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

Studies were designed to determine whether angiotensin II has a direct stimulatory effect on arginine-vasopressin in man and to determine the role, if any, played by angiotensin II in the control of vasopressin release in physiological and pathological conditions. Acute infusion of angiotensin II in normal volunteers produced small but definite increases in plasma levels of arginine-vasopressin (5-4+/-0-3(S.E.M.) to 6-4+/-0-2 pg/ml) only when plasma angiotensin II levels were supraphysiological. Concurrent measurements of plasma arginine-vasopressin and angiotensin II were made during acute changes in fluid balance and posture in normal volunteers and in clinical conditions characterized by high plasma levels of angiotensin II (Addison's disease and Bartter's syndrome). The results of these studies allow us to conclude that there is little to suggest a direct effect of angiotensin II which is likely to be relevant to the normal physiological control of arginine-vasopressin in man.
 ...
PMID:Effects of angiotensin II on arginine-vasopressin in physiological and pathological situations in man. 30 1

This review provides a summary and assessment of research involving renal prostaglandins. Arachidonic acid released from phospholipids is converted by prostaglandin cyclo-oxygenase in the kidney to PGF2, PGF2alpha, PGD2, and, possibly, to PGI2 and thromboxane A2. Production of PGE2 and PGF2alpha is predominately but not exclusively in the medulla, whereas degradative enzymes are present in both cortex and medulla. Prostaglandins enter the tubular lumen by facilitated transport and are partially reabsorbed from the urine in the distal nephron. Urine prostaglandins probably reflect renal synthesis. PGE2 and endoperoxides stimulate and PGF2alpha and indomethacin inhibit renal renin synthesis. In response to ischemia, vasoconstriction, or angiotensin II the kidney increases prostaglandin synthesis to modulate renal vascular resistance. In conscious animals or man no role has been established for prostaglandins in the maintenance of basal renal blood flow or renal sodium excretion. PGE influences renal water excretion by inhibiting the action vasopressin. Despite conflicting data there is evidence that renal prostaglandins are involved either primarily or secondarily in many types of hypertension. Inhibitors of prostaglandin cyclooxygenase have been used with success in Bartter's syndrome. Conflicting results in many areas of investigation may be resolved by the use of more accurate and reliable assays, careful handling of samples, and the use of urine to further investigate renal prostaglandin synthesis.
 ...
PMID:Prostaglandins and the kidney. 33 46

We have investigated the effect of indomethacin and DDAVP on water excretion in a patient with familial Bartter's syndrome in whom urinary concentration was impaired during ad libitum fluid intake without any decrease in maximal concentrating ability. In response to indomethacin urine osmolality and free water reabsorption increased, simultaneously with the decrease in the excretion of prostaglandin E2. The indomethacin induced improvement was however less than that obtained after DDAVP with or without indomethacin. The results can be interpreted on the basis of either a direct "vasopressin-like" action of indomethacin or abolishment of the peripheral vasopressin--prostaglandin interaction. The clinical implication is that the theoretical possibility of indomethacin-induced inappropriate ADH syndrome should be borne in mind when a patient is treated with this drug on a long term basis.
 ...
PMID:Pharmacologic studies in Bartter's syndrome: effect of DDAVP and indomethacin on renal concentrating operation. Part II. 63 67

The factors involved in renin release have been extensively evaluated. The primary determinants are the transmural pressure at the afferent arteriole, sodium delivery to the macula densa, and the activity of the adrenergic nervous system. Other possible factors include circulating catecholamines, the serum and cerebrospinal fluid sodium concentration, serum potassium concentration, angiotensin II concentration, and antidiuretic hormone release. There is no convincing evidence that the renin-angiotensin system mediates renal autoregulation. Plasma renin activity is altered in a number of clinical settings. This parameter is elevated in most patients with cirrhosis and the nephrotic syndrome as well as in individuals with severe congestive heart failure. Despite inappropriately large weight gains, plasma renin suppresses normally with increased salt intake in edematous patients who have a normal glomerular filtration rate. The mechanisms of the alteration in the renin-angiotensin system in Bartter's syndrome is still not clear.
 ...
PMID:Renin and the kidney. 110 Oct 89

A 32-year-old man was diagnosed as having pseudo-Bartter syndrome due to surreptitious habitual vomiting and to maldigestion related to decayed teeth. His chief complaints were muscle pain and weakness. In this case, metabolic alkalosis, hypokalemia, hypochloremia, increased plasma renin activity and aldosterone levels were noticed with marked decreases in urinary chloride excretion. Creatinine clearance (GFR) and renal plasma flow (RPF) were also decreased. Blood pressure was normal, but the pressor response to angiotensin II was attenuated. Before treatment with 0.9% saline infusion, plasma vasopressin (AVP) was not suppressed sufficiently by lowering the plasma osmolality (Posm) with an oral water load (WL), but it normally responded to a rise in Posm due to hypertonic saline infusion. Moreover, plasma AVP was normally suppressed by WL after the replenishment of saline. Plasma atrial natriuretic peptide (ANP) was low before WL, but increased normally in response to WL. However, inconsistent with the normal response in this case, decreases in plasma AVP failed to dilute urinary osmolality and to increase urine flow, irrespective of the levels of plasma ANP. These results indicate that chronic inanition due to surreptitious vomiting causes impaired renal diluting ability through decreases in GFR and RPF, irrespective of the levels of plasma AVP and ANP.
 ...
PMID:Impaired water diuresis in a patient with pseudo-Bartter syndrome. 153 41

A great deal of information has been accumulated on the synthesis and release of AVP, oxytocin, and their associated neurophysins under normal circumstances. In 1957, Schwartz and Bartter first described SIAD in patients with lung cancer and postulated that the clinical findings were the results of excessive vasopressin secretion. Tumors have been known since 1964 to produce vasopressin, and small cell (oat cell) carcinoma of the lung is by far the most frequent malignant cause of SIAD. The biosynthetic pathway for the synthesis of AVP and its associated neurophysin (and to a lesser extent, oxytocin and its neurophysin) is well described and is similar if not identical to the synthesis of these peptides in the hypothalamus. However, there is little reliable information on the control of peptide synthesis and release by these tumors. The clinical picture of SIAD is well described and occurs in 20% to 40% of patients with SCCL, although up to 88% of patients with extensive SCCL have elevated circulating levels of one or more neurohypophyseal peptides. This information has led to considerable interest in the use of these peptides as tumor markers for the diagnosis, evaluation, and assessment of therapy in these patients. With the recognition of the high incidence of secretion of neurohypophyseal peptides by SCCL, studies have been initiated to determine the value of radioactive vasopressin neurophysin antibodies in localizing tumors that synthesize these peptides. The studies provide potentially useful information in diagnosing and following patients with SCCL and also offer some promise that radiolabeled antineurophysins could eventually be used to treat these patients.
 ...
PMID:Ectopic secretion of neurohypophyseal peptides in patients with malignancy. 193 17

We have suggested that the renal tubular signal for renin release is related to alterations of sodium chloride cotransport in the TALH. Renin release is inhibited by increased sodium chloride transport and stimulated by interrupted sodium chloride transport. Because of the different affinities of the carriers for sodium and chloride, chloride rather than sodium is rate limiting for this cotransport process. Consequently, renin release is related to alterations of chloride delivery rather than sodium delivery to the TALH. The reduction of PRA by selective chloride loading and by short-term infusion of chloride salts is related to increased chloride delivery to the loop and hence increased chloride transport. Alternatively, chlorpropamide and antidiuretic hormone may inhibit renin release by increasing chloride delivery to the loop. Stimulation of renin release may likewise be related either to decreased chloride delivery and hence decreased transport in the loop (hypochloremia related to selective chloride deprivation) or to an intrinsic alteration in the transporting capacity of the loop (loop diuretics, potassium depletion, glucocorticoid deficiency, Bartter's syndrome). The intermediate steps between alterations of sodium chloride transport in the TALH and renin release remain to be defined.
 ...
PMID:Renal tubular chloride and renin release. 331 41

Two patients with a Bartter-like syndrome, who had been hypokalaemic for 129 and 55 months, and 13 normokalaemic control subjects were investigated during 24 h of water deprivation. The hypokalaemic patients had urine volumes, urine osmolalities, osmolar clearances and tubular capacities for water reabsorption within the normal range. During thirst, plasma-arginine vasopressin increased much more markedly in the patients (3.4 to 11.1 pmol/l and 3.0 to 17.7 pmol/l) than in the control subjects (2.1 pmol/l (median), range 1.0-3.1, to 3.7 pmol/l, range 1.7-6.4). Plasma angiotensin II increased during water deprivation in the patients (33 to 53 pmol/l and 147 to 208 pmol/l) but not in the control subjects (9 pmol/l (median), range 3-15, to 11 pmol/l, range 3-15). Plasma aldosterone was the same in patients and control subjects and did not change in response to thirst. It is suggested that renal concentrating ability can be preserved in patients with chronic potassium depletion by means of a compensatory increase in the secretion of antidiuretic hormone.
 ...
PMID:Effect of chronic hypokalaemia on renal concentrating ability and secretion of arginine vasopressin. 357 9

A new rat model of the Schwartz--Bartter syndrome was created by the administration of 1-deamino-8-D-arginine vasopressin together with a forced water intake. The treatment led to water retention, hypernatriuria, marked hyponatraemia (in 4-5 days) and severe cerebral oedema. These changes could be prevented by the simultaneous administration of [1-(beta-mercapto-beta, beta-cyclopentamethylene-propionic acid)- 2-o-ethyltyrosine-4-valine] arginine vasopressin. The observations indicate that this vasopressin antagonist analogue might be of use in the future as an effective drug against the Schwartz--Bartter syndrome.
 ...
PMID:Experimental water intoxication induced by dDAVP in rat, and its prevention with the vasopressin antagonist d(CH2)5Tyr(Et)VAVP. 358 72

The stable prostaglandin analogue 9-deoxo-16, 16-dimethyl-9-methylene-PGE2 (9-methylene-PGE2) was infused intravenously (0.5 ml/min) in the dosage of 20 micrograms/min for 2 h in conscious euhydrated man. The administration of 9-methylene-PGE2 rapidly induced an increase in urine flow (from 1.2 +/- 0.07 to 5.35 +/- 1.07 ml/min) concomitantly with a decrease in urine osmolality (from 827 +/- 40 to 193 +/- 44 mOsm/kg). Parallel to this tubular reabsorption of sodium (Na+), calcium (Ca2+) and magnesium (Mg3+) increased and that of potassium (K+) decreased as shown by a reduction in the clearance for respective ion divided by the clearance of inulin. Apparently the water diuresis was mediated by an inhibition of arginine vasopressin's (AVP) antidiuretic effect. The mechanism behind the increase in renal tubular reabsorbtion of Na+ could possibly be a 9-methylene-PGE2 mediated modulation of the renal aldosterone effect. However the protocol followed did not provide any evidence for this, or any other explanation of the observed renal retention of Na+, Ca2+ and Mg2+. The results reported here indicate that 9-methylene-PGE2 may have a future use as a water diuretic agent in patients suffering from water retention and dilutional hyponatraemia such as seen in the syndrome of inappropriate antidiuretic hormone (AVP) release commonly known as SIADH or Schwartz-Bartter's Syndrome.
 ...
PMID:Water diuretic effect of intravenously administered 9-deoxo-16, 16-dimethyl-9-methylene-PGE2 in conscious man. 654 32


1 2 3 Next >>