arterial blood pressure regulation. definitions arterial blood pressure mean arterial pressure –=...
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ARTERIAL BLOOD PRESSURE REGULATION
• Arterial blood pressure
• Mean arterial pressure– = Diastolic + 1/3 pulse pressure
• Systolic blood pressure
• Diastolic blood pressure
Physiological variations in BP
• Body mass index.
Determinants of ABP
• Total peripheral resistance.
• Cardiac output.
• Blood viscosity.
• Blood volume.
ABP = CO X TPR
Site of Resistance in the circulation: arteries Or capillaries?
Total Peripheral Resistance
Factors affecting diameter of arterioles
• Vasodilator agents:– Atrial natriuretic peptide (ANP)– Histamine– Adrenomedullin– Nitric oxide– Prostacyclin
• Vasoconstrictor agents:– Noradrenaline– Sympathomimetic drugs.– Vasopressin– Angiotensin II– Endothelin-1
Blood viscosity: Hematocrit
• Plasma Proteins:Normal Plasma protein level:
Plasma protein blood viscosity
• Effect of Blood Volume :
• Changes in blood volume affect arterial pressure by changing cardiac output:
• An increase in blood volume increases central venous pressure. right atrial pressure, right ventricular end-diastolic pressure and volume. ventricular preload ventricular stroke volume by the Frank-Starling mechanism.
• right ventricular stroke volume pulmonary venous blood flow to the left ventricle, thereby increasing left ventricular preload and stroke volume.
• stroke volume cardiac output and arterial blood pressure.
Regulation of ABP
• Short-term regulation:– Baroreceptor reflexes.– Chemoreceptor reflexes.– Atrial reflexes.– CNS-ischemic response.
• Long-term regulation:– Role of the kidney.
• Intermediate regulation:– Capillary fluid shift
Higher Control of ABP
BaroreceptorsOf these two sites for arterial baroreceptors, the carotid sinus is quantitatively the most important for regulating arterial pressure. The carotid sinus receptors respond to pressures ranging from 60-180 mmHg (Figure 2). Receptors within the aortic arch have a higher threshold pressure and are less sensitive than the carotid sinus receptors. Maximal carotid sinus sensitivity occurs near the normal mean arterial pressure; therefore, very small changes in arterial pressure around this "set point" dramatically alters receptor firing so that autonomic control can be reset in such a way that the arterial pressure remains very near to the set point. This set point changes during exercise, hypertension, and heart failure. The changing set point explains how arterial pressure can remain elevated during exercise or chronic hypertension .
Long-Term: Blood volume regulation by kidneys
• Blood volume is determined by the amount of water and sodium ingested, excreted by the kidneys into the urine, and lost through the gastrointestinal tract, lungs and skin. The amounts of water and sodium ingested and lost are highly variable. To maintain blood volume within a normal range, the kidneys regulate the amount of water and sodium lost into the urine. For example, if excessive water and sodium are ingested, the kidneys normally respond by excreting more water and sodium into the urine. The details of how the kidneys handle water and sodium are beyond the scope of this cardiovascular web site; therefore, the reader is encouraged to consult general medical physiology textbooks to learn more about this topic. The following paragraphs briefly describe how renal excretion of water and sodium are regulated and how blood volume affects cardiovascular function.
Regulation of Blood Volume by Renal Excretion of Water and Sodium
• The primary mechanism by which the kidneys regulate blood volume is by adjusting the excretion of water and sodium into the urine.
• Mechanisms:• Pressure Natriuresis:
– ed blood volume arterial pressure, renal perfusion, and glomerular filtration rate. This leads to an increase in renal excretion of water and sodium (Pressure natriuresis).
– In certain types of renal disease, the pressure natriuresis relationship is altered so that the kidneys retain more sodium and water at a given pressure, thereby increasing blood volume.
Renin Angiotensin System
• The renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating blood volume and systemic vascular resistance, which together influence cardiac output and arterial pressure.
Functions of Ang II
1. Constricts resistance vessels (via AII [AT1] receptors) thereby increasing systemic vascular resistance and arterial pressure2. Acts on the adrenal cortex to release aldosterone, which in turn acts on the kidneys to increase sodium and fluid retention3. Stimulates the release of vasopressin )antidiuretic hormone, ADH) from the posterior pituitary, which increases fluid retention by the kidneys4. Stimulates thirst centers within the brain5. Facilitates norepinephrine release from sympathetic nerve endings and inhibits norepinephrine re-uptake by nerve endings, thereby enhancing sympathetic adrenergic functionStimulates cardiac hypertrophy and vascular hypertrophy