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Regulation of arterial blood pressure (The Guyton and Hall Physiology)
The document discusses the regulation of arterial blood pressure, detailing definitions such as systolic and diastolic pressures, pulse pressure, and mean arterial pressure. It describes short-term and long-term regulatory mechanisms involving nervous, hormonal, and miscellaneous processes, emphasizing the roles of baroreceptors and the renin-angiotensin system. The effects of catecholamines and various reflex pathways are also examined as they contribute to maintaining blood pressure within normal ranges.
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Regulation of arterial blood pressure (The Guyton and Hall Physiology)
- 1. Regulation of Arterial BloodPressure Maryam Fida (o-1827) Source: The Guyton and Hall Physiology
- 2. Definitions BLOOD PRESSURE The pressure exerted by the blood on vessel wall is known as blood pressure. SYSTOLIC BLOOD PRESSURE The maximum pressure exerted in the arteries during systole of heart. Normal systolic pressure: 120 mm Hg. DIASTOLIC BLOOD PRESSURE The minimum pressure exerted in the arteries during diastole of heart. Normal diastolic pressure: 80 mm Hg. PULSE PRESSURE The difference between the systolic pressure and diastolic pressure. Normal pulse pressure: 40 mm Hg (120 – 80 = 40). MEAN ARTERIAL BLOOD PRESSURE The average pressure existing in the arteries. Mean Arterial Blood Pressure = Diastolic Pressure + 1/3 Pulse Pressure Pulse Pressure = (Systolic – Diastolic) Mean Arterial Blood Pressure =Diastolic Pressure+1/3(Systolic – Diastolic)
- 3. Blood Pressure Blood Pressure= Cardiac Output X Peripheral Resistance Blood Pressure = (Stroke Volume X Heart rate) X Peripheral Resistance Factors which effect Stroke Volume, Heart rate and Peripheral Resistance ultimately effects Blood Pressure
- 4. Regulation of BloodPressure Short Term Regulation Long Term Regulation
- 5. Short Term Regulationof Blood Pressure Nervous Mechanisms Baroreceptor Reflex CNS Ischemic Response Cushing’s Reflex / Cushing’s Reaction Chemoreceptors Hormonal Mechanisms Catecholamines Renin Angiotensin system Vasopressin / ADH Miscellaneous Mechanisms Capillary Fluid Shift Stress Relaxation and reverse stress relaxation
- 6. Nervous Mechanism • 1.Baroreceptor Reflex Becomes activated within few seconds. Baroreceptors are the stretch receptors in the walls of the carotid arteries and arch of aorta Impulses are carried from these receptors by hering’s nerve and vagi to the vasomotor centre in brain stem which consists of three parts i.e. Vasoconstrictor Vasodilator Sensory part Lateral and medial parts: Lateral part increases heart rate and medial part decreases heart rate. Baroreceptors remain stimulated when mean blood pressure is between 60 -180 mm of hg, however fopr carotid above range is 210. If blood pressure falls below 60 or above 210 or 180 baroreceptor don’t remain active. Baroreceptors remain stimulated when mean blood pressure is between 60 -180 mm of hg, however fopr carotid above range is 210. If blood pressure falls below 60 or above 210 or 180 baroreceptor don’t remain acti Baroreceptors remain stimulated when mean blood pressure is between 60 -180 mm of hg, however fopr carotid above range is 210. If blood pressure falls below 60 or above 210 or 180 baroreceptor don’t remain activ When blood pressure rises above normal, baroreceptors are stretched more than normal sending more impulses to the vasomotor center and bringing back the blood pressure. When there is fall in the blood pressure below normal, stretch of receptors decreases so the discharge of impulses decreases and this decrease discharge stimulates the vasomotor center, leading to the rise back of blood pressure. As barorecpetors prevent change in blood pressure, they are known as pressure buffer system. Baroreceptors remain stimulated when mean blood pressure is between 60 -180 mm of hg, however for carotid above range is 210. If blood pressure falls below 60 or above 210 or 180 baroreceptor don’t remain active.
- 8. 2. CNS IschemicResponse When mean blood pressure falls below 60 mm of hg, it becomes activated There is impaired blood flow to the brain, leading to ischemia of brain including vasomotor centre. Ischemic neurons of vasomotor centre discharge excessively along sympathetic pathways leading to tachycardia and raised blood pressure This ischemic response is very powerful activator of vasomotor sympathetic system This is the last ditch response to maintain the blood pressure Cushing’s Reaction Specialized CNS ischemic response It is initiated when there is high intracranial pressure. Raised intracranial pressure compresses the cerebral blood vessels leading to ischemia of brain causing stimulation of CNS ischemic response. As a result, blood pressure rises which restores the blood flow to the brain. So it’s a protective mechanism. In case of ischemic stroke, don’t lower the blood pressure. Average CSF pressure is 12 cm of H20. Cushing’s reflex is activated when intracranial pressure rises up to 45 cm of H20.
- 9. Chemoreceptors • These arepresent in aortic bodies and carotid bodies • These are important when blood pressure falls to very low i.e. up to 50 mm of Hg. • At this pressure there is increased PCO2, increased H+ ions and Decreased P02, which stimulates the peripheral chemoreceptors. • Impulses are carried along glossopharyngeal and vagi to vasomotor centre bringing back the blood pressure.
- 10. Hormonal Mechanisms Catecholamines When bloodpressure falls, there is sympathetic stimulation and as a part of this stimulation large amounts of catecholamines are released from adrenal medulla, they remain in system for few minutes exerting the same effect as the direct effect of nervous stimulation. VASOPRESSIN/ADH • It causes vasoconstriction, so as vasopressin it is involved in short term regulation. • ADH is also involved in long term regulation.
- 11. Miscellaneous Mechanisms CapillaryFluid Shift When blood pressure increases, there is increased capillary hydrostatic pressure leading to increase in the filtration of fluid into interstitial space causing decreased blood pressure This again causes less filtration from capillaries and so blood volume increases and this will try to bring back the blood pressure. Stress relaxation and reverse stress relaxation • When blood pressure increases due to increased blood volume, the smooth muscle in the vessel wall undergoes relaxation to accommodate the increased blood volume without rise in blood pressure. (Stress Relaxation) • When blood pressure falls due to blood loss, the smooth muscle in the vessel wall contracts around the decreased blood volume so that decreased blood volume can adequately fill the blood vessel. (Reverse stress relaxation) • This is one of the mechanisms which prevents the development of circulatory shock.
- 12. Long Term Regulationof B.P Long term regulation maintains the blood pressure for days, weeks, months and years. It is through renal body fluid pressure control systems The renal body fluid pressure control system is assisted by 4 mechanisms: 1.. Renin angiotensin mechanism 2.. ADH mechanism 3.. Aldosterone mechanism 4.. Sympathetic impulses to kidney
- 13. 1. Renin AngiotensinSystem • whenever blood pressure falls to low value: renal blood flow decreases GFR decreases Concentration of NaCl at macula densa decreases. This causes release of renin. Sympathetic stimulation also causes renin release. Renin once released remains in system for 1 hour.
- 14. Rennin acts onAngiotensinogen (which is formed in liver) and converts it into angiotensin - I Angiotensin-I (decapeptide) goes to lungs where Angiotensin Converting Enzyme converts it into Angiotensin-II in lungs which is a octa peptide. A small amount of angiotensin 3 is also formed which is not physiologically active. Angiotensin-II once formed remains in blood for 2 to 3 minutes.
- 15. Angiotensin-II exerts differenteffects i.e. Vasoconstriction (Short term Regulation) It acts on adrenal cortex to release aldosterone. (Long term regulation) It acts on hypothalamus to stimulate thirst centre. (Long term regulation) It also causes release of ADH from hypothalamo neurohypop[hyseal system. (Long term regulation) It also causes release of norepinephrine from the sympathetic post ganglionic nerve endings. (Long term regulation) So we can say that hormonal mechanism is involved in both short term and long term regulation. It becomes activated in about 20 minutes
- 17. 2. SYMPATHETIC IMPULSESTO KIDNEY: Whenever the blood pressure falls, there is increased sympathetic discharge which leads to renal vasoconstriction causing retention of salt and water.
- 18. ADH MECHANISM: When blood pressure falls there is release of ADH, which causes water reabsorption from the distal part of renal tubules. ALDOSTERONE MECHANISM: SO all the four mechanisms causes salt and water retention. When blood pressure increases above normal all of the above mechanisms are reversed.