Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renin-angiotensin system has a range of physiological actions concerned with the control of the circulation. Angiotensin II has both an immediate and a delayed pressor effect; it stimulates the secretion of aldosterone and antidiuretic hormone, promotes thirst, stimulates the sympathetic nervous system at various sites while inhibiting vagal tone, and has a range of direct effects on the kidney. Several aspects of this range of actions can become deranged in a number of forms of hypertension as well as in congestive cardiac failure. Hence much effort has been directed in recent years to the development of agents designed to interfere with the renin-angiotensin system and to apply these clinically in the treatment of hypertension and congestive cardiac failure. Orally active converting enzyme inhibitors are of proven benefit not only in renovascular hypertension, but also, when combined with loop diuretics, in the treatment of intractable hypertension as well as, both alone and in combination with thiazide diuretics, in the treatment of essential hypertension. In congestive cardiac failure controlled trials have shown that converting enzyme inhibitors can improve exercise tolerance while diminishing lassitude, correct potassium deficiency, and limit ventricular arrhythmias. Energetic efforts are being made to develop orally active inhibitors of the enzyme renin itself, since these should be more specific in action than the presently available and very successful converting enzyme inhibitors.
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PMID:Circulatory basis for the use of angiotensin converting enzyme inhibitors in hypertension and cardiac failure. 242 88

The renin-angiotensin system has a range of physiological actions concerned with the control of the circulation. Angiotensin II has both an immediate and a delayed pressor effect, it stimulates the secretion of aldosterone and antidiuretic hormone, promotes thirst, stimulates the sympathetic nervous system at various sites while inhibiting vagal tone, and has a range of direct effects on the kidney. Several aspects of this range of actions can become deranged in a number of forms of hypertension as well as in congestive cardiac failure. Hence much effort has been directed in recent years to the development of agents designed to interfere with the renin-angiotensin system and to apply these clinically in the treatment of hypertension and congestive cardiac failure. Orally active converting enzyme inhibitors are of proven benefit not only in renovascular hypertension, but also, when combined with loop diuretics, in the treatment of intractable hypertension as well as, both alone and in combination with thiazide diuretics, in the treatment of essential hypertension. In congestive cardiac failure controlled trials have shown that converting enzyme inhibitors can improve exercise tolerance while diminishing lassitude, correct potassium deficiency and limit ventricular arrhythmias. Energetic efforts are being made to develop orally active inhibitors of the enzyme renin itself, since these would be more specific in action than the presently available and very successful converting enzyme inhibitors.
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PMID:The clinical use of angiotensin converting enzyme inhibitors in hypertension and cardiac failure. 303 14

This chapter reviews the disturbances of the serum sodium and potassium concentrations, acid-base imbalances, and acute renal dysfunction that are seen frequently in alcoholic patients. The hyponatremia common in decompensated cirrhotics is caused by an impairment of renal free water clearance and concomitant water ingestion. Excessive proximal renal tubular sodium reabsorption and nonosmotic vasopressin release underlie the defect in renal water excretion in cirrhosis. Restriction of water intake is the principal therapeutic measure for hyponatremia. Hypokalemia is common in alcoholics but when observed does not always represent true potassium depletion. Although most cirrhotics have a diminished total body potassium content, intracellular potassium concentration is usually normal. In some patients gastrointestinal and renal potassium losses and nutritional potassium deficiency may cause true potassium depletion. Respiratory and metabolic alkalosis are the acid-base disturbances seen most frequently in alcoholics. Acidosis is relatively uncommon and is usually due to renal insufficiency, lactic acid or keto-acid accumulation. Toxin ingestion (methanol, ethylene glycol, or isopropanol) may also cause severe acidosis. Rhabdomyolysis, common in severe alcoholism, may produce various electrolyte disturbances and acute renal failure. The prognosis for recovery is good although temporary dialysis may be necessary.
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PMID:Disorders of the serum electrolytes, acid-base balance, and renal function in alcoholism. 370 21

The effect of potassium depletion on urinary prostaglandin E and cyclic AMP excretion was studied in female Sprague-Dawley and in Brattleboro rats. The animals were fed a potassium-free diet for 20 days which resulted in an average decrease in serum potassium of 25% in both strains. In the Sprague-Dawley rats, potassium depletion increased urine volume from 5.5 +/- 0.9 ml/day to 25.9 +/- 3.5 ml/day (p less than 0.001), decreased urinary osmolality from 1483 +/- 87 mosmol/kg H2O to 372 +/- 12 mosmol/kg H2O (p less than 0.001) and suppressed urinary cyclic AMP excretion from 56.95 +/- 3.81 nmoles/day to 0.83 +/- 0.40 nmoles/day (p less than 0.001). Potassium depletion in the Brattleboro rats did not affect these parameters. Excretion of prostaglandin E-like immunoreactivity in urine did not change in either strain with potassium depletion. The findings support the hypothesis that prostaglandins do not play a significant role in the polyuria caused by potassium deficiency in rats. Hypokalemia may cause polyuria by suppression of vasopressin-sensitive cyclic AMP generation, leading to a decrease in water permeability.
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PMID:The role of urinary prostaglandin E and cyclic AMP in the polyuria of hypokalemia in rats. 624 32

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions. Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and prostaglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by beta 1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II. Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified natriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide). Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure. Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion. Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected. The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.
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PMID:Endocrine physiology of electrolyte metabolism. 638 78