Pituitary volume, increase

The permeability properties of the distal convoluted tubule are regulated by antidiuretic hormone (ADH, or vasopressin). In hypotonic conditions, ADH secretion by the posterior pituitary is suppressed and the distal convoluted tubule is impermeant to water. Conversely, in hypertonic or volume-contracted states, ADH is released by the posterior pituitary and increases the permeability and water reabsorption by the distal convoluted tubule. 

The most obvious manifestation of iodine deficiency is goiter, an increased thyroid volume. An assumption about goitrogenesis is that, in iodine deficiency, a fall in the blood level of thyroxine (T4) leads to increased thyroid-stimulating hormone (TSH) output from the pituitary. TSH increases the uptake of iodide by the thyroid, with increased turnover of iodine associated with hyperplasia of the follicular cells of the thyroid. The size of the gland... 

Clofibrate 2 g daily reduced the volume of urine exereted by 2 patients with pituitary diabetes insipidus, but when glibenclamide was also given the volume increased once again. Without treatment they excreted 5.8 and 6.5 litres of urine daily, and this reduced to only 2.4 and 1.7 litres while taking clofibrate, whereas with glibenclamide and clofibrate they excreted 3.6 and 3.7 litres daily, respectively. ... 

Logically, ADH receptor antagonists, and ADH synthesis and release inhibitors can be effective aquaretics. ADH, 8-arginine vasopressin [113-79-17, is synthesized in the hypothalamus of the brain, and is transported through the supraopticohypophyseal tract to the posterior pituitary where it is stored. Upon sensing an increase of plasma osmolaUty by brain osmoreceptors or a decrease of blood volume or blood pressure detected by the baroreceptors and volume receptors, ADH is released into the blood circulation it activates vasopressin receptors in blood vessels to raise blood pressure, and vasopressin V2 receptors of the nephrons of the kidney to retain water and electrolytes to expand the blood volume. 

The potent antidiuretic hormone AVP orchestrates the regulation of free water absorption, body fluid osmolality, cell contraction, blood volume, and blood pressure through stimulation of three G-protein-coupled receptor subtypes Vi-vascular types a and b, V2-renal, and V3-pituitary. Increased AVP secretion is the trademark of several pathophysiological disorders, including heart failure, impaired renal function, liver cirrhosis, and SIADH. As a consequence, these patients experience excess water retention or inadequate free-water excretion, which results in the dilution of sodium concentrations, frequently manifesting as clinical hyponatremia (serum sodium concentration <135mmol/L). This electrolyte imbalance increases mortality rates by 60-fold. Selective antagonism of the AVP V2 receptor promotes water... 

The antidiuretic hormone is an octapeptide released from the posterior lobe of pituitary gland. It is used in the treatment of diabetes insipidus. ADH reduces the total urine volume and absence of this hormone cause diabetes insipidus. ADH acts on collecting duct cells to increase their water permeability. It acts on V2 receptors in collecting duct and regulate their water permeability through cAMP production. 

Thirst is sensed in the hypothalamus and occurs when extracellular volume decreases or osmotic pressure increases. ADH is then released from the posterior pituitary, increases water reabsorption in the nephron and reduces the volume of urine produced. 

It was concluded from these and other studies in hypophysectomized animals that ACTH had no effect on aldosterone release. The volume-sensitive renal mechanism appears to be mainly responsible for postoperative aldosterone changes (S4), but it would now appear that ACTH also plays a part in regulating aldosterone secretion (S4). Removal of the pituitary leads to an immediate fall in aldosterone levels in adrenal venous blood (H9). A linear dose response relationship exists between the infusion rate of ACTH and aldosterone secretion rates (H9). Volume receptors in the right atrium and in the vascular tree respond to minor reductions in blood volume and play an important part in stimulating the aldosterone response (Bl, FI). Patients with suppression of cortisol production due to prolonged administration of steroids continue to secrete aldosterone and are able to increase their output after stress indicating the presence of another trophic factor as well as ACTH (T3). 

The autonomous, sustained production of AVP in the absence of known stimuli for its release is called SIADH. In this syndrome, plasma AVP concentrations are inappropriately increased relative to a low plasma osmolality and to a normal or increased plasma volume. SIADH may be the result of one of several factors production of vasopressin by a malignancy (such as a small cell carcinoma of the lung), the presence of acute and chronic diseases of the central nervous system, pulmonary disorders, or a side effect of certain drug therapies. In addition, as many as 10% of patients undergoing pituitary surgery have a transient SIADH approximately 8 to 9 days after surgery (when the patient is at home), which responds to water restriction (2 to 3 days) and resolves without recurrence. In SIADH, a primary excess of AVP, coupled with unrestricted fluid intake, promotes increased reabsorption of free water by the kidney. The result is a decreased urine volume and an increased urine sodium concentration and urine osmolality. As a consequence of water retention, these patients become modestly volume expanded. The increase in intravascular volume causes hemodilution accompanied by dilutional hyponatremia and a low plasma osmolality. Volume expan-... 

One of the posterior pituitary hormones—antidiuretic hormone (ADH, vasopressin)—may play a part in the metabolic response to injury. The reduced blood volume and increased plasma electrolyte concentration found after trauma may be expected to stimulate ADH secretion and the oliguria or anuria often found to follow injury would surest this is so (J2). 

Alcohol inhibits the release of vasopressin (antidiuretic hormone see Chapter 29) from the posterior pituitary gland, resulting in enhanced diuresis. The volume loading that accompanies imbibing complements the diuresis that occurs as a result of reduced vasopressin secretion. Alcoholics have less urine output than do control subjects in response to a challenge dose with ethanol, suggesting that tolerance develops to the diuretic effects of ethanol. Alcoholics withdrawing from alcohol exhibit increased vasopressin release and a consequent retention of water, as well as dilutional hyponatremia. 

B. Effects and Clinical Uses ADH and desmopressin reduce urine volume and increase its concentration. ADH and desmopressin are useful in pituitary diabetes insipidus. They are of no value in the nephrogenic form of the disease, but salt restriction, thiazides, and loop diuretics may be used. These therapies reduce blood volume, a very strong stimulus to proximal tubular reabsorption. The proximal tubule thus substitutes— in part— for the deficient concentrating function of the collecting tubule. 

Vasopressin (At)N) is released front the posterior pituitary gland. It increases the number of water channels in the collecting ducts allow ing the passive reahsorption of water. In cranial diabetes insipidus, absence of, VDH causes the excretion of large volumes of hypotonic urine. This is iremed with vasopressin or desmopressin, a longer acting analogue. 

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