HORMONES INFLUENCING RENAL ACTIVITY

The distal convoluted tubule (DCT) in the kidney cortex functions to reabsorb Na+ and secrete K+. This is regulated by the adrenal hormone, aldosterone, as stimulated by angiotensin II, which will increase reabsorption of Na+ and secrete K+. The DCT also functions in the continuation of bicarbonate ion reabsorption with hydrogen ion secretion. The terminal portion of the DCT is sensitive to antidiuretic hormone (ADH) from the neurohypophysis, which acts to increase the permeability of the tubule to water, resulting in concentrating the urine. 

B i.e. Aldosterone in collecting duct

A i.e. Regulated by ADH

–         100 mOsm/ kg H20. It does not mean that urine osmolality is greater than that of plasma. It only means that the urine is less than maximally diluted. And urine osmolality is not necessarily elevated inappropriately at all levels of plasma osmolality. 4. Elevated urinary sodium excretion (Turinary Na*) on a normal salt & water intake. It is present in most patients but is neither 100% diagnostic nor its absence rules out the diagnosis. ” align=”left” height=”278″ width=”339″>Concentration and dilution of urine i.e. free water and osmolar clearances are regulated by antidiuretic hormone (ADH) or vasopressinQ.

SIADH is characterized by relatively excessive ADH levels, euvolemia, hypoosmolality (decreased osmolality) of serum, hyponatremia (.1sertim Na*), inappropriately high urine osmolality and elevated urinary Na* excretionQ

Syndrome of Inappropriate ADH Secretion (SIADH)

–  Syndrome of inappropriate ADH secretion (SIADH) is characterized by relatively excessive ADH levels or plasma ADH levels that are elevated above what would be expected on the basis of body fluid osmolality, blood volume and

blood pressure – hence named inappropriate ADH secretion. Patients with SIADH retain water and their body fluids (eg serum) becomes progressively hypoosmotic. In other words, decreased excretion of excess water results in reduced (low)

plasma osmolality (ie hypoosmotic body fluids), hyponatremia (reduced plasma Na*) but the urine is hyper-osmotic (more concentrated) and contain increased urinary

Na* than would be expected on the basis of low body fluid osmolality.

– SIADH is characterized by low plasma osmolality,

hyponatremia (decreased plasma / serum Na*), inappropriately high urine osmolality and significant amounts of sodium in urine (Turinary Na*)

In SIADH, restricted Ovate intake is necessary to prevent cellular overhydration. Declomycin , an agent causing reversible nephrogenic diabetes insipidus (ie ADH deficiency 1/t dehydration, polyduria & polydipsia), may also be useful.

– Bartter & Schwartz clinical criteria for diagnosis of SIADH include

1. SIADH is most common cause of euvolemic-hypoosmolality. Euvolemia is defined clinically on the basis of absence of signs of hypovolemia (ie tachycardia, orthostatic or postural hypotension decreased skin turgor & dry mucous membranes ) or hypervolemia (generalized edema, ascites etc). Other causes of euvolemic hypoosmolality such as hypothyroidism, hypocortisolism (pituitary ACTH deficiency or Addison’s disease) and diuretics must be excluded.
2. Hypoosmolality (decreased effective osmolality) of ECF or serum (20) and hyponatremia (reduced plasma Na*); however, pseudo hyponatremia or hyper glycemia must be excluded.
3. Inappropriately high urine osmolality (concentration) ie > 100 mOsm/ kg H₂0. It does not mean that urine osmolality is greater than that of plasma. It only means that the urine is less than maximally diluted. And urine osmolality is not necessarily elevated inappropriately at all levels of plasma osmolality.
4. Elevated urinary sodium excretion (Turinary Na*) on a normal salt & water intake. It is present in most patients but is neither 100% diagnostic nor its absence rules out the diagnosis.

Nephrogenic Syndrome of Inappropriate Antidiuresis

Nephrogenic syndrome of inappropriate antidiuresis (NSIA) occurs d/t gain of function (activating) mutations is V, receptor gene resulting in its constitutive activation even in the absence of ADH. It present with same laboratory findings as those of SIADH including hypoosmolar serum, hyponatremia (4,serum Na*), hyperosmolar urine and Turine Nat But unlike SIADH (where high ADH levels are responsible for water retention by kidneys) patients with NSIA have undertrevels levels of ADH in their plasma.

Ans. is ‘c’ i.e., ADH

Anterior pituitary has two types of cells : ‑

1. Acidophilic cells

o Somatotrophs            –>         Secrete growth hormone

o Lactotrophs               –>          Secrete prolactin

2. Basophilic cells

o Corticotrophs            –>           Secrete ACTH, POMC, MSH

o Thyrotrophs             –>            Secrete TSH

o Gonodotrophs          –>            Secrete FSH, LH Posterior pituitary secretes ADH and oxytocin.

Ans is ‘d’ i.e., Collecting duct

The characteristic feature of cells lining the collecting duct is their responsiveness to Antidiuretic hormone (AD.11).

Ans. C: Collecting tubule

ANP act on the collecting tubule and duct to increase Na+ excretion.

It produce this effect by dilating afferent arterioles and relaxing mesangial cells. Both of these actions increase glomerular filtration. In addition, it act on the renal tubules to inhibit Na+ reabsorption. Other actions include an increase in capillary permeability, leading to extravasation of fluid and a decline in blood pressure. In addition, it relax vascular smooth muscle in arterioles and venules. These peptides also inhibit renin secretion and counteract the pressor effects of catecholamines and angiotensin II.

In the brain, ANP is present in neurons, and an ANP-containing neural pathway projects from the anteromedial part of the hypothalamus to the areas in the lower brainstem that are concerned with neural regulation of the cardiovascular system. In general, the effects of ANP in the brain are opposite to those of angiotensin II, and ANP-containing neural circuits appear to be involved in lowering blood pressure and promoting natriuresis.

Ans. A: DCT

Aldosterone acts on the principal (P) cells of DCT and collecting tubules

Aldosterone

• It increases the reabsorption of sodium ions and water and the secretion of potassium ions in the collecting ducts and distal convoluted tubule of the kidneys’ functional unit, the nephron.
• This increases blood volume and, therefore, increases blood pressure.
• Drugs that interfere with the secretion or action of aldosterone are in use as antihypertensives.
• One example is spironolactone, which lowers blood pressure by blocking the aldosterone receptor.
• Aldosterone is part of the renin-angiotensin system.
• Aldosterone is a yellow steroid hormone (mineralocorticoid family) produced by the outer-section (zona glomerulosa) of the adrenal cortex.
• The overall effect of aldosterone is to increase reabsorption of ions and water in the kidney. Its activity is reduced in Addison’s disease and increased in Conn’s syndrome.