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)

Specific binding sites for atrial natriuretic peptide have been identified in membrane of the phaeochromocytoma cell line PC12. Scatchard analysis of binding studies revealed a Kd of 794 pM and a density (Bmax) of 254 fmol/mg protein. Hormones unrelated to ANP such as angiotensin II, bradykinin and arginine-8-vasopressin did not complete for the binding sites. Of the ANP-related peptides which competed for the binding sites, the following order of affinity was established; rANP (8-33) greater than rANP (28 amino acid) greater than rat atrial peptide fragment (13-28) greater than a-hANP (28 amino acid) greater than atrial peptide fragment (1-11) greater than atriopeptin I.
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PMID:Characterization of specific binding of atrial natriuretic peptide (ANP) to rat PC12 phaeochromocytoma cells. 285 Apr 20

Changes in levels of plasma immunoreactive atrial natriuretic peptide (IR-ANP) were measured in response to administration of isoproterenol in the anesthetized, vagotomized rabbit. A dose-dependent increase in plasma IR-ANP was seen in response to 10 min isoproterenol infusions between 0.1 and 10.0 micrograms/kg/min. The time course of these responses showed the maximum levels of IR-ANP to be attained 10 min after the cessation of infusion. In rabbits in which plasma vasopressin (AVP) levels were also measured, the maximum levels of AVP were attained during the infusion period. There was no correlation between levels of AVP and IR-ANP suggesting that AVP released into the plasma did not affect directly the release of IR-ANP. The changes in IR-ANP in response to isoproterenol were significantly reduced in rabbits which had been administered the beta-1-adrenoceptor blocking agent, atenolol. In six rabbits in which the vagi remained intact, the increases in IR-ANP were reduced and became significant only with 10 micrograms/kg/min isoproterenol infusion. The results demonstrate that isoproterenol infusion increases the level of plasma IR-ANP in the anesthetized rabbit and suggest that this is through an effect on the heart rather than on peripheral vessels.
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PMID:Influence of isoproterenol on plasma immunoreactive atrial natriuretic peptide and plasma vasopressin in the anesthetized rabbit. 288 66

ANP receptor binding and desensitization were demonstrated in the A10 vascular smooth muscle cell (VSMC) line. Concomitantly, the ANP receptor coupled guanylate cyclase activity was reduced by the receptor down-regulation with ANP. The ANP stimulated cGMP accumulation is modulated by arginine-vasopressin, while the arginine-vasopressin mediated cAMP system remained unaffected by ANP. Results suggest negative coupling of arginine-vasopressin receptors to the guanylate cyclase activity, and indicate that the vasorelaxant activity of ANP might be regulated in part by arginine-vasopressin via specific receptor sites.
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PMID:Modulation of ANP receptor-mediated cGMP accumulation by atrial natriuretic peptides and vasopressin in A10 vascular smooth muscle cells. 289 30

The disappearance and metabolic clearance rate (MCR) of alpha human atrial natriuretic peptide (alpha h-ANP) has been studied in normal man by radioimmunoassay of the atrial peptide in plasma and plasma extracts. After an intravenous (iv) bolus injection of 100 micrograms alpha h-ANP, levels of immunoreactive alpha h-ANP (IR-alpha hANP) in unextracted plasma fell rapidly and exponentially during the first 10 min (t1/2 = 2.5 min), after which levels declined more slowly to reach basal values 30 min after injection. Venous plasma extracts, purified by Sep Pak cartridges, were used to calculate the MCR of IR-alpha hANP under steady state conditions of constant iv infusion (200 micrograms over 60 min) in healthy volunteers. Calculated MCR from venous samples was 2.4 L/min and volume of distribution 10.7 L. After cessation of infusions, the disappearance rate (rapid phase) of IR-alpha hANP was 3.1 min. These studies show that alpha h-ANP is rapidly metabolized at rates similar to other vasoactive hormones such as angiotensin II and vasopressin.
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PMID:Metabolic clearance rate and plasma half life of alpha-human atrial natriuretic peptide in man. 293 12

Plasma levels of immunoreactive alpha human atrial natriuretic peptide (IR-ANP) were measured in nine patients with chronic renal failure before and after removal of 1.3-3.7 litres of fluid by ultrafiltration and again during volume repletion with intravenous sodium chloride solution (150 mmol/l: saline). Baseline levels of IR-ANP were elevated but fell by 22% during ultrafiltration. Saline infusion induced a rapid and steep rise in IR-ANP levels which were 150% of baseline while body weight was still 2% below baseline. Changes in plasma renin, angiotensin II, aldosterone and vasopressin during the study were slight compared with the change in IR-ANP, but noradrenaline levels rose threefold during ultrafiltration. There was a significant positive relationship between arterial pressure and IR-ANP levels before and after ultrafiltration. These results lend support to the suggestion that atrial peptides are of physiological importance, especially in states of chronic fluid overload such as chronic renal failure.
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PMID:Exaggerated responsiveness of immunoreactive atrial natriuretic peptide to saline infusion in chronic renal failure. 294 53

Plasma levels of ANP were measured during a 4 hrs head-down tilt at -6 degrees in 5 healthy male volunteers (aged 20-22 M.2). The experiments took place from 8 to 14 hrs, (day), and from 22 to 7 hrs (night). The control period was 1 hr. in a seated position (8 to 9 hrs. for day and 22 to 23 hrs. for night). Blood samples were collected at 9 and 23 hrs. and every 20 min. during the first hours, and every hours thereafter. Electroencephalograms were continuously recorded during night. Our results showed a similar increase in ANP during both experimental conditions. During night there was no correlations between ANP and sleep stages. Finally the differences observed in renal responsiveness to central volume expansion during day or night could not be explained by a difference in renin, aldosterone, vasopressin (previously demonstrated in several studies) or ANP secretion.
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PMID:[Plasma variation of atrial natriuretic peptide in central hypervolemia (diurnal or nocturnal) induced by antiorthostatic decubitus at -6 degrees]. 295 28

Continuous intravenous infusion of rat atrial natriuretic peptide (rANP) was carried out for 60 min in urethan-anesthetized rats. Plasma rANP (PANP) levels during 0, 12.5, and 50 ng/min rANP infusion reached 20.9 +/- 3.4, 61.2 +/- 12.3, and 228 +/- 30.6 pg/ml, respectively. Urinary sodium excretion (UNaV) remained unchanged during the 0 and 12.5 ng/min rANP infusion. In contrast, the 50 ng/min rANP infusion resulted in a 5.6-fold increase in UNaV without significant changes in plasma aldosterone levels and glomerular filtration rate. Isotonic saline infusion (116 microliter/min for 60 or 120 min) caused a significant increase in UNaV. UNaV in an experimental model of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) was 5.0 times greater than in control animals. PANP levels in 60- or 120-min saline-infused and SIADH rats were 46.3 +/- 6.7, 39.0 +/- 9.0, and 35.6 +/- 3.2 pg/ml, respectively. These values were significantly higher than control values but failed to achieve a level at which natriuresis occurred during the infusion of rANP. These results suggest that endogenous ANP may not play a critical role in the induction of acute natriuresis in volume-expanded states, although it could be partially involved in such a natriuretic response.
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PMID:Role of atrial natriuretic peptide in natriuresis in volume-expanded rats. 296 11

ANP harbors truly remarkable properties in having demonstrable interactions at several key loci of the systems that control blood pressure and extracellular fluid volume. The discovery of ANP by deBold and colleagues succeeded in bringing together neighboring scientists (that is, nephrologists, endocrinologists, cardiologists, and vascularologists), whose research efforts do not often coalesce, in attempts to define the pharmacology and physiology of this peptide. Although we have witnessed a tremendous explosion of interest and work over the past 6 years, several areas of research need to be pursued to obtain these goals. ANP appears to lower blood pressure by reducing either afterload or preload, with the sympathetic state of the individual having an important modulating effect. ANP causes an increased renal secretion of electrolytes, although there is yet to be uniform agreement on the underlying mechanism(s). The depressor and natriuretic effects of ANP act in harmony with an inhibitory effect on the release of aldosterone, renin, and vasopressin. Although this intriguing pharmacologic foundation of ANP has been laid, the physiologic role or importance is still in question. Nonetheless, as we gain further insight into the pharmacology, we stand to advance our knowledge of, and hopefully develop more useful regimens for, cardiovascular and renal pathologic states. As would be expected of an agent that may interact at multiple regulatory sites for control of hemodynamics and fluid volume, differences will most likely exist among species in the pharmacology of ANP, not only as a function of structure-activity relationships but also as a consequence of phylogenic differences in the integration of cardiovascular control.
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PMID:Pharmacologic effects of atrial natriuretic peptide. 296 64

Human alpha-atrial natriuretic peptide (h-alpha ANP) makes the urine of dehydrated volunteers hypotonic to plasma despite high circulating concentrations of antidiuretic hormone. Urinary dilution with h-alpha ANP also occurs in subjects receiving indomethacin. Therefore, h-alpha ANP antagonises effects of antidiuretic hormone on distal tubular V2-receptors in man, probably without involving prostaglandins.
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PMID:Antagonism of V2-receptor effect of antidiuretic hormone by atrial natriuretic peptide in man. 296 73

Previous investigations have shown that rat atrial natriuretic peptide (r-ANP,5-28, atriopeptin III), antagonizes the effects of various pressor hormones (angiotensin II, vasopressin and norepinephrine) but is ineffective against pressor responses to acute spinal cord stimulation. Because the latter are believed to be mediated by intrajunctional alpha-1 adrenoceptors, whereas the others are thought to involve mainly extrajunctional receptors, we explored the possible specificity of r-ANP for alpha adrenoceptor subtypes, by comparing r-ANP, the calcium channel blocker nifedipine and the vasodilator sodium nitroprusside in their ability to inhibit pressor responses to the alpha-2 and alpha-1 adrenoceptor agonists, clonidine and phenylephrine, in pithed, vagotomized rats. Acute pressor responses to bolus-injected clonidine were dose-dependently attenuated by both r-ANP (up to 21%) and nifedipine (up to 37%), but acute pressor responses to phenylephrine were unaffected. Sodium nitroprusside inhibited pressor responses to clonidine (up to 67%) and phenylephrine equally (up to 66%). Pressor responses during constant infusions of clonidine and phenylephrine were attenuated similarly by r-ANP and nifedipine. This pattern of results, alpha-2 adrenoceptor specificity during immediate pressor responses but not during sustained pressor responses, suggests that r-ANP, like nifedipine, attenuates those adrenoceptor-mediated pressor responses which depend on slow transmembrane calcium fluxes.
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PMID:Differential inhibition of alpha adrenoceptor-mediated pressor responses by rat atrial natriuretic peptide in the pithed rat. 299 43


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