Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pathophysiological mechanisms are reviewed concerning the onset and the perpetuation of the clinical features of congestive heart failure. This syndrome is a severe condition of poor prognosis and bad life quality which in the last decades has reached, in the western industrial countries, the highest levels of general mortality, mainly due to the high prevalence of hypertensive and ischaemic myocardiopathies in the last years. To the clinical features of heart failure mainly contributes a deregulation of the physiological compensatory mechanisms contemporarily and concurrently activated following the primary deficiency of the heart pump function. In physiological conditions, following the myogenic adapting mechanisms reflex mechanisms intervene, activated by intracardiac and aortic and carotid-sinus mechanoreceptors following the variations in intracardiac and intravascular pressure and generally evoking negative feed-back effects. In patients with heart failure arterial high pressure mechanoreceptors respond to the reduction in effective arterial pressure thus provoking a deactivation of the tonic inhibition on the sympathetic cardiovascular drive. This leads to an activation of peripheral and renal vasoconstrictor tone, to a raised medullary catecholamine incretion, to heart rate and inotropism stimulation, and to an increase in pituitary gland ADH production as well as to an activation of renin-angiotensin-aldosterone system (RAAS). Analogous vasoconstrictive, and sodium and water retentive effects can be elicited by endothelin produced by endothelial cells and found in high plasma levels in CHF. These excitatory effects, leading to a rise in systemic vascular resistance and to hydro-electrolytic retention with volume expansion, are not efficiently counteracted by the opposite effects triggered by cardiopulmonary vagally mediated mechanoreceptors activated by the raised cardiac filling pressure and leading to sympathetic nervous inhibition, peripheral and renal vasodilation, ADH and RAAS inhibition. Analogous effects should be provoked by the raised production, due to enhanced heart wall distension, of atrial natriuretic factor leading to vasodilation, natriuresis and diuresis. Reduced sensitivity of cardiopulmonary baroreceptors and lowered production of ANF due to structural cardiac changes could represent, according to most opinions, the main factors responsible for the prevailing sympathetic activation and hydro-saline retention in CHF. The activation of cardiopulmonary sympathetic positive-feed back afferents, could be also involved in the characteristic alteration of the vago-sympathetic balance in heart failure. The persistent reduction in heart pump function could lead to the instauration of vicious circles among the various regulatory systems and create an overcompensation condition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The physiopathological aspects and new therapeutic approaches in cardiac-circulatory failure]. 149 59

The heart is the major source of atrial natriuretic peptides (ANP). A propeptide is stored in atrial myocytes. In normal humans, atrial distension secondary to volume overload and/or increased atrial pressures are thought to stimulate the secretion of biologically active alpha-ANP (ANF-[99-126], 28 amino residues) into the circulation. Plasma immunoreactive ANP (irANP) rises in response to acute sodium-volume loading, the central shift of volume produced by lying down or by immersion, acute increases in blood pressure (BP), dynamic exercise, or the administration of glucocorticoids or mineralocorticoids. Plasma irANP also rises with aging. Synthetic alpha-ANP infused acutely i.v. can lower BP, reduce plasma volume by an extravascular shift, cause baroreflex-mediated sympathetic activation, directly inhibit adrenal steroidogenesis and lower plasma aldosterone and cortisol, directly inhibit renal renin release, elevate plasma insulin; diuresis, free water clearance and natriuresis increase already in response to low alpha-ANP doses that raise plasma irANP within the physiological-pathological range. It follows that in addition to direct influences on cardiovascular and renal function, the ANP system may comprise a cardio-adrenal feedback mechanism and perhaps also modulate insulin and the release of ADH. The major although yet unproven physiological role of the ANP system may be the protection of the heart against volume and/or pressure overload. The pathophysiological, diagnostic and therapeutic aspects of elevated plasma irANP values, ANP measurements, or administration of synthetic ANP, respectively, in various diseases are currently under intense study and of great potential interest.
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PMID:Atrial natriuretic peptide in man. 252 24

The atria play a major role in the regulation of body fluids. Since the work of Henry and col., techniques of atrial distention have shown the existence of volume receptors which perceive the fulness of blood volume, the left atrium in particular. When blood volume increases, receptors originate a neuro-humoral reflex in which the afferent path would be the vagus nerve, the hypotalamus would be the center, and the efferent path would be the inhibition of the hypophysis ADH secretion, provoking a decreased water reabsorption and, consequently, diuresis. This mechanism would have precedence over the osmotic regulation. Added to the investigations of the authors, these experiments also point to an increased sodium excretion, for which release of a natriuretic factor in a non-determined site was claimed as responsible. In 1981, de Bold and col. reported a hormone produced in atrial cardiocites (ANF) that would be released upon stretching of the atrium and that would act upon the nephron through different mechanisms to cause deep diuresis and natriuresis. This publication gave origin to numerous investigations. The formula of the responsible peptide was determined. The hormone was sinthesized and the pharmaceutical industry launched many synthetic products. The physiologic and physiopathologic implications of this discovery and the therapeutic potential of these synthetic derivatives are discussed.
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PMID:[Role of the atria in controlling body fluids]. 253 86

The effects of intracerebroventricular (ICV) infusion of atrial natriuretic factor (ANF; atriopeptin III) on renal function, plasma concentrations of antidiurectic hormone, aldosterone, and plasma renin activity (PRA) were examined in anesthetized rats and sodium-depleted conscious sheep. The results were compared with those obtained by intravenous infusion of the same dose of ANF. In both rats and sheep, urine volume was increased four- to sixfold over basal values by ICV infusion of ANF. The response was not associated with increased excretion of sodium or potassium. However, urine osmolality was decreased, and free water clearance increased. Intravenous infusion of the same dose of ANF was without effect. Neither mean arterial blood pressure nor heart rate was changed by the ICV infusion of ANF. In the sheep, renal plasma flow showed no significant changes and glomerular filtration rate was unaltered with the exception of a single experimental period out of four periods of ICV ANF infusion. Plasma concentration of ADH was decreased and PRA increased, whereas aldosterone levels remained unchanged as a function of ICV ANF. In the rat, the diuretic response to ANF was prevented by continuous intravenous infusion of a subpressor dose of ADH. These results suggest that ANF within the central nervous system inhibits secretion of ADH.
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PMID:Centrally administered atrial natriuretic factor increases renal water excretion. 295 69

VPA-985 is an orally active, competitive vasopressin V(2) receptor antagonist that in normal human beings increases water excretion without affecting solute excretion. Whether solute excretion is affected in patients with hyponatremia resulting from inappropriate secretion of antidiuretic hormone (SIADH) or from cirrhosis treated with VPA-985 is unknown. Six hyponatremic patients with SIADH and 5 hyponatremic patients with cirrhosis with ascitis (CWAs) were treated with 50 or 100 mg VPA-985 twice daily. Evolution of creatinine, urea, uric acid, sodium, potassium, and osmotic clearance were determined. Volume hormones (plasma renin [PR], aldosterone, antidiuretic hormone [ADH], atrial natriuretic factor [ANF]) were also determined before and after treatment. In patients with SIADH, serum sodium concentration (SNa) was generally corrected in 1 day (SNa: 126 +/- 4.5 mmol/L at t = 0 hours and 133 +/- 5.6 mmol/L at t = 24 hours) and associated with a decrease in sodium excretion (from 82 +/- 22 mmol/24 hours to 45 +/- 21 mmol/24 hours; P < 0.05) without modification in potassium excretion. Despite an increase in diuresis (from 0.84 +/- 0.2 ml/min to 1.46 +/- 0.4 ml/min) urea and uric acid clearances decreased. Urine osmolality decreased from 414 +/- 148 mOsm/kg H(2)O to 209 +/- 55 mOsm/kg H(2)O. Volume hormones did not change. In the CWAs the rise of SNa was more progressive (SNa: 126 +/- 2.8 mmol/L at t = H0 to 133 +/- 4.9 mmol/L at t = 48 hours) and parallel to an augmentation in sodium excretion (from 23 +/- 18 mmol/24 hours to 65 6 60 mmol/24 hours the second day of VPA administration). The higher sodium excretion was also connected with a progression in potassium excretion (from 22 6 7 mmol/24 hours to 36 +/- 18 mmol/24 hours). The increase in diuresis under VPA from 0.42 +/- 0.2 mL/min to 1.7 +/- 0.9 mL/min resulted in a higher urea clearance. Urine osmolality decreased from 509 +/- 142 mOsm/kg H(2)O before VPA to 194 +/- 106 mOsm/kg H(2)O after VPA. ADH increased in CWAs treated with VPA, from 1.9 +/- 1.2 pg/mL to 5.3 +/- 2.8 pg/mL (P <.05) while other volume hormones did not change. VPA-985 is a highly effective drug in the short-term management of hyponatremic patients with SIADH or CWAs. SNa correction is associated with urinary sodium retention in SIADH, whereas in CWAs a mild increase in sodium excretion is observed.
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PMID:Difference in solute excretion during correction of hyponatremic patients with cirrhosis or syndrome of inappropriate secretion of antidiuretic hormone by oral vasopressin V2 receptor antagonist VPA-985. 1175 87