pituitrin and Potassium-Deficiency

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.

Topics: Acute Disease; Analgesics; Humans; Hypercalcemia; Immune System Diseases; Kidney Calculi; Kidney Concentrating Ability; Kidney Diseases; Kidney Tubular Necrosis, Acute; Necrosis; Nephrosis; Nephrotic Syndrome; Potassium Deficiency; Proteins; Tetracyclines; Ureteral Diseases; Ureteral Obstruction; Urologic Neoplasms; Vascular Diseases; Vasopressins

Topics: Animals; Diuresis; Furosemide; Kidney; Kidney Cortex; Kidney Medulla; Kidney Tubules, Distal; Kidney Tubules, Proximal; Loop of Henle; Ouabain; Potassium Deficiency; Rats; Vasopressins

Topics: Acid-Base Equilibrium; Aldosterone; Amino Acids; Angiotensin II; Animals; Diabetes Insipidus; Glomerular Filtration Rate; Glucose; Humans; Inulin; Juxtaglomerular Apparatus; Kidney; Kidney Tubules; Oxygen Consumption; Potassium Deficiency; Proteins; Sodium; Urea; Uric Acid; Vasoconstrictor Agents; Vasopressins

Topics: Alcohols; Body Water; Central Nervous System Diseases; Child; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diuresis; Edema; Ethanol; Histiocytosis, Langerhans-Cell; Homeostasis; Humans; Hyponatremia; Infant; Infant, Newborn; Kidney Diseases; Nicotine; Physiology; Pituitary Gland; Pituitary Gland, Posterior; Potassium Deficiency; Prednisone; Pyloric Stenosis; Vasopressins; Water

In industrialized countries, a large part of the population is daily exposed to low K(+) intake, a situation correlated with the development of salt-sensitive hypertension. Among many processes, adaptation to K(+)-restriction involves the stimulation of H,K-ATPase type 2 (HKA2) in the kidney and colon and, in this study, we have investigated whether HKA2 also contributes to the determination of blood pressure (BP). By using wild-type (WT) and HKA2-null mice (HKA2 KO), we showed that after 4 days of K(+) restriction, WT remain normokalemic and normotensive (112 ± 3 mmHg) whereas HKA2 KO mice exhibit hypokalemia and hypotension (104 ± 2 mmHg). The decrease of BP in HKA2 KO is due to the absence of NaCl-cotransporter (NCC) stimulation, leading to renal loss of salt and decreased extracellular volume (by 20 %). These effects are likely related to the renal resistance to vasopressin observed in HKA2 KO that may be explained, in part by the increased production of prostaglandin E2 (PGE2). In WT, the stimulation of NCC induced by K(+)-restriction is responsible for the elevation in BP when salt intake increases, an effect blunted in HKA2-null mice. The presence of an activated HKA2 is therefore required to limit the decrease in plasma [K(+)] but also contributes to the development of salt-sensitive hypertension.

Topics: Animals; Blood Pressure; Dinoprostone; H(+)-K(+)-Exchanging ATPase; Hypertension; Kidney; Mice; Mice, Inbred C57BL; Potassium; Potassium Deficiency; Solute Carrier Family 12, Member 3; Vasopressins

Resistance to the pressor effects of angiotensin II, but not norepinephrine, has been observed in sodium depletion, potassium depletion, and cirrhosis. We tested the response to arginine vasopressin (AVP) in each of these conditions. Male Sprague-Dawley rats were made sodium depleted with furosemide and a low-sodium diet for 3 days, potassium depleted by feeding a low-potassium diet for 14-21 days, or cirrhotic by inhalation of carbon tetrachloride for 8 wk. In conscious rats, the pressor response to graded doses of AVP was reduced in sodium depletion by 27-43% compared with control rats. Sodium-depleted rats were also found to have enhanced baroreceptor reflexes, since the decrease in heart rate for a given increase in mean arterial pressure was greater than in control rats. When the ganglionic blocker pentolinium tartrate was given to sodium-depleted rats the pressor response to AVP was restored to control levels. In potassium-depleted rats the pressor response to AVP was 21-52% lower than that in controls, whereas cirrhotic rats also had a blunted response to AVP (14-41% lower than control). However, there was no evidence in either of these two states of enhanced baroreceptor activity, and pretreatment with pentolinium tartrate did not restore the pressor response to normal. Therefore, although resistance to the pressor effect of AVP was found in all three conditions, the mechanism of this effect was different in sodium depletion compared with potassium depletion and cirrhosis. We conclude that resistance to the pressor action of AVP in sodium depletion was secondary to resetting of the baroreceptors.

Topics: Animals; Blood Pressure; Dose-Response Relationship, Drug; Ganglionic Blockers; Liver Cirrhosis, Experimental; Male; Pentolinium Tartrate; Potassium Deficiency; Pressoreceptors; Rats; Rats, Inbred Strains; Reflex; Sodium; Vasopressins

The effects of PDN on VP-sensitive cAMP metabolism were examined in MCT and MAL microdissected from the rat kidney. VP-sensitive adenylate cyclase activity was significantly reduced (delta -46%; p less than 0.05) in MAL of PDN rats but, in sharp contrast, was significantly increased (delta +79%; p less than 0.02) in MCT of PDN rats compared to controls. cAMP phosphodiesterase activity was significantly increased in both MAL (delta +59%; p less than 0.005) and MCT (delta +79%; p less than 0.001) of PDN rats compared to controls. The increase in cAMP accumulation in MAL measured in response to VP in intact tubules did not differ between PDN and controls, whereas cAMP accumulation in response to VP was significantly higher (delta +127%; p less than 0.001) in MCT of PDN rats compared to controls. The present results would indicate that the observed in vivo resistance to the antidiuretic effect of VP that occurs in PDN is not due to an impairment in VP-sensitive cAMP accumulation in MCT, but would rather suggest that a defect exists at a cellular step subsequent to cAMP generation. In addition, our results illustrate that the extent and directionality of in situ accumulation of cAMP measured in intact tubules cannot always be predicted from rhe activities of enzymes controlling its synthesis and degradation (adenylate cyclase and cAMP phosphodiesterase), which are measured in vitro in disrupted tubules.

Topics: Adenylyl Cyclases; Animals; Arginine Vasopressin; Cyclic AMP; Kidney Medulla; Kidney Tubules; Kidney Tubules, Collecting; Loop of Henle; Male; Potassium Deficiency; Proteins; Rats; Rats, Inbred Strains; Vasopressins

Topics: Blood Volume; Female; Humans; Hypercalcemia; Kidney Diseases; Lupus Erythematosus, Systemic; Nephrotic Syndrome; Potassium Deficiency; Retroperitoneal Fibrosis; Urogenital Neoplasms; Vasopressins

The possibility that an alteration of the vasopressin-dependent cyclic AMP system plays a pathogenic role in the urinary concentrating defect in K+ depletion was investigated in the rat. The antidiuretic response to vasopressin was significantly less in K+-depleted rats. In these K+-depleted rats, the increase in urinary cyclic AMP excretion in response to vasopressin was also significantly less. However, repletion of K+ for 1 wk by feeding high-K+ diets restored the ability to increase urinary cyclic AMP excretion in response to vasopressin. In the in vitro incubation of renal medullary slices, the increase in cyclic AMP concentration in response to vasopressin was also significantly less in the slices obtained from K+-depleted rats than in those obtained from control rats. These findings suggest that, in K+ depletion, there is a reversible impairment of the vasopressin-dependent cyclic AMP system in the renal medulla; this impairment may play a pathogenic role in the urinary concentrating defect in K+ depletion.

Topics: Animals; Cyclic AMP; Diet; Glomerular Filtration Rate; Kidney; Kidney Concentrating Ability; Potassium Deficiency; Rats; Sodium; Vasopressins

Topics: Aged; Body Weight; Diuretics; Humans; Hypertension; Hyponatremia; Polythiazide; Potassium; Potassium Chloride; Potassium Deficiency; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Body Composition; Body Water; Dogs; Humans; Mathematics; Parenteral Nutrition; Potassium; Potassium Deficiency; Radioisotope Dilution Technique; Regression Analysis; Sepsis; Sodium; Sodium Isotopes; Starvation; Surgical Procedures, Operative; Tritium; Uremia; Vasopressins

Topics: Adenine Nucleotides; Anemia, Sickle Cell; Animals; Cyclic AMP; Humans; Kidney; Kidney Concentrating Ability; Potassium Deficiency; Rats; Vasopressins

Topics: Alkalosis; Bicarbonates; Blood Pressure; Blood Urea Nitrogen; Diet, Sodium-Restricted; Diuresis; Edema; Ethacrynic Acid; Female; Furosemide; Humans; Hyponatremia; Hypotension, Orthostatic; Kidney Concentrating Ability; Middle Aged; Potassium Deficiency; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Aged; Cerebrovascular Disorders; Coma; Female; Humans; Hyponatremia; Hypopituitarism; Potassium Deficiency; Vasopressins

Topics: Central Nervous System Diseases; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Humans; Infant; Infant Nutrition Disorders; Kidney Function Tests; Metabolism; Potassium Deficiency; Sodium; Urine; Vasopressins; Water

Topics: Adrenal Cortex Hormones; Aldosterone; Arginine Vasopressin; Electrolytes; Intestinal Obstruction; Metabolism; Physiology; Potassium Deficiency; Sodium Chloride; Vasopressins; Water; Water-Electrolyte Balance

Topics: Antidiuretic Agents; Arginine Vasopressin; Humans; Hypokalemia; Leadership; Potassium; Potassium Deficiency; Vasopressins

Topics: Aldosterone; Animals; Hyperaldosteronism; Hypokalemia; Potassium; Potassium Deficiency; Rats; Vasopressins