiving chemoreceptors, which sensitive to the action of special chemical substances, mechanical and chemical stimulus, namely taste and olfactory receptors, c) respectively1. auditory nerves, d) visual receptors, which Mechanoreceptors in the stimulated by agents from external cardiovascular system are known as environment but can be associated to certain baroreceptors since they respond to cardiovascular response (conditional stretching usually caused by changes in reflexes)1. pressure (baro = pressure). High blood baroreceptors, which located in the 2 Afferent nerve fibers adventitial layer of the carotid sinus and a. The glossopharyngeal nerve (the IXth aortic arch (thus they are known also as cranial nerve) arterial baroreceptors), are sensitive to Through with the impulses from changes in arterial blood pressure2. Low baroreceptors in the carotid sinus and pressure baroreceptors, which lies on the chemoreceptors in the carotid bodies walls of the right and left atria near the ascend to cardiovascular centre2.

44 Ikhlas Muhammad Jenie, Refleks Cardiovascular ...... b. The (the Xth cranial nerve) consequence, heart rate will be increased Through with the impulses from (positively effect) and baroreceptors in the aortic arch, veno- contractility of the will be atrial stretch receptors, the stretch strengthened (positively inotropic effect). receptors in the pulmonary artery, and Sympathetic tone to most vessels will be chemoreceptors in the aortic bodies is increased to cause except transmitted to cardiovascular centre2. in the skeletal muscle, cardiac muscle, liver, c. The cardiac sympathetic nerves and brain. CAC will also stimulate adrenal Through with the impulses from the medulla to release circulating epinephrine stretch receptors in the left is in the blood4. travelled to cardiovascular centre2. c. Cardiac-inhibitory centre (CIC) d. Small myelinated (group III) and small CIC is the nucleus ambiguus of the unmyelinated nerve fibres (group IV) vagus nerve. When NTS is stimulated, CIC They carry excitatory input from will be activated, and then will increase vagal skeletal muscle2. tone causing a decrease in heart rate. When NTS is inhibited by impulses from peripheral 3. Cardiovascular centre receptors or the higher centres, CIC will be The location of cardiovascular centre depressed to inhibit the . In turn, is in the . It consists of: heart rate will be increased (vagal a. Sensory centre withdrawal) 4. It is the nucleus tractus solitarius (NTS), As we note, it exists the influence from which located on the dorsomedial part of the higher nervous centre such as medulla, is the site of the synapse for the and cerebral cortex to the cardiovascular cardiovascular afferents from the centre. Many parts of hypothalamus and baroreceptors, cardio-pulmonary receptors, cerebral cortex can inhibit or excite CAC5. arterial chemoreceptors, pulmonary stretch Under normal condition, cerebral cortex receptors, and muscle receptors as well as inhibits cardiovascular reflexes exerted by from the higher centres, namely the interoceptors. Direct stimulation of the hypothalamus, limbic system, and cerebral cerebral cortex leads to a decrease in the cortex. NTS evaluates and processes reflex reaction caused by stimulation of the sensory information, which its output is interoceptors. If the influence of cerebral relayed to hypothalamus and cerebellum as cortex to the cardiovascular center is blocked, well as to various parts of the medulla, e.g. stimulation of interoceptors causes greater to cardiac-acceleratory centre and cardiac- changes in cardiovascular reflexes1. inhibitory centre2. b. Cardiac-acceleratorycentre (CAC) 4. Efferent nerve fibres It has intrinsic activity. However, when The heart receives endings of NTS is stimulated by impulses from parasympathetic and sympathetic nerve peripheral receptors, the cardiac- fibres. The preganglionic parasympathetic acceleratory centre will be inhibited. CAC nerve to the heart arises in the nucleus then will depress the spinal centre of the ambiguus in the medulla. These fibres are sympathetic nervous system. In turn, heart carried by the vagus nerve, whose ganglions rate will be decreased (negatively are clustered in the heart. The chronotropic effect) and contractility of postganglionic fibres of the right vagus nerve cardiac muscle be weakened (negatively are connected chiefly with the sinu-atrial inotropic effect). Reduced sympathetic tone node and atrial muscle. Its stimulation leads will cause vasodilatation of most vessels. to a slowing down of heart rate (negatively When NTS is inhibited by impulses from chronotropic effect). The postganglionic peripheral receptors or higher centres, CAC fibres of the left vagus nerve mainly go to will be excited and activate the spinal centre the atrio-ventricular node. Its excitation of sympathetic nervous system. As a depresses conductivity of this node1.

45 Mutiara Medika Vol. 7 No. 1: 43-50, Januari 2007

Acetylcholine released by the postganglionic the effects of its metabolic products. As a parasympathetic nerve terminal binds to consequence, the next will become muscarinic (M2) receptors in the cell stronger than before. Therefore, the membrane of sinu-atrial node, atrio- negatively chronotropic effect of vagus nerve ventricular node, and atrial muscle2. The will enhance the positively inotropic action preganglionic sympathetic nerve to the heart of sympathetic nerves1. arises in the grey matter of the lateral horns Blood vessels receive three kinds of of the spinal cord segments T1 to T5. These autonomic vasomotor nerves: a) preganglionic nerves then enter the sympathetic vasoconstrictor nerves, b) sympathetic chain and terminate on the parasympathetic vasodilator nerves, c) stellate ganglion. The postganglionic sympathetic vasodilator nerves. The sympathetic fibres surround subclavian sympathetic preganglionic neurons are artery form the so-called loop of Vieussens, located in the grey matter of the and enter the rami of the cardiac nerves, intermediolateral columns of the spinal cord where it frequently mixes with the segments T1 to L3. The postganglionic preganglionic parasympathetic fibres of neurons are located in the sympathetic vagus nerves. The postganglionic ganglia or more distant ganglia, such as the sympathetic nerve fibres end in the celiac ganglia, hypogastric ganglia, and the ventricular muscle as well as in the atrial adrenal medulla. In most vessels, they end muscle, sinu-atrial node and atrio-ventricular in the tunica media, but in the veins, they node1. released by the penetrate into the inner part. The postganglionic sympathetic fibres terminal sympathetic vasoconstrictor nerves richly innervate small arteries and large arterioles binds to the 1 adrenergic receptors either in the cell membrane of sinu-atrial and atrio- but poorly innervate terminal arterioles. ventricular node to increase heart rate They also innervate most of venous vessels (positively chronotropic effect) or in the atrial but poorly innervate venous vessels of the muscle and ventricular muscle to increase splanchnic vasculature and even do not the force of myocardial contraction (positively innervate venous vessels of skeletal muscle. inotropic effect)2. Both sympathetic and Norepinephrine released by the terminal parasympathetic systems exert tonic effect fibres binds to adrenergic receptors on to the heart. However, vagal inhibition the cell membrane of the vascular smooth predominates. It can be seen that, when muscle. 1 adrenoceptors are well both systems are blocked, intrinsic heart rate distributed over vascular smooth muscle in a young adult at rest turns out to be whereas 2 adrenoceptors lie on certain around 105 beats per minute. During blood vessels, such as on vessels of the skin, physiological alterations, both systems and as prejunctional receptors on the exhibit reciprocal changes. During hard sympathetic preganglionic nerve fibres. muscular work, vagal tone decreases Stimulation of the 1 adrenoceptors elicits whereas sympathetic activity increases, vasoconstriction, which increases total resulting in -induced tachycardia. peripheral resistance and reduces the blood However, it is the activity of parasympathetic flow. Neurotransmitters other than nerve to the heart, not the activity of the norepinephrine released by the sympathetic systems, which accounted for postganglionic sympathetic vasoconstrictor beat-to-beat differences in heart rate nerve are neuropeptide Y and ATP. The because the onset and decay of the effect sympathetic vasoconstriction nerves are of acetylcholine is faster than that of constantly in a state of tonic excitation. norepinephrine2. Although both systems Therefore, the circular vascular smooth seem having antagonistic action to each muscle cells are maintained in a certain other, they actually exert synergic actions to degree of constriction. If the tone increases, the heart. Systole retardation caused by the arterioles would constrict much more. If stimulation of the vagus nerve provides the the tone decreases, the arterioles would ventricular muscle longer time to neutralize reduce the constriction (dilate). Moreover,

46 Ikhlas Muhammad Jenie, Refleks Cardiovascular ...... the activity of the sympathetic vasodilator nerves causes endothelium- vasoconstrictor nerves to each organ is independent vasodilatation. These fibres independently regulated. The also release other vasodilator agents, such parasympathetic preganglionic nerve fibres as nor-adrenergic nor-cholinergic (NANC) leave the central nervous system in two and vasoactive polypeptide (VIP). Unlike outflows: the cranial nerves and sacral spinal the sympathetic vasoconstrictor nerves, nerves. Within the end organ they synapse parasympathetic vasodilator nerves are not with the postganglionic parasympathetic tonically active. They would be active only neurons, which send short axons to the when the organ function demand rise in the arterioles. The arterioles innervated by the blood flow 2. vasodilator nerves as well as by the The sympathetic vasodilator nerves vasoconstrictor nerves are found just in a differ from the sympathetic vasoconstrictor few tissues: in the salivary glands, exocrine nerves in several aspects as shown by Table pancreas, gastrointestinal mucosa, genital 1. This system is a part of alerting response erectile tissue, cerebral and coronary to mental stress, fear, danger, or simply arteries. Acetylcholine released by the anticipation of exercise2. postganglionic fibres of the parasympathetic

Table 1. Differential properties of the sympathetic vasoconstrictor and vasodilator nerves2

Properties Sympathetic vasoconstrictor Sympathetic vasodilator nerves nerves Main neurotransmitter Norepinephrine Acetylcholine Distribution Most organ and tissues Restricted in the skeletal muscle and sweat glands Tone Yes No The centre Medulla oblongata Forebrain regulation Yes No

5. Effectors baroreceptors. Opening of this The working organs of the cardiovascular mechanosensitive Na+-Ca2+ channels allows system are the heart and blood vessels. The Na+ and Ca2+ influx and depolarizing the heart is a pump that generates motive force endings. Sufficient depolarization opens to move the blood through the vessels, voltage-dependent Na+ and K+ channels at which act as a tube, but not a rigid one6. the spike initiating zone, triggering at frequency related to the Cardiovascular reflexes magnitude of depolarization7. Impulses from 1. Cardiovascular reflex to stimulation the carotid sinus is transmitted to NTS in of high pressure baroreceptors the medulla oblongta through the (baroreflex) glossopharyngeal nerve (the IXth cranial At the normal level of blood pressure, arterial nerve), while impulses from aortic arch baroreceptors (ARBs) burst at a slow rate. ascends through the vagus nerve (the Xth It tonically inhibits resting sympathetic nerve cranial nerve)2. Receiving these impulses, activity. A rise in arterial blood pressure NTS in turn stimulate CIC and inhibit CAC. causes vascular distension that stretches the As CIC is stimulated, the vagal tone to the carotid sinus and aortic arch, stimulating heart is increased and heart rate will drop. ARBs at a higher rate3. Cellular events can Whereas, as CAC is inhibited, spinal centre be described as follows: It is the role of of sympathetic nerves is depressed, the mechanoreceptors ion channels on the sympathetic tone to the heart and blood nerve endings that mediate vessels are decreased, resulting in mechanoelectrical transduction in bradycardia and vasodilatation, which

47 Mutiara Medika Vol. 7 No. 1: 43-50, Januari 2007 decreases cardiac output and total pressure) as well as to mean arterial blood peripheral resistance, respectively. pressure. The greater the oscillation in blood Therefore, these baroreflex will restore high pressure (meaning the greater the variance arterial blood pressure back to the normal in ), the greater ARBs would levels (depressor reflex) 4. When there is a be stimulated, thus, the greater would be drop in arterial blood pressure, the carotid the depressor reflex. This signalling of pulse sinus and aortic arch are less stretched and pressure is important during orthostasis or ARBs will be excited at a slower rate3. NTS postural changes and behavioural stress2. will receive fewer ascending impulses2. In ARBs also tonically inhibit the release of turn, it will excite CAC and inhibit CIC. As vasopressin and angiotensin II (AngII). CAC is stimulated, the spinal centre of When blood pressure drops, the decrease sympathetic nerves is more excited and thus in the impulses of ARBs evokes increase in sympathetic tone to the heart and blood the sympathetic activity, which in turn will vessels are increased. As CIC is inhibited, stimulate the juxtaglomerular cells in the vagal tone to the heart is decreased and kidneys to release renin. As a consequence, heart rate will rise. The overall results are the renin-angiotensin-aldosteron system tachycardia and vasoconstriction, which (RAAS) is activated. AngII will enhance the causes an increase in cardiac output and pressor reflex. In the kidneys, AngII and total peripheral resistance, and finally a rise aldosteron cause salt retention. The in blood pressure4. decrease in the ARBs traffic also stimulates ARBs provide moment-to-moment the posterior pituitary gland to release negative feedback of blood pressure arginine vasopressin to the blood to enhance regulation7. The carotid baroreceptors are peripheral vasoconstriction and water sensitive to pulse pressure (the difference retention (anti diuresis) as well2. It can be between systolic and diastolic blood summarized in the below table.

Table 2. Hormonal changes during baroreflexes2 ARBs are stimulated ARBs are inhibited RAAS Decrease Increase Vasopressin Decrease Increase

The decrease or increase of ABR done by invasive (intra-arterial blood activity to stimuli is known as baroreceptor pressure measurement) or non-invasive sensitivity (BRS). BRS is defined as measurement of arterial blood pressure8. changes in the R-R interval (reciprocal of The Japanese researcher has invented the the heart rate) on the electrocardiogram new non-invasive diagnosis tool for the (ECG) plotted as a function of the change quantitative evaluation of BRS. The in blood pressure during the preceding measurement uses ECG and pulse wave . Change in BRS can be monitoring. It observes time series induced by any physiological or sequence of heart rate changes in pharmacological maneuver. The corresponding to the blood pressure assessment can be done qualitatively and changes. The time series data is inputted quantitatively. Qualitatively, BRS can be into a personal computer system and is measured at bedside by the change in heart analyzed by special software. The rate from baseline during the Valsava fluctuation of the heart rate variability reflects maneuver for 15 seconds. The heart rate autonomic nerve function9. BRS decreases usually increases 10 – 30 bpm by the end of with age, therefore the result should be the maneuver. Quantitatively, assessment compared with the response obtained in of BRS requires continuous monitoring of normal subjects of comparable age8. the ECG and arterial pressure. It can be

48 Ikhlas Muhammad Jenie, Refleks Cardiovascular ......

Table 3. Physiological and pharmacological maneuvers that modulate arterial baroreflex8

Activate Deactivate Neck pressure Neck suction Phenylephrine Nitroglycerin Angiotensin II Amylnitrite Valsava Nitroprusside

2. Cardiovascular reflex to stimulation cardiopulmonary baroreceptors modify input of low pressure baroreceptors from arterial baroreceptors. They are (cardiopulmonary baroreceptors) sensitive to small changes in cardiac stretch Two types of veno-atrial stretch receptors, and affect sympathetic discharge during low a) type A, which discharges during atrial grade physiological change not detected by systole, b) type B, which discharges during arterial baroreceptors10. atrial filling, detect changes in the volume of the blood through changes in the central 3. Cardiovascular reflex of stimulation venous pressure Any increase in blood of peripheral chemoreceptors volume will activate type B receptors. The Nerve endings in the carotid and aortic impulses are then transmitted to NTS in the bodies are stimulated by hypoxia, medulla through the afferent fibres of the hypercapnia, hyperkalemia, and acidosis. vagus nerves, resulting in tachycardia, The impulses are transmitted to the natriuresis, and diuresis. The atrial cardiovascular centre in the medulla through natriuretic peptide, hormone released by the afferent fibres of the IXth and Xth cranial atrial muscle, acts as the intermediary link nerves, respectively. It actually causes of the natriuresis and diuresis effect. Atrial bradycardia reflex and vasoconstriction of systole stimulates type A receptors. Similar the resistance vessels except in the skin. to type B receptors, the impulses from type However, the inspiratory centre in the A receptors are then transmitted to NTS in medulla is stimulated also, which in turn the medulla oblongata through vagus nerves. causes an increase in tidal volume and It is followed by inhibition to cardiac and excites the stretch receptor within the lungs. peripheral sympathetic outflow but excitatory The final result is tachycardia and to cardiac vagal outflow, resulting in vasodilatation in most vascular beds2. bradycardia and vasodilatation2. The clinical Stimulation of metaboloreceptors in the syndrome of vasovagal syncope may occur skeletal muscle by the chemical released 10 + by this mechanism . The stimulation of type during exercise, notably K ions, H----2---PO4 A veno-atrial stretch receptor is associated ions, and H+ ions, will result in tachycardia, with the inhibition of the release of increased myocardial contractility and angiotensin II, catecholamine, and peripheral vasoconstriction, resulting in rise vasopressin2. The mechanoreceptors in the of blood pressure2, known as the exercise walls of the left ventricle are stimulated pressor reflex11. during ventricle systole since these receptors Chemoreflex and baroreflex interact are sensitive to changes in the intra to each other. Inputs from arterial ventricular pressure. The reflex responses baroreceptor may modulate responses to of their stimulation are bradycardia and chemoreceptor stimulation. A line of vasodilatation2. The stretch receptors in the evidences showed that chemoreflex pulmonary artery are excited by a rise in the vasoconstriction is enhanced at high levels pressure of the pulmonary artery. The of baroreceptor stimulation, but is reduced vessels of the systemic circulation dilate in at low levels of baroreceptor stimulation. response to the excitation of these Thus, hypotension will enhance, whereas mechanoreceptors and lead to a drop in hypertension will inhibit, vasoconstriction blood pressure1. The signals from those responses to hypoxic hypercapnia

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(asphyxia). Teleologically, this interaction is 3. Ganong WF. Review of medical important to survival fitness. However, physiology. 16th ed. Norwalk: Appleton inputs from chemoreceptors alter baroreflex & Lange; 1993. function in more complicated ways. Both 4. Chauduri SK. Concise medical hypocapnia and hypercapnia will result in physiology. 2nd ed. Calcutta: New tachycardia12. Central Book Agency; 1993. 5. Guyton AC, Hall JE. Text book of medical 4. Cardiovascular reflex of stimulation physiology. 9th ed. Philadelphia: W.B. of exteroceptors Saunders Company; 1996. Stimulation of the exteroceptors causes 6. Bijlani RL. Understanding medical reflex constriction of the vessels and physiology: A text book for medical sometimes also acceleration of the cardiac student. 2nd ed. New Delhi: Jaypee activity1. Cold applied to the skin is followed Brothers Medical Publishers; 1997. by constriction of the blood vessels of the 7. Chapleau MW. Arterial baroreceptors. In: skin, especially the arterio-venous Izzo JL, Black HK, editors. Hypertension anastomoses. Sudden load noise or primer: The essential of high blood unpleasant sight also could increase blood pressure. 2nd ed. Maryland: Lippincott pressure and elicit tachycardia2. Somatic Williams & Wilkins; 1999. pain is associated with the increase in 8. Taylor A. Evaluation of aortocarotid sympathetic activity (somato-sympathetic . In: Izzo JL, Black HK, reflex) 3. However, severe visceral pain is editors. Hypertension primer: The associated with bradycardia, hypotension essential of high blood pressure. 2nd ed. and even painting2. Maryland: Lippincott Williams & Wilkins; 1999. Conclusion 9. Yambe T, Yoshizawa M, Sugita N, Cardiovascular reflexes are part of Tanaka A, Maruayam M, Konno S. homeostasis mechanism. Arterial baroreflex Invention of the new diagnosis tool for is response to changes in blood pressure. the quantitative evaluation of the Cardiopulmonary baroreflex is response to Baroreflex sensitivity. The 21st Scientific small changes in blood volume. Meeting of the International Society of Cardiovascular reflex of stimulation of Hypertension: Abstract CD-ROM; 2006. peripheral chemoreceptors is response to 10. Mohanty PK. Cardiopulmonary changes in blood pH and gas partial baroreceptors. In: Izzo JL, Black HK, pressure. Cardiovascular reflex associated editors. Hypertension primer: The to stimulation of exteroceptors is conditioned essential of high blood pressure. 2nd ed. reflex, such as seen in fight and flight Maryland: Lippincott Williams & Wilkins; mechanism. Interactions among these 1999. reflexes are seen clinically. All these reflexes are to maintain blood flow to part of body, 11. Kluess HA, Wood RH. Heart rate mainly vital and demanded active organs. variability and the exercise pressor reflex during dynamic handgrip exercise and References postexercise occlusion. Am J Med Sci 2005; 329(3):117-123. 1. Bykov KM, Konradi G. Text book of 12. Henry RA, I-Li Lu, Beightol LA, Eckberg nd physiology. 2 ed. Moscow: Peace DL. Interactions between CO2 Publishers; 1953. chemoreflexes and arterial baroreflexes. 2. Levick JR. An introduction to Am J Physiol 1998; 274:H2177-H2187. cardiovascular physiology. 3rd ed. London: Arnold; 2000.

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