Page 505 - ACCCN's Critical Care Nursing

482 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

Along with blood pressure, the sodium content of the also increases the reabsorption of salt and water in the
extracellular fluid is critical in maintaining fluid balance, tubule and stimulates the release of renin.
as it constitutes the major electrolyte and osmotic agent
of the glomerular filtrate. It is imperative that sodium Antidiuretic Hormone
intake and loss is equally balanced, as excessive losses The antidiuretic hormone (ADH) is excreted from the
will result in associated fluid loss and excessive intake will pituitary gland under regulation of hypothalamic osmo-
result in fluid retention. If sodium balance is not main- receptors (thirst centre), and reduces kidney diuresis (the
tained, other compensations such as a rise in blood pres- excretion of water). By enhancing the kidney’s ability to
sure may result to restore fluid balance. As blood pressure concentrate urine, it ensures that the excretory functions
rises, the excretion of sodium also increases by way of the of waste products and electrolytes continue while limit-
production of additional glomerular filtrate. In this way, ing fluid loss. ADH is essential to surviving limited
water and sodium balance are inextricably linked. 10 periods of fluid deprivation and fine-tuning the urine
volume production on a continuous basis.
HORMONAL AND NEURAL REGULATION
OF RENAL FUNCTION Renin–Angiotensin–Aldosterone

Various feedback mechanisms exist that assist in precisely System (RAAS)
adjusting the final amount of fluid and electrolyte to be Renin is the chemical trigger to initiate a cascade system
excreted from the kidney. These include the sympathetic that results in two powerful hormones acting on the
nervous system response, angiotension II, aldosterone, kidney to significantly influence sodium and water excre-
antidiuretic hormone and atrial natriuretic peptide. All tion (see Figure 18.4). Renin is produced and released
these mechanisms work in synchrony with blood pres- from the juxtaglomerular apparatus, a collection of cells
sure and sodium balance in ensuring a highly regulated in the macula densa of the distal tubule, and the adjacent
circulating and extracellular fluid volume. 10 afferent arteriole next to the glomerulus, which monitors
blood sodium concentration. When released, renin stim-
Sympathetic Nervous System ulates the activation of angiotensin I from angiotensino-
Stimulation of the sympathetic nervous system (SNS) by gen. Under the influence of coenzyme A, angiotensin I
loss of blood volume occurs by reflex via the low-pressure converts to angiotensin II, a potent vasoconstrictor and
volume sensors in the pulmonary and venous circula- stimulus to reabsorb sodium and water. The vasoconstric-
tions. This is complemented by further stimulation if tor effect raises blood pressure and flow to the glomeru-
arterial pressure falls. The SNS widely innervates the lus, inhibiting further renin release (a negative feedback
kidney and is able to reduce the filtration rate by con- mechanism) as perfusion pressure normalises. This allows
stricting the afferent arteriole of the glomerulus, thus the return of natriuresis (sodium excretion) and diuresis.
inhibiting blood flow and pressure necessary to create the This response is essential in assisting with retaining fluid
glomerular filtration rate. This stimulation of the SNS in the event of a falling blood pressure, or boosting fluid

+
Low (Na ) ECF RBPF/P Renal sympathetic
Renin
Angiotensinogen release from the renal JG apparatus

Angiotensin I
Adrenal cortex + angiotensin II + ACE

Aldosterone release Vasoconstriction
Thirst
+
Na (Cl + H O)
2
reabsorb DCT & CD TPR
ADH
ECF volume BP

Abbreviations
ACE = angiotension-converting enzyme ECF = extracellular fluid
ADH = antidiurectic hormone JG = juxtaglomerular
BP = blood pressure RBF/P = renal blood flow/pressure
CD = collecting duct TPR = total peripheral resistance
DCT = distal collecting duct
FIGURE 18.4 Renin–angiotensin–aldosterone system (RAAS).