How the nervous, endocrine, renal, respiratory and cardiovascular system works together to help maintain homeostasis in blood volume, blood pressure and blood PH?
When the blood pressure in the aorta rises, the arterial wall stretches and excites increased activities within the baroreceptors. Next, the information is conveyed through the nerves to the cardio regulator center which triggers the mechanism that lowers the blood pressure to a normalized level. When lowering the blood pressure, there is a decline in the sympathetic input (SI) as well as a rise in the parasympathetic input (PI) to the cardiovascular system (Blaustein et al. H1031). However, when the sympathetic stimulation is shut, and parasympathetic stimulation is boosted, it results to a decline in the pulse rate as well as stroke volume which then lowers the CO (cardiac output) and BP. Also, when the baroreceptors sense that the BP is too elevated, the cardio regulatory center lowers the SI to the blood vessels which leads to vasodilation that causing a decline in the total resistance pressure as well as a decline in the BP. The opposite occurs when the aorta baroreceptors detect a decline in BP. A drop in the BP causes a decline in action potential sent to the regulatory center of the cardio. Hence to raise BP, the body creates an upsurge in sympathetic nerve activity (SNA) via the SA node making it often fire thus increasing the pulse rate. (Chovatiya et al. 282) Also, the heart muscle is forced to pump with greater force thus increasing the stroke volume.
The normal blood PH is 7.4. When a person has a PH below than 7.4 he’s considered to have acidosis while a rise above the normal PH is alknanosis. To maintain a normal PH, the body fluids should be buffered. This is a blend of compounds that can reduce hydroxyl ions or Hydrogen ions to keep a normal PH. in the blood and within cells, proteins are the most effective buffers and hemoglobin absorbs excess H+ when not transporting oxygen (Kohan et al. 70). The concentration of buffering substances such as carbonates and phosphates is present in the blood and the tissue fluids and is regulated by the kidney or the lungs. When the concentration of H+ in the blood is very high, the respiratory center of the brain is sparked and the breathing rate rises. As the CO2 is expelled, the PH goes back to normal since the gas is acidic. The kidneys also good mechanisms through which the blood PH can be controlled. They can either form an alkaline or acidic urine, this bringing the H+ concentration to normal. According to Putnam et al. (H1219), when the kidneys form an acidic urine, H+ are expelled and in alkaline urine HCO3- are expelled. However, it should be noted that the blood PH is regulated in three ways. Buffers within the body fluids and the cells react to control the H+ and OH- concentration. Ultimately, the pulmonary system requires some time to bring the effects as the kidney takes up to twenty hours.
Blood is filtered in the glomerulus. The filtrate comprises of water, sodium plus other substances. When the filtrate passes through the kidney, the concentration of sodium is affected via transport of sodium in the tubular wall where it diffuses into intracranial capillaries (Wiig et al. 2803). The water leaves through the tubular section since they are permeable. However, the primary mechanism through which kidney regulates blood volume is through adjustment of sodium and water lost during elimination of urine from the body. At certain regions in the proximal tubules, the transport of sodium is controlled by angiotensin that rises sodium transport hence resulting in sodium retention. In the collecting tubules, the aldosterone hormone is used to speed sodium transport thus resulting in sodium retention and fluid retention in the body. Also, the ADH hormone rises water permeability in the distal tubules thus allowing water to diffuse from the tubular fluid into a highly concentrated solution hence reducing both water loss as well as urine volume. Activation of the RAAS or renin-angiotensin aldosterone systems can also lead to increased water loss in the urine thus leading to an increase in the blood volume. The activation of RAAS occurs during heart failure thus causing fluid retention into the body (Wilding 1230). However, drugs that hinder the formation of angiotensin II boosts the loss of water and sodium hence reducing blood volume. Ultimately, any drug or mechanism that changes the activity of renin angiotensin-aldosterone structure affects the volume of blood in the body.
Blaustein, Mordecai P., et al. "How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension." American Journal of Physiology-Heart and Circulatory Physiology 302.5 (2012): H1031-H1049.
Chovatiya, Raj, and Ruslan Medzhitov. "Stress, inflammation, and defense of homeostasis." Molecular cell 54.2 (2014): 281-288.
Kohan, Donald E., et al. "Regulation of blood pressure and salt homeostasis by endothelin." Physiological reviews 91.1 (2011): 1-77.
Putnam, Kelly, et al. "The renin-angiotensin system: a target of and contributor to dyslipidemias, altered glucose homeostasis, and hypertension of the metabolic syndrome." American Journal of Physiology-Heart and Circulatory Physiology 302.6 (2012): H1219-H1230.
Wiig, Helge, et al. "Immune cells control skin lymphatic electrolyte homeostasis and blood pressure." The Journal of clinical investigation 123.7 (2013): 2803.
Wilding, John PH. "The role of the kidneys in glucose homeostasis in type 2 diabetes: clinical implications and therapeutic significance through sodium glucose co-transporter 2 inhibitors." Metabolism 63.10 (2014): 1228-1237.
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