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The cardiovascular system is responsible for maintaining an adequate flow of blood to all cells in the body. Carried in the blood are nutrients essential for cell survival and function, such as oxygen and glucose, cell waste products such as carbon dioxide and urea are also transported in the blood from cells to sites where they may be excreted from the body.

The cardiovascular system is regulated by various receptive mechanisms that include baroreceptors, which are responsible for detecting changes in blood pressure, and chemoreceptors, which detect changes in the chemical composition of the blood. There are autonomic and humoral mechanisms in place that as a result of stimulation of these receptors cause changes in heart rate, cardiac output, stroke volume, blood pressure and composition of the blood.

In response to gravitational (orthostatic) stress, the cardiovascular system is required to alter its performance. On earth because of the downward pull of gravity the body easily supplies blood to the lower limbs. However, the body is naturally challenged in supplying blood to areas that lie superiorly to the heart, and so has developed protective reflexes that act primarily through the actions of the autonomic nervous system to ensure sufficient blood flow reaches the head. The problem of orthostatic intolerance has been highlighted in certain groups such as endurance athletes1, astronauts returning from space flights2, and in diabetic patients suffering from autonomic neuropathies3, this has led to a significant increase in the number of groups researching the mechanisms responsible for the

se occurences and how they can be utilised to develop preventative treatments. It is therefore essential that the protective mechanisms that exist to combat orthostatic stress are fully understood. When discussing the effects of gravity on the cardiovascular system the baroreceptors involvement in maintainence of cardiovascular function has been shown to be the main receptive mechanism. There are two main groups of baroreceptors whose actions have been shown to be involved in protecting the body against orthostatic stress, these are the carotid and aortic arch. Their responses are mediated through the autonomic nervous system, which primarily through the sympathetic division have been shown to be the main immediate mechanism that aids humans in avoiding postural hypotension.






Venous pressure 0 - 90 Mean Arterial pressure

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Figure 15. Demonstrates the hydrostatic pressure effects in man in an upright position. The arterial and venous pressures are both increased by some 85mmHg at the ankle whilst pressure in the vessels found superiorly to the heart decrease.

Immediate Cardiovascular responses to posture changes and blood volume distribution

The hydrostatic indifference point (HIP), a term first used by Wagner in 1886, represents the natural reference point of hydrostatic pressure shifts in the cardiovascular system. Upon assuming an upright position, intravascular pressures in inferior regions of

the body rise, in superior regions pressure would fall and it is assumed there is a region between the superior and inferior regions where assuming an upright position would not alter intravascular pressures (HIP). The HIP in man has been located at about 5 to 8 cm below the diaphragm4, if the HIP were at the same level as the heart, posture changes would have little effect on cardiac output. In changing from a supine to an upright position, intravascular pressures decrease above the HIP and rise in the lower regions of the body (figure 1). As a result the most extensive pressure increase must takes place in the arteries as they do not contain valves, however the veins also show a marked increase in intravascular pressure. The increase in venous pressure and their relatively low elastic recoil causes the veins to distend, it is in these regions that blood pools. The venous volume of the legs increases by about 500ml4. Most of the translocated volume is contained in the deep intra and intermuscular leg veins and it is here that the intravascular pressure greatly increases. Approximately 200ml-300ml is transferred to the veins in the buttock and pelvic area6. It is thought that the translocated volume is derived principally from the intrathoracic compartment of the low pressure system7. It is the intrathoracic vessels that function as a blood reservoir, and their storage capacity is of great importance when the upright position is assumed, as there is a sudden drop in venous return. Approximately 70% of the total blood volume is now contained in the systemic veins; the heart and lungs account for about 15%, the systemic arteries for 10%, and the capillaries for 5%8. The increased venous pressure causes capillary pressure to rise, there is then a resultant loss of plasma fluid from the circulation. It has been shown that plasma volume falls by 13% over the first 14 minutes9 (figure 2). The lymphatic system is responsible for ‘recycling’ the excess plasma fluid and returning it to the systemic circulation. Like ve

nous return, the return of lymphatic fluid to the circulation is dependant upon limb muscular activity. When a person is upright and active, the decreased circulating blood volume (CBV) should not affect the venous return of blood to the heart as the excess lymph would be recycled as quickly as it is produced. However, in prolonged standing with minimal leg movement, the pooling of both blood and lymph can impair venous return to the extent that cardiac output is reduced by about 25%. It has been shown that individuals with a large CBV are able to withstand orthostatic stress better than those with a lower CBV3.

The bodies main concern when in the upright position is maintaining blood pressure, as blood pressure determines especially in the arterial system, blood flow to organs, which determines the supply of essential nutrients and removal of waste products. On the assumption of an upright position the baroreceptors induce changes in peripheral resistance and cardiac function, which results in the maintenance of mean arterial pressure11. When in a supine position, the gravitational effects on the circulation are minimal, blood pressure lies well within homeostatic parameters, venous return and cardiac output are more than adequate to meet the demands of the body. Heart rate is kept low as a reflex bradycardia is induced by vagal impulses acting at the SA node. Upon assumption of an upright position, blood shifts to the lower regions of the body, away from the head and neck regions. This shift is detected by arterial baroreceptors as a fall in blood pressure, a compensatory increase in heart rate (figure 3) is initiated through increased sympathetic nerve activity acting at the SA node. The increase in heart rate acts to increase both cardiac output and blood pressure, however, due to blood pooling in the venous system there is a marked decrease in venous return. Harms et al, 1999 demonstrated a reduction in the end diastolic filling of the left

ventricle causing a reduction in stroke volume and up to 20% fall in cardiac output under orthostatic conditions12. However, responses of heart rate have been shown to be of little importance in the maintenance of blood pressure during orthostatic stress13. It is now thought that the main mechanism responsible for maintenance of blood pressure when cardiac output is decreased is an increase in vascular resistance. An increased vascular resistance would act to decrease blood pooling and increase venous return. However, the exact mechanisms responsible for these changes remain unclear.

Baroreceptors- regulatory mechanisms

Afferent fibres from the baroreceptors travel in the aortic and carotid sinus nerves, which join the vagus and glossopharyngeal nerves, respectively, and connect with the cardiovascular centres in the medulla. The sensory endings of the baroreceptors are transducers of mechanical deformations, and it is the pressure induced deformation of the vessel wall and thus of the endings rather than the pressure itself that determines the discharge frequency at the baroreceptors. There is a small tonic discharge from baroreceptor afferents under normal blood pressure conditions. As blood pressure increases the frequency of discharge from the baroreceptors increases. However, as seen under conditions of orthostatic stress, as the blood pressure decreases (as interpreted by baroreceptors), the frequency of baroreceptor discharge decreases. The interaction between the carotid and aortic baroreceptors and the significance of the role each plays in combating orthostasis is unknown. It has been suggested that the carotid baroreceptors are more important in dictating the reflex adjustments. The carotid baroreceptors are located superiorly to the heart and so on assumption of an upright position the blood pressure in those areas would drop significantly. If you compare that with the location of the aortic baroreceptors, just above heart level, these receptors will recognise an increase in mean pr

essure. The carotid baroreceptors are more effectively positioned to ‘report’ blood pressure changes when in the upright position. It has also been shown that surgical denervation of the carotid baroreceptors leads to impaired orthostatic blood pressure control14.

Suggestions have been made that the mechanisms responsible for counteracting orthostatic stress are a result of a change in baroreceptor sensitivity. Victor and Mark15, suggest that there is an increase in baroreceptor sensitivity under conditions of orthostatic stress, however, Bevegard et al16, have suggested that there is no change or even a decrease in baroreceptor sensitivity under these conditions. To contradict things further Vukasovic et al17 suggest that orthostatic conditions have no effect on baroreceptor control of vascular resistance.

Adaptations in peripheral vasculature

From the fall in cardiac output in the face of a constant mean arterial pressure on assumption of the upright position, an increase in the total peripheral resistance of approximately 30-40% is seen4. This can be a quite confusing concept at it was earlier said that under the increased venous pressure inferior veins can distend, but yet they are still able to provide resistance which acts to increase blood pressure. It is assumed therefore that the resistance is provided through neurogenic and myogenic mechanisms. Neurogenic control of peripheral vascular tone is mediated through the cardiovascular control centres, vasomotor and cardiac, which are located in the medulla oblongata and lower pons. The vasomotor centre supplies nervous innervation to the peripheral vasculature and the cardiac centre to the heart. Within the vasomotor centre there are thought to be two distinct regions, the vasoconstrictor area and the vasodilatory area. The vasoconstrictor area contains a high concentration of neurons that synapse with adrenergic neurons of the sympathetic nervous system (SNS) which subsequently secrete nor-adrenaline. Nor-adrenaline acts at the á recepto

rs located in the mucularis layer of the peripheral vessels, or those found in precappilary sphincters. Studies by Donald and Shepard, 1980, demonstrated that the SNS has a greater importance than the Parasympathetic Nervous System (PNS) in regulating vascular tone18. The importance of the degree on SNS stimulation on the venous circulation is, however, to increase or reduce venous capacitance. A small change in venous capacitance can produce large alterations in venous return, as upto 80% of the total blood volume can be stored in the veins. Myogenic adaptations to long term orthostatic stress have been demonstrated in the lower extremity veins, with an increase in the diameter of the vessels and an increase in smooth muscle cell count in the vessel wall19. However vessel wall thickness did not change dramatically20.

Humoral control

Under orthostatic stress there are various short and long term humoral mechanisms in place to maintain cardiovascular function. The long term regulation of blood volume is controlled primarily by the renal system. During prolonged orthostasis the Renin-Angiotensin-Aldosterone system is activated21 which acts to increase the blood volume by drawing fluid from the interstitium into the circulation. Responses of the kidney to orthostatic stress shows a decrease in sodium excretion9. It has been shown that changes in Na+ intake can alter baroreflex sensitivity and sympathetic activity22. Increasing salt (NaCl) intake has been shown to increase plasma volume and increase orthostatic tolerance in patients with unexplained syncope23. This suggests a dual role of Na+ in combating orthostatic stress as it influences positively both neural and hormonal anti-gravity defence mechanisms. Increases in plasma nor-adrenaline and spillover are seen, probably due to efferent sympathetic activity under orthostatic conditions9. A slight increase is seen in plasma ADH levels after LBNP (-37.5 mmHg) as is a slight increase in plasma renin concentration24. However, these changes were not

seen in heart transplant recipients suggesting that aortic arch and/or cardiac receptors have a role in regulating renal blood volume control. ACTH and corticosterone (stress hormones) were found to rise above normal resting values upto 24 hours after assuming upright posture25. However, these results are taken from the rat model, so cannot be taken at face value when discussing effects of orthostasis in humans as there may be interspecies and biped/quadraped differences. The results do however add to the weight of evidence that suggests humoral adaptations play a major role in combating orthostatic stress long term.

Autonomic Neuropathies

Postural hypotension can develop in patients with long standing diabetes. When this occurs it is termed autonomic neuropathy as the diabetes causes damage to the autonomic nerves that control the heart, regulate blood pressure and control blood glucose. Autonomic neuropathy has been shown to affect upto 40% of the diabetic population26. As a result, upon standing blood pressure drops sharply as there is no sympathetic stimulation of peripheral vessels, causing a person to feel dizzy and they may possibly faint. The aetiology of diabetic neuropathy has not yet been pinpointed, suggested mechanisms include modification and inactivation of proteins critical to neural function by non-enzymatic glycosylation27, altered neural polyol metabolism28, microvascular disease with impaired bloodflow29 and ischaemia in diabetic nerves. Patients with Insulin Dependant Diabetes Mellitus (IDDM), especially those who are young but have a long disease duration, appear to be at a higher risk of developing autonomic neuropathy than those with Non Insulin Dependant Diabetes Mellitus (NIDDM). Studies have confirmed that the prevalence of diabetic neuropathy increases both with the duration of diabetes and with worsening hyperglycemia30.

Glucose uptake into peripheral nerves is determined by blood glucose concentration. Glucose is converted by aldose reductase (rate-limiting enzym

e of polyol pathway) to sorbitol, which can then be further metabolised to fructose. The nerve cell membrane is relatively impermeable to sorbitol and fructose, which tend to accumulate within the nerve28. The presence of sorbitol and fructose creates an osmotic potential which results in an inflow of water from the interstitium into the nerve, which impairs conduction and damages the nerve. It has been shown that the increased activity of the polyol pathway due to hyperglycaemia can lead to the production of highly reactive sugars that may glycate nerve proteins, which could damage nerve function in several ways. For example, glycation of tubulin, the monomer that polymerises to form microtubules, could interfere with axonal transport27. Nitric oxide (NO) is the free radical responsible for similar actions to that of Endothelium Derived Relaxing Factor (EDRF), in that it acts as a local vasodilator, released from endothelial cells. NO formation requires the co-factor NADPH, which is also required as a co-factor by aldose reductase. The increased activity of aldose reductase in hyperglycaemic conditions may reduce the amount of NADPH available for use by Nitric Oxide Synthase (NOS), with a resultant decrease in production of NO that could reduce nerve blood flow29.


Diabetic neuropathies amongst other autonomic neuropathies have been key in highlighting the importance of the effects of the autonomic nervous system in combating orthostatic stress. It is this initial response of the autonomic nervous system, through sympathetic stimulation that prevents a person from fainting upon standing and allows the body to maintain adequate circulation of blood to the head despite the increased pull of gravity on the circulating fluid. The Renin-Angiotensin-Aldosterone system plays a role in maintaining blood volume and blood pressure during prolonged orthostatic stress. A fall in an elderly person could severely affect their mobility and independence and therefore quality of life. It has been show

n that the elderly are more likely to develop postural hypotension as there is a reduced compliance in venous vessels31. Anti-hypertensive medication such as á-blockers can also lead to hypotension, as the blocking of á-receptors in the peripheral vasculature prevents vasoconstriction, and there is consequently a large volume of blood pooled. Clinicians should be aware of the consequences of prescribing anti-hypertensive therapy to elderly patients as the development of hypotension and the increased risk of consequent fall could be more damaging to the individual in both psychological (loss of confidence) and physical (decreased mobility) terms.


1. Sawka M.N, Convertino V.A, Eichner E.R, Schnieder S.M, Young A.J (2000). Blood volume: importance and adaptations to exercise training, environmental stresses, and trauma/sickness. Med Sci Sports Exerc 32, 332-348

2. Fritsh J.M, Charles J.B, Bennett B.S, Jones M.M, Eckberg D.L (1992). Short-duration spaceflight impairs human carotid baroreceptor-cardiac reflex responses. J Appl Physiol 73: 664-671

3. Cameron, N.E, Cotter, M.A (1994). The relationship of vascular changes to metabolic factors in diabetic mellitus and their role in the development of peripheral nerve complications. Diabetes Metabolic Review. 10:189-224

4. Gauer OH, Thron HL. Postural changes in the circulation. In: Handbook of physiology. Circulation, edited by W.F.Hamilton, Washington D.C: Am Physiol Soc, 1965, Sect 2, vol III, chap 67, p 2409-2439.

5. Lamb J.F, Ingram C.G, Johnston I.A, Pitman R.M. The Cardiovascular system. In: Essentials of Physiology. Blackwell Scientific Publications 1980. Chapter 5, pp 87-140.

6. White D.D, Montgomery L.D (1996). Pelvic blood pooling of men and women during lower body negative pressure. Aviat Space Environ Med 67: 555-559.

7. Sjostrand, T. Volume and distribution of blood and their significance in regulating the circulation. Physiol Rev. 33: 202, 1953

8. Sjostrand, T. The regulation of the blood volume regulat

ion in man. Acta Physiol. Scand. 26: 312-327, 1962

9. Jacob G, Ertl A.C, Shannon J.R, Furlan R, Robertson R.M, Robertson D (1998). Effect of standing on neurohormonal responses and plasma volume in healthy subjects. J Appl Physiol 84:914-921.

10. Borst C, Wieling W, Van Brederode J.F.M, Hond A, De Rijk L.G, Dunning A.J (1982). Mechanisms of initial heart rate response to postural change. Am J Physiol 243 (Heart Circ. Physiol.12): H676-681.

11. Cooper V.L, Hainsworth R (2001). Carotid baroreceptor reflexes in humans during orthostatic stress. Experimental Physiology 86.5, 677-681.

12. Harms M.P, Wesseling K.H, Pott F, Jenstrup M, Van Goudoever J, Secher N.H, Van Lieshout JJ (1999). Continuous stroke volume monitoring by modelling flow from non-invasive measurement of arterial pressure in humans under orthostatic stress. Clin Sci 97, 291-301.

13. Hainsworth R (2000). Heart rate and orthostatic stress. Clinical Autonomic Research 10, 323-325

14. Palatini P, Pessina A.C (1987). Valsalva’s manoeuvre for evaluating the integrity of baroreceptor reflex arc. Archives of Internal Medicine 17, 614-615 (Abstract).

15. Victor R.G, Mark A.L (1985). Interaction of cardiopulmonary and carotid baroreflex control of vascular resistance in humans. Journal of Clinical Investigation 76, 1592-1598.

16. Bevegard S, Castenfors J, Lindblad L.E, (1977). Effects of changes in blood volume distribution on circulatory variables and plasma rennin activity in man. Acta Physiologica Scandinavica 99, 237-245.

17. Vukasovic J.L, Al-Timman J.K.A, Hainsworth R (1990). The effects of lower body negative pressure on baroreceptor responses in humans. Experimental Physiology 75, 81-93.

18. Donald D.E, Shepard J.T (1980). Autonomic regulation of the peripheral circulation. Ann Rev Physiol 42: 429-39

19. Monas E, Lorent M, Dornyei G, Berczi V, Nadasy G (2003). Long term adaptation mechanisms in extremity veins supporting Orthostatic Tolerance. News Physiol Sci 18:210-214

20. Monas E (1993). How does

vein wall respond to pressure? News Physiol Sci 8:124-128.

21. Egan, B. M., S. Julius, C. Cottier, K. J. Osterziel, and H. Ibsen (1983). Role of cardiovascular receptor on the neural regulation of renin release in normal men. Hypertension 5: 779-786.

22. Grassi G, Cattaneo B.M, Seravalle G, Lanfranchi A, Bolla G, Mancia G (1997). Baroreflex impairment by low Na+ diet in mild or moderate Essential Hypertension. Hypertension 29: 802-807.

23. El-Sayed H, Hainsworth R (1996). Salt supplement increases plasma volume and orthostatic tolerance in patients with unexplained syncope. Heart, vol 75, 134-140.

24. Giannattasio C, Del Bo A, Cattaneo B.M, Cuspidi C, Gronda E, Frigerio M, Mangiavacchi M, Marabini M, De Vita C, Grassi G (1993). Reflex vasopressin and renin modulation by cardiac receptors in humans. Hypertension, vol 21, 461-469.

25. Monas E, Berczi V, Nadasy G L (1995). Local control of veins: biomechanical, metabolic and humoral aspects. Physiol Rev 75: 611-666.

26. Pickup J.C, Williams G (1997). Clinical features of Diabetic Neuropathy. In: Textbook of Diabetes, 2nd Edition, Blackwell Science, Chapter 50, p50.01-50.20.

27. Cullum N.A, Mahon J, Stringer K, McLean W.G (1991). Glycation of rat sciatic nerve tubulin in experimental diabetes mellitus. Diabetologica 34:387-389.

28. Greene D.A, Lattimer S.A, Seemer A.A.F (1987). Sorbitol, phosphoinositides and sodium-potassium ATP-ase in pathogenesis of Diabetic complications. N Engl J Med 316: 599-606

29. Cameron N.E, Cotter M.A (1994). The relationship of vascular changes to metabolic factors in diabetes mellitus and their role in the development of peripheral nerve complications. Diabetes Metab Rev 10: 189-224

30. Thomas P.K (1992). Diabetic neuropathy: models, mechanisms and mayhem. Can J Neurol Sci 19: 1-7

31. Huisman HW, Pretorius PJ, Van Rooyen JM, Malan NT, Eloff FC, Laubscher PJ, Steyn HS (1999). Hemodynamic changes in the cardiovascular system during the early phases of orthostasis. Acta Physiol Scand 166(2):145-9


Edited by doctor_mani

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Sat Sri Akal:

With all due respect and no malice intended:


You got something against gravity? And what this gotta do with Sikhism?

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maybe because he thinks he's a doctor he can come educate all these sikhs, that don't know anything about the world.

seems like a moderate :@

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Guest balwinderkaur

just take it as general knowledge......this site is also for youth to learn more about the world and interact with one another positively besides learning about sikhee. let's not create another war......we dont know if this mani person is a moderate so lets not point fingers.

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your absolutely right, balwinderkaur. i kinda felt bad after writing my previous post.

sorry if i'm wrong, doctor_mani

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Guest SikhForLife

perhaps that somsa post should go here too



UK docs warn about Samosas.



"Diabetes among the city's Sikhs is now three times higher than within the white European population - and heart disease is one-and-a-half times more prevalent." - BBC


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i know when u use it in dhal or rejmaa saag :@ ... da taste is just wonderful :@

well i dunno our ancesestors use to take loads of kiooo but they use to do loads of heavy work too.. so dat kinda balance it off.. we nowadays are lazy bumps.. tongue.gif so if u like kiooo work out too.. at least it'll be balanced :@

  • Like 1

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Guest mehtab

S1ngh Posted on Dec 19 2003, 10:43 PM

all punjabi families use SOOOOOOOO MUCH OIL and SOOOO much fat.. :@
aithey motta fer nai koi hunda tongue.gif

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Guest balwinderkaur
all punjabi families use SOOOOOOOO MUCH OIL and SOOOO much fat.. :@

heyy dont generalise tongue.gif i never let more than 1 tsp of oil enter my cooking pot if i ever use it tongue.gif . I prefer baking,steaming, boiling or stir-frying in non-stick pan(so no need for oil). VERY HEALTHY COOKING. tongue.gif:@ Hmmm market for fat free samosas, my mouth is watering now..ooooooo when will your shop open amar?? Now can someone plz courier some fat free samosas to me????? Yummmm.

rochak virji u are in need of kioooo

No need for ghee bhainjee tongue.gif We just bring him to taste all our local delicacies like mee goreng, mee rebus,mee siam, NASI LEMAK, roti prata, roti john, roti jala, ondeh-ondeh,ice kacang etc and he will immediately pork up......INSTANT BOOM tongue.gif:@ hhaha.

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