- suction, vomitting, diarrhea, fistulas (loss Na)
there are baroreceptors located in the low-pressure side of the circulation (walls of the cardiac atria and large pulmonary vessels) that respond primarily to fullness of the circulation. Baroreceptors are also present in the high-pressure arterial side of the circulation (aortic arch and carotid sinus) that respond primarily to changes in the arterial pressure. The activity of both types of receptors regulates renal sodium and water elimination by modulating sympathetic nervous system outflow and antidiuretic hormone (ADH) secretion
•SNS-The sympathetic nervous system
responds to changes in arterial pressure and blood volume by adjusting the glomerular filtration rate and thus the rate at which sodium is filtered from the blood. Sympathetic activity also regulates tubular reabsorption of sodium and renin release. ADH, which is secreted from the posterior pituitary glands, controls the permeability of the collecting tubules and ducts of the kidney to water, thereby regulating the amount of water that is lost in the urine.
- (vasoconstriction, water retention, corticotrophin)
- in hypothalamus
•Thirst ;polydipsia - excessive thirst. hypodipsia - decrease in ability to sense thirst
•ANP- An additional mechanism that influences sodium excretion by the kidney is the atrial natriuretic peptide (ANP). ANP, which is released from the heart in response to atrial stretch and overfilling, increases the excretion of sodium by the distal and collecting tubules of the kidney
•RAAS - Pressure-sensitive receptors in kidney, particularly in the afferent arterioles, respond directly to changes in arterial pressure through stimulation of the sympathetic nervous system and release of renin with activation of the renin-angiotensin-aldosterone system (RAAS).11 The RAAS exerts its action through angiotensin II and aldosterone (see Chapter 18). Angiotensin II acts directly on the renal tubules to increase sodium reabsorption. It also acts to constrict renal blood vessels, thereby decreasing the glomerular filtration rate and slowing renal blood flow so that less sodium is filtered and more is reabsorbed. Angiotensin II is also a powerful regulator of aldosterone, a hormone secreted by the adrenal cortex. Aldosterone acts at the level of the cortical collecting tubules of the kidneys to increase sodium reabsorption while increasing potassium elimination.
- fluid deficit or excess vs. hyponatremia or hypernatremia
Isotonic fluid volume deficit results when water and electrolytes are lost in isotonic proportions. It is almost always caused by a loss of body fluids and is often accompanied by a decrease in fluid intake The manifestations of fluid volume deficit reflect a decrease in ECF volume. They include thirst, loss of body weight, signs of water conservation by the kidney, impaired temperature regulation, and signs of reduced interstitial and vascular volumes
Hyponatremia or hypernatremia that is brought about by disproportionate losses or gains in sodium or water exerts its effects on the ICF compartment, causing water to move in or out of body cells. Many of the manifestations of changes in sodium concentration reflect changes in the intracellular volume of cells, particularly those in the nervous system.