Blood pressure regulation -
During exercise, blood is diverted to the skeletal muscles through vasodilation while blood to the digestive system would be lessened through vasoconstriction. The blood entering some capillary beds is controlled by small muscles, called precapillary sphincters, illustrated in [link].
If the sphincters are open, the blood will flow into the associated branches of the capillary blood. If all of the sphincters are closed, then the blood will flow directly from the arteriole to the venule through the thoroughfare channel see [link]. These muscles allow the body to precisely control when capillary beds receive blood flow.
Varicose veins are veins that become enlarged because the valves no longer close properly, allowing blood to flow backward. Varicose veins are often most prominent on the legs. Why do you think this is the case?
Proteins and other large solutes cannot leave the capillaries. The loss of the watery plasma creates a hyperosmotic solution within the capillaries, especially near the venules. The fluid in the lymph is similar in composition to the interstitial fluid. The lymph fluid passes through lymph nodes before it returns to the heart via the vena cava.
Lymph nodes are specialized organs that filter the lymph by percolation through a maze of connective tissue filled with white blood cells. The white blood cells remove infectious agents, such as bacteria and viruses, to clean the lymph before it returns to the bloodstream.
After it is cleaned, the lymph returns to the heart by the action of smooth muscle pumping, skeletal muscle action, and one-way valves joining the returning blood near the junction of the venae cavae entering the right atrium of the heart. Evolution Connection Vertebrate Diversity in Blood Circulation Blood circulation has evolved differently in vertebrates and may show variation in different animals for the required amount of pressure, organ and vessel location, and organ size.
Animals with longs necks and those that live in cold environments have distinct blood pressure adaptations. Long necked animals, such as giraffes, need to pump blood upward from the heart against gravity. These checks and balances include valves and feedback mechanisms that reduce the rate of cardiac output.
Long-necked dinosaurs such as the sauropods had to pump blood even higher, up to ten meters above the heart. This would have required a blood pressure of more than mm Hg, which could only have been achieved by an enormous heart.
Evidence for such an enormous heart does not exist and mechanisms to reduce the blood pressure required include the slowing of metabolism as these animals grew larger. It is likely that they did not routinely feed on tree tops but grazed on the ground.
Living in cold water, whales need to maintain the temperature in their blood. This is achieved by the veins and arteries being close together so that heat exchange can occur.
This mechanism is called a countercurrent heat exchanger. The blood vessels and the whole body are also protected by thick layers of blubber to prevent heat loss. In land animals that live in cold environments, thick fur and hibernation are used to retain heat and slow metabolism. The pressure of the blood flow in the body is produced by the hydrostatic pressure of the fluid blood against the walls of the blood vessels.
Fluid will move from areas of high to low hydrostatic pressures. In the arteries, the hydrostatic pressure near the heart is very high and blood flows to the arterioles where the rate of flow is slowed by the narrow openings of the arterioles. During systole, when new blood is entering the arteries, the artery walls stretch to accommodate the increase of pressure of the extra blood; during diastole, the walls return to normal because of their elastic properties.
The blood pressure of the systole phase and the diastole phase, graphed in [link] , gives the two pressure readings for blood pressure.
Throughout the cardiac cycle, the blood continues to empty into the arterioles at a relatively even rate. This resistance to blood flow is called peripheral resistance. Blood Pressure Regulation Cardiac output is the volume of blood pumped by the heart in one minute.
It is calculated by multiplying the number of heart contractions that occur per minute heart rate times the stroke volume the volume of blood pumped into the aorta per contraction of the left ventricle. Therefore, cardiac output can be increased by increasing heart rate, as when exercising.
However, cardiac output can also be increased by increasing stroke volume, such as if the heart contracts with greater strength. Stroke volume can also be increased by speeding blood circulation through the body so that more blood enters the heart between contractions. During heavy exertion, the blood vessels relax and increase in diameter, offsetting the increased heart rate and ensuring adequate oxygenated blood gets to the muscles.
Stress triggers a decrease in the diameter of the blood vessels, consequently increasing blood pressure. These changes can also be caused by nerve signals or hormones, and even standing up or lying down can have a great effect on blood pressure.
Blood primarily moves through the body by the rhythmic movement of smooth muscle in the vessel wall and by the action of the skeletal muscle as the body moves. Blood is prevented from flowing backward in the veins by one-way valves. The vasculature of the skin, kidney, spleen and mesentery has extensive sympathetic innervation although vascular beds of the heart, brain and skeletal muscle have less [18].
Intrinsic: Arterial baroreceptors are specialised pressure-responsive nerve endings situated in the walls of the aortic arch and internal carotid artery just above the sinus bifurcation [19]. Afferent fibres relay with the CCC.
There is basal discharge from baroreceptor afferents at physiological arterial pressures. When receptor endings are stretched, AP are generated and transmitted at a frequency roughly proportional to the pressure change. Afferent input results in negative chronotropic and inotropic effects, in addition to a reduction in vasoconstrictory tone of arterioles and venules.
Hence, increased BP provides a reflex negative feedback loop to maintain homeostasis, with responses greatest to changes in blood pressure in the physiological range mmHg. Clinically, this reflex is evident in the acute setting such as when standing from a sitting position with the kidneys playing a more prominent role in mediation of long-term pressure regulation [20].
A reduction in responsiveness can occur with age, hypertension and coronary disease. Baroreceptors are also present to a lesser extent in the atria, vena cavae and ventricles. The aortic and carotid bodies also contain chemoreceptors, which respond to reductions in the arterial partial pressure of oxygen PaO2 and increases in arterial partial pressure of carbon dioxide PaCO2.
Afferent pathways are located in the same nerves as adjacent baroreceptors. Their primary function is to increase respiratory minute volume, but sympathetic vasoconstriction occurs as a secondary effect [21]. Extrinsic: Extrinsic influences play a smaller and less consistent role in circulatory regulation.
Nonetheless, they become of increased relevance in states of stress, including pain, central nervous system CNS ischaemia and the Cushing reflex. Pain can produce variable responses. Mild-moderate severity may generate a tachycardia and increases in arterial BP mediated by the somatosympathetic reflex [22].
Severe pain, however, may elicit bradycardia, hypotension and symptoms of shock. The CNS ischaemic response occurs when severe hypotension mean BP The adrenal medulla is unique in that the gland is innervated by preganglionic SNS fibres which originate directly from the spinal cord [25].
The adrenal medulla secretes adrenaline and NA in response to stimulation and function as hormones by entering the bloodstream and exerting distant effects on target organs.
In view of this, activity is prolonged in comparison to NA release as a neurotransmitter. The RAA system does not play a major role in health, but is rather of increased relevance in BP maintenance during periods of hypovolaemia or impaired cardiac output when renal perfusion is compromised [26].
The enzyme renin initiates the cascade and is secreted by juxtaglomerular cells, which are modified VSMCs located in the media of the afferent arteriole immediately proximal to the glomerulus. Renin secretion is primarily secondary to renal hypoperfusion, but also occurs via SNS activation of β1-adrenergic receptors.
Renin cleaves angiotensinogen, synthesised in the liver, to angiotensin I. This is physiologically inactive but rapidly hydrolysed by angiotensin-converting enzyme ACE , found in high concentrations in pulmonary vascular endothelium, to form angiotensin II.
Angiotensin II directly mediates arteriolar vasoconstriction in most vascular beds which increases TPR and BP.
It also stimulates transmission in the SNS. Additionally, it stimulates the zona glomerulosa of the adrenal cortex to synthesise and secrete aldosterone which targets the sodium-potassium exchanger in the distal collecting tubule and collecting duct of nephrons to cause sodium and water retention.
This results in an increase in circulatory volume [27]. Angiotensin II also activates secretion of antidiuretic hormone ADH , otherwise known as vasopressin. This peptide is synthesised in the brainstem and transported for storage in the posterior lobe of the pituitary gland [28].
In addition to angiotensin II, secretion is also triggered by increased plasma osmolality detected by receptors in the hypothalamus and decreased plasma volume detected by receptors in the atria.
ADH induces translocation of aquaporin-2 channels in collecting ducts to enhance free water permeability and resorption anti-diuresis. ADH also has direct vasoconstrictory effects which are generalised and affect most regional circulations. Angiotensin II is metabolised by aminopeptidases to angiotensin III.
This is a less potent vasoconstrictor but has comparable activity in stimulating aldosterone secretion. NO is deemed to be one of the most important mediators of vascular health. For all three, NO synthesis depends upon binding of eNOS to the calcium-regulatory protein calmodulin. It is the constitutively active eNOS that is implicated in production of NO within the vascular endothelium.
The amino acid L-arginine is the main substrate for synthesis, with the requirement of several co-factors to produce NO and L-citrulline as a by-product. Once synthesised, NO diffuses across the cell membrane of endothelial cells and enters VSMCs where activation of guanylate cyclase occurs.
This catalyses conversion of GTP to cGMP, which is an important secondary messenger and mediates several biological targets implicated in vascular function [30]. eNOS expression can be regulated by multiple stimuli including insulin, shear stress and vascular endothelial growth factor VEGF [31].
There is continuous, basal synthesis of NO to relax VSMCs and maintain vasodilatory tone in vessels, with most of its effects exerted in the arterial rather than venous system.
Pharmacological agents such as glyceryl trinitrate GTN and sodium nitroprusside SNP exert their effects via cGMP-dependent mechanisms after conversion into NO [32]. Indeed, the beneficial effects of ACE-I may be related, in part, to amplification of the actions of bradykinin, which potentiates NO release.
Beyond vasomotor function, NO also has inhibitory effects on platelet adhesion and aggregation, local inflammatory responses and mitogenesis [33]. Hence, NO participates heavily in the provision of an overall anti-atherogenic and anti-thrombotic environment within the vasculature to preserve normal physiology.
Atrial natriuretic peptide ANP is synthesised directly by atrial myocytes in response to chamber distension and hormones such as adrenaline and ADH [34]. It directly relaxes VSMCs and inhibits renin, therefore having an overall natriuretic effect to reduce BP.
No direct inotropic or chronotropic effects have been documented. Some vascular beds have the ability to locally regulate blood flow in a phenomenon termed autoregulation [35]. This occurs markedly in arterioles in the heart, kidneys and brain, and to lesser effect in the skin and lungs.
This negative feedback mechanism maintains constant perfusion despite changes in arterial BP. In the absence of autoregulation, a linear relationship exists between pressure and flow.
Vasodilatation and vasoconstriction allow a constant flow to be achieved despite alterations in BP. This response is greatest in organs with the smallest neurogenic tone and is largely intrinsic, with only marginal influence from neural and humoral mediators.
In clinical contexts such as states of malignant hypertension, for instance, close assessment and regulation of BP is paramount to ensure that cerebral autoregulatory mechanisms are maintained to prevent linearity in pressure-flow dynamics. Order for reprints. PTZ: We're glad you're here.
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Toggle navigation. ISSN: X. Mini Review Open Access Peer-Reviewed. Author and article information. patel leeds. DOI : Received: 26 May, Accepted: 21 June, Published: 22 June, Cite this as Patel PA, Ali N Mechanisms involved in regulation of Systemic Blood Pressure. Arch Clin Hypertens 3 1 : DOI: Main article text.
Neural Control Cardiovascular control centres CCC The cardiovascular control centres CCC of the central nervous system CNS are located in the lower pons and medulla oblongata i.
Vasomotor tone Vasomotor tone is the sum of the muscular forces intrinsic to the blood vessel opposing an increase in vessel diameter [6]. Autonomic nervous system ANS As indicated, the CCC modulates the ANS which directly innervates cardiac muscle and VSMCs. Reflexes Intrinsic: Arterial baroreceptors are specialised pressure-responsive nerve endings situated in the walls of the aortic arch and internal carotid artery just above the sinus bifurcation [19].
The CNS ischaemic response occurs when severe hypotension mean BP Humoral Control Catecholamines The adrenal medulla is unique in that the gland is innervated by preganglionic SNS fibres which originate directly from the spinal cord [25].
Renin-angiotensin-aldosterone RAA system The RAA system does not play a major role in health, but is rather of increased relevance in BP maintenance during periods of hypovolaemia or impaired cardiac output when renal perfusion is compromised [26].
Nitric oxide NO NO is deemed to be one of the most important mediators of vascular health. Atrial natriuretic peptide ANP Atrial natriuretic peptide ANP is synthesised directly by atrial myocytes in response to chamber distension and hormones such as adrenaline and ADH [34].
Local autoregulation Some vascular beds have the ability to locally regulate blood flow in a phenomenon termed autoregulation [35]. Funding sources: There are no external funding sources to disclose. Izzo, JL Jr The sympathoadrenal system in the maintenance of elevated arterial pressure. J Cardiovasc Pharmacol 3: S J Physiol Nat Rev Neurosci.
Anesth Prog Med Sci Sports Exerc S Cardiovasc Res PLoS One e Pharmacol Rev Microcirculation Am J Physiol H
Regulation Coenzyme Q supplements the regilation system to maintain a Circadian rhythm mental health arterial Blood pressure regulation is Presssure in ensuring adequate perfusion to meet metabolic requirements of tissues. Bloood regulatory mechanisms are coordinated regulwtion the cardiovascular regulationn centres Rainbow Fish Colors the brainstem, which are themselves influenced by impulses from other neural centres in addition to sensors both intrinsic and extrinsic to the circulation. However, certain organs such as the heart, kidneys and brain have the ability to coordinate blood flow locally, i. This enables alterations in regional perfusion without perturbations of BP. This mini-review provides an exploratory discussion of neural and humoral mechanisms that underpin regulation of systemic BP.
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