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)

Intrathecal (IT) injection of arginine vasopressin (AVP) in rats caused a transient (less than 30 min), dose-related paralysis of the hindlimbs, loss of hindlimb and tail nociceptive responsiveness, and increased mean arterial pressure. Motor dysfunction was produced with comparable potency by lysine vasopressin (LVP) and arginine vasotocin (AVT); oxytocin (OXY) was approximately 1000 times less potent. Paralysis induced by these peptides was selectively blocked following IT pretreatment with 0.5 nmoles of the vasopressin V1 receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine] Arg8-vasopressin (d(CH2)5[Tyr(Me2)]AVP). Pressor and antinociceptive responses to AVP were also blocked by this compound. However, at higher doses (2-5 nmoles, IT), d(CH2)5[Tyr(Me2)]AVP produced hindlimb paralysis, antinociception, and pressor responses by itself. In contrast to the fiber degeneration, cell loss, and necrosis found in lumbosacral cords of rats persistently paralyzed by other peptides (dynorphin A, somatostatin, and ICI 174864), neuropathological changes were not evident in spinal cords of rats transiently paralyzed by IT AVP. These results indicate that AVP-related peptides affected diverse spinal cord functions through interactions with a V1-like receptor. The similar pattern of cardiovascular and antinociceptive responses to other peptides (dynorphin A, somatostatin, and ICI 174864), which also caused hindlimb paralysis, suggests that the former responses may actually reflect the nonselective consequences of a peptide-induced disruption of spinal cord function, rather than specific shared pharmacological effects.
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PMID:Hindlimb paralytic effects of arginine vasopressin and related peptides following spinal subarachnoid injection in the rat. 324 52

The presence of vasopressin receptors of the V1 (vascular) type and of oxytocin receptors in the rat kidney was investigated using an autoradiographical approach. Rat kidney sections were incubated with tritiated vasopressin ([3H]vasopressin, 1.5 nM) or oxytocin ([3H]oxytocin, 3 nM). The ligand selectivity of the [3H]vasopressin binding sites detected was deduced from competition experiments using one selective unlabeled ligand for V2 (antidiuretic) vasopressin receptors (1-deamino-[8-D-arginine]-vasopressin, dDAVP) and one selective unlabeled ligand for V1 receptors (des-glycineamide-[1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid]-arginine vasopressin, des(Gly(NH2)9d(CH2)5-AVP). Specific and dense [3H]vasopressin labeling was observable in the medullopapillary and cortical portions of the kidney. Specific [3H]vasopressin binding in the cortex was insensitive to the V1-selective ligand, des(Gly(NH2)9d(CH2)5-AVP, but was inhibited by dDAVP. Glomerular structures identified as such by microscopical observation of the kidney sections were specifically labeled with [3H]oxytocin and [125I]-SAR1-angiotensin II but not with [3H]vasopressin. It is concluded that V1 receptors which have been evidenced on mesangial cells in culture are not expressed in a detectable quantity on mesangial cells in situ. The specific [3H]oxytocin binding to glomeruli might reflect the presence on glomerular structures of oxytocin receptors involved in the effects of the hormone on renal hemodynamics, and possibly in some of the effects ascribed to vasopressin.
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PMID:Autoradiographic localization of vasopressin and oxytocin binding sites in rat kidney. 339 84

Non-steroidal anti-inflammatory drugs represent the most heavily prescribed and used class of drugs in human medicine. Most are derivatives of either salicylates, propionic acid, indoleacetic acid, anthranilic acid, pyrazolone, or oxicams. They depress the synthesis of prostaglandins from arachidonic acid by reversible inhibition of the enzyme cyclooxygenase. In the kidney, prostaglandins PGE2 and PGI2 modulate the vasoconstrictor effects of angiotensin II, norepinephrine, and vasopressin. In the presence of volume contraction, anesthesia, or disease states associated with high levels of these hormones, prostaglandins regulate glomerular filtration, vascular resistance, and renin secretion. They additionally influence urine volume and sodium content. In man, a syndrome of analgesic abuse that has been identified worldwide occurs more frequently in females than males and can result in severe renal damage, most notably renal papillary necrosis. Most common laboratory animals are relatively resistant to developing the renal lesion associated with NSAIDs unless high doses are given over long periods of time and some withholding of water is introduced into the protocol. Diuresis with 5% dextrose and water is protective. Studies of paracetamol and salicylate have demonstrated that these compounds concentrate in the papillary tip of the kidney at concentrations of 4 to 13 times the plasma levels in dogs and rabbits, respectively. Renal papillary necrosis has been described in horses on maintenance doses of phenylbutazone where dehydration or reduced water consumption has occurred. The lesion can be reproduced experimentally if water is withheld during a portion of the dosing interval. An increased incidence of uroepithelial tumors have been reported in patients with a history of analgesic abuse.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal toxicity of non-steroidal anti-inflammatory drugs. 348 6

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.
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PMID:Experimental water intoxication induced by dDAVP in rat, and its prevention with the vasopressin antagonist d(CH2)5Tyr(Et)VAVP. 358 72

In view of our previous findings that a specific antidiuretic (V2) agonist, 4-valine-8-D-arginine vasopressin, acutely increased cardiac output and heart rate in dogs, we examined the hypothesis that interaction with V2-like receptors might contribute to the hemodynamic response seen after blockade of the vasoconstrictor (V1) effect of arginine-vasopressin in dehydrated dogs. After 48 hours of water restriction which increased plasma vasopressin to 10.6 +/- 2.0 pg/ml, the V1 antagonist 1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid) 2-(O-methyl)tyrosine arginine-vasopressin, 10 micrograms/kg, was injected intravenously into six conscious dogs, and the combined V1 + V2 antagonist 1-(beta-mercapto-beta,beta,cyclopentamethylene propionic acid) 2-(O-ethyl)-D-tyrosine, 4-valine arginine-vasopressin, 10 micrograms/kg, was administered to another six dogs. Mean arterial pressure, cardiac output (electromagnetic flowmeter), and regional blood flows (radioactive microspheres) were measured before and 20-30 minutes after antagonist administration. Mean arterial pressure did not change significantly in either instance. Cardiac output increased by 31.0 +/- 7.1% after V1 blockade, but by only 10.8 +/- 2.1% following V1 + V2 blockade. Blood flow increased significantly and to a similar extent in the skin, the skeletal muscles, and the fat following both antagonists. Conversely, kidney, arterial liver, and bone blood flow increased only after V1 blockade. In six additional, normally hydrated conscious dogs, it was shown that the V1 + V2 antagonist had no significant hemodynamic effects, a finding previously established for the V1 antagonist. The V1 + V2 antagonist completely prevented the hemodynamic effects associated with administration of the V2 agonist 4-valine-8-D-arginine vasopressin, 200 ng/kg, whereas the V1 antagonist did not. Both antagonists had similar effects on the hemodynamic changes induced by nitroprusside infusion, namely a potentiation of the blood pressure lowering action. These results suggest that part of the hemodynamic response to blockade of the vasoconstrictor action of vasopressin in dehydration is caused by unmasking cardiovascular effects linked to the antidiuretic activity of the arginine-vasopressin molecule.
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PMID:Cardiovascular effects associated with antidiuretic activity of vasopressin after blockade of its vasoconstrictor action in dehydrated dogs. 375 91

The hemodynamic changes associated with the onset of one-kidney, figure-8, renal-wrap hypertension were monitored in rats fed a high-sodium diet. In addition, the hemodynamic contributions of the sympathetic nervous system (SNS) and arginine vasopressin (AVP) were assessed during the 1st week of hypertension. Renal wrapping caused mean arterial pressure (MAP) to increase significantly from 108 +/- 4 to 140 +/- 4 mmHg on day 5 after renal surgery. The hypertension was associated with a significant bradycardia and no significant change in cardiac output (CO), as measured with an electromagnetic flow probe. Total peripheral resistance (TPR) was significantly elevated to 140% above control value on day 5 after renal surgery. Ganglionic blockade caused similar decreases in MAP and TPR in normotensive and hypertensive animals. Sympathetic blockade after pretreatment with a specific vascular antagonist of AVP, [1-beta-mercapto-beta, beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine]Arg8-vasopressin ([d(CH2)5Tyr(Me)]AVP), caused a greater depressor response in the renal-wrapped animals as compared with the effect of ganglionic blockade alone in these animals. The effect of [d(CH2)5Tyr(Me)]AVP alone on the hemodynamics was not different between the two groups of rats. After ganglionic blockade pretreatment, [d(CH2)5Tyr(Me)]AVP caused a significant decrease in MAP and TPR in the renal-wrapped animals. In addition, the difference in MAP and TPR between the two groups of rats was eliminated after combined blockade of AVP and the SNS. The results of this study indicated that the onset of hypertension was a result of an activation of neurohumoral mechanisms to increase TPR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic changes during onset of high-sodium one-kidney figure-8 renal hypertension. 377 99

The pathophysiological role of an increase in circulating vasopressin in sustaining global and regional vasoconstriction in patients with congestive heart failure has not been established, particularly in patients with hyponatraemia. To assess this further, 20 patients with congestive heart failure refractory to digoxin and diuretics were studied before and 60 minutes after the intravenous injection (5 micrograms/kg) of the vascular antagonist of vasopressin [1(beta-mercapto-beta,beta-cyclopentamethylene-propionic acid), 2-(0-methyl) tyrosine] arginine vasopressin. Ten patients were hyponatraemic (plasma sodium less than 135 mmol/l) and 10 were normonatraemic. In both groups of patients the vascular vasopressin antagonist did not alter systemic or pulmonary artery pressures, right atrial pressure, pulmonary capillary wedge pressure, cardiac index, or vascular resistances. Furthermore, there was no change in skin and hepatic blood flow in either group after the injection of the vascular antagonist. Only one patient in the hyponatraemic group showed considerable haemodynamic improvement. He had severe congestive heart failure and a high concentration of plasma vasopressin (51 pmol/l). Plasma renin activity, vasopressin, or catecholamine concentrations were not significantly changed in response to the administration of the vasopressin antagonist in either the hyponatraemic or the normonatraemic groups. Patients with hyponatraemia, however, had higher baseline plasma catecholamine concentrations, heart rate, pulmonary pressure and resistance, and lower hepatic blood flow than patients without hyponatraemia. Plasma vasopressin and plasma renin activity were slightly, though not significantly, higher in the hyponatraemic group. Thus the role of vasopressin in sustaining regional or global vasoconstriction seems limited in patients with congestive heart failure whether or not concomitant hyponatraemia is present. Vasopressin significantly increases the vascular tone only in rare patients with severe congestive heart failure and considerably increased vasopressin concentrations. Patients with hyponatraemia do, however, have raised baseline catecholamine concentrations, heart rate, pulmonary arterial pressure and resistance, and decreased hepatic blood flow.
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PMID:Hormonal, global, and regional haemodynamic responses to a vascular antagonist of vasopressin in patients with congestive heart failure with and without hyponatraemia. 379 Mar 79

Arginine-vasopressin (AVP) acts on vasoconstriction and diuresis through two different types of receptors (V1 and V2, respectively). Since AVP also modifies ACTH release, we have attempted to determine which class of receptors mediates the capacity of AVP to increase ACTH secretion and to potentiate the effect of corticotropin-releasing factor (CRF) on the pituitary using two AVP antagonists: [1-deaminopenicillamine-2-(O-methyl)tyrosine]arginine-vasopressin [dPTyr(Me)-AVP], which blocks V1 receptors, and [1-beta-mercapto-beta,beta-cyclopentamethylene propionic acid)2-D-leucine-4-valine]arginine vasopressin [d(CH2)5DLeuValAVP], which interferes with V2 receptors. dPTyr(Me)AVP, but not d(CH2)5DLeuValAVP, inhibited the ACTH-releasing as well as the CRF-potentiating effects of both AVP and its antidiuretic analog [1-deamino-8-D-arginine]vasopressin (dDAVP). These results suggest that the actions of AVP and dDAVP on the corticotrophs is primarily mediated through V1 (pressor-like) receptors.
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PMID:Studies of the nature of the interaction between vasopressin and corticotropin-releasing factor on adrenocorticotropin release in the rat. 608 90

This study was designed to investigate the possible role of angiotensin and vasopressin in the maintenance of arterial blood pressure during acute blockade of the autonomic nervous system. Two groups of eight dogs each were anesthetized with pentobarbital sodium, and autonomic ganglia were blocked with hexamethonium (20 mg/kg). Thirty minutes later group 1 received the vasopressin antagonist 1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine arginine vasopressin (10 micrograms/kg) followed after a 30-min interval by captopril (1 mg/kg). Group 2 received the same drugs, except the order of administration of vasopressin antagonist and captopril was reversed. Vasopressin antagonist during ganglionic blockade (group 2) produced a greater fall in blood pressure than did captopril during ganglionic blockade (group 1). These data indicate that vasopressin plays a greater pressor role than angiotensin in the acute response to ganglionic blockade. Additional studies were performed to determine if the autonomic nervous system alone can support the resting blood pressure in the anesthetized dog. Combined blockade of angiotensin and vasopressin without autonomic blockade produced a significant decrease in blood pressure, suggesting that the autonomic nervous system alone is not able to support the control blood pressure in the anesthetized dog.
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PMID:Role of angiotensin and vasopressin on blood pressure of ganglionic blocked dogs. 612 7

Two antagonists of the pressor action of arginine-vasopressin (AVP) were studied in conscious, normally hydrated dogs: 1-deaminopenicillamine-4-valine-8-D-arginine-vasopressin, or dPVDAVP, and 1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid)2-(O-methyl)tyrosine arginine-vasopressin, or d(CH2)5Tyr(Me)AVP. We first examined the hemodynamic effects of these antagonists when given alone. The infusion of dPVDAVP, 200 ng/kg/min, increased cardiac output (measured with an aortic electromagnetic flowmeter) by 23% and heart rate by 27%, leaving arterial pressure unchanged. Most of the change in cardiac output reflected a large increase in skeletal muscle blood flow, as determined by radioactive microspheres. The injection of d(CH2)5Tyr(Me)AVP, 10 micrograms/kg, had little effect on cardiac output, arterial pressure, and heart rate. We then examined the ability of the two antagonists to block the hemodynamic responses to injections of AVP. In the absence of the antagonists, AVP induced dose-related increases in mean arterial pressure and total peripheral resistance, as well as decreases in heart rate and cardiac output. The antagonist dPVDAVP shifted the dose-response curves to the right without changing their slope. On the contrary, the hemodynamic response to AVP was strikingly modified following blockade with d(CH2)5Tyr(Me)AVP. Cardiac output and heart rate increased, whereas total peripheral resistance decreased, for doses of AVP between 25 and 400 ng/kg. It is concluded that some antagonists of the pressor action of vasopressin may influence hemodynamics of conscious dogs by effects other than competitive antagonism at the level of vascular receptors.
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PMID:Hemodynamic effects of antagonists of the vasoconstrictor action of vasopressin in conscious dogs. 620 31


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