The Clinical Biology of Sodium. The Physiology and by A. R. Michell

By A. R. Michell

A e-book for clinicians and easy scientists

The pathophysiology of sodium is critical to the administration of a variety of medical stipulations, significantly liver sickness, renal affliction, cardiac failure, high blood pressure (including high blood pressure in pregnancy), oedema, diarrhoea, hypovolaemia, surprise, the behavioural results of hyper- or hyponatraemia and diverse endocrine problems. extensive care and fluid remedy count crucially on sound administration of sodium stability. No unmarried scientific discovery has kept extra lives at much less fee than the truth that the elemental impression of diarrhoea rests on disturbances of enteric sodium stability: the facility to revive web uptake via oral rehydration has switched over cholera from a killer to a home-nursing disorder. but if we glance at animals, in addition to people, we recognize that the intestine isn't just a resource of sodium disturbances yet, probably, an important regulator of sodium stability. We additionally realize that until h

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Example text

T h e stimulatory effect of potassium at the external site, though real, has often been thought unimportant because it saturates at 1 mmol/1, well below the E C F concentration (4—5 mmol/1). Recent evidence suggests that this may result from the use of broken cell preparations and that in intact renal tubule fragments, for example, stimulation continues until a maximum is reached at 5 mmol/1 (Katz, 1988). N a - K ATPase plays a crucial role in the renal adaptation to potassium loads and in the heightened ability of surviving nephrons to maintain adequate potassium excretion until the advanced stages of chronic renal failure (Stanton, 1987).

Medullary washout' undermines urinary concentrating capacity. It Renal Sodium Regulation 47 Loop of Henlé Descending limb t A Thick ascending limb (TAL) Thin ascending limb FIG. 4. Basic principles of counter current multiplication. g. as a result of chronic overdrinking (psychogenic polydipsia) or diversion of R B F from the cortex to the medulla in acute renal failure, hence the paradoxical urine of typical A R F ; small in volume (as in a dehydrated patient) yet, unlike a dehydrated patient, dilute.

Another aspect of the proximal tubular contribution to acid-base regulation is the production of ammonia buffer which, together with phosphate buffer, may be the limiting factor in acid excretion. Ammonia synthesis depends on delivery of glutamine to tubular cells. This depends on the sodium gradient and potential difference generated by N a - K ATPase. Ammonia synthesis is regulated by glucocorticoids. T h e adaptive increase in response to an established metabolic acidosis is glucocorticoid-dependent and excess glucocorticoid sufficiently enhances acid excretion to cause metabolic alkalosis (Welbourne, 1990).

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