Metabolism of Neurohypophyseal Hormones: Considerations from a Molecular Viewpoint1

Walter, R.; Simmons, William H.

doi:10.1159/000400594

Cited by 21 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, Shimizu et al (1980) showed that dDAVP was resistant to the homogenates of the rat kidneys or liver, which might partly explain the elongated antidiuretic effect of dDAVP compared with AVP. Although there is no direct evidence that the AVP degrading enzymes or reagents employed in the present study play a role in inactivating AVP or dDAVP in vivo, it has been suggested that enzymes which possess chymotrypsin-like or trypsinlike activity may inactivate AVP in vivo by releasing glycinamide (Gly-NH2) and that aminopeptidase in rat kidney plays a significant role in inactivating AVP (Walter and Simmons 1977). Furthermore, thiol-disulfide oxydoreductase isolated from rat liver has also been felt to inactivate AVP by reducing disulfide (Walter and Simmons 1977).…”

Section: Discussionmentioning

confidence: 70%

“…Late pregnancy plasma has been reported to contain a cystine aminopeptidase, vasopressinase or oxytocinase, which inactivates AVP and oxytocin by splitting the bond between the amino-terminal hemicystine and tyrosine at positions 1 and 2 (Tuppy 1968;Walter and Simmons 1977). Accordingly, it is likely that deamination of hemicystine at position 1 causes resistance to the action of vasopressinase.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Resistance of 1-deamino-(8-D-arginine)-vasopressin to in vitro degradation as compared with arginine vasopressin.

et al. 1985

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Resistance of 1-deamino-(8-D-arginine)-vasopressin to in vitro degradation as compared with arginine vasopressin.

et al. 1985

View full text Add to dashboard Cite

show abstract

“…Indeed, our present data indicate that levels of AVP were significantly higher in the anephric rats than in those with kidneys in situ (Groups 2 and 3 vs Groups 6 and 7 in table 1), which is compatible with knowledge of the kidney's participation in the clearance of AVP. 9 Catecholamines also tended to be higher in anephric rats than in their counterparts with intact kidneys, but only the levels of epinephrine were significantly higher in the anephric model with intact sympathetic system. Treatment with combination of reserpine and metyrosine was chosen as an effective and rapid way to eliminate catecholamines.…”

Section: Discussionmentioning

confidence: 89%

Interaction of the sympathetic nervous system with vasopressin and renin in the maintenance of blood pressure.

Gavras¹,

Hatzinikolaou²,

North³

et al. 1982

Hypertension

View full text Add to dashboard Cite

SUMMARY To evaluate the partial contributions and interaction of three vasopressor systems in blood pressure maintenance, nephrectomized rats and rats with intact kidneys were submitted sequentially to catecholamine depletion, elimination of vasopressin's vasoconstrictor action, and (for those with kidneys in situ) angiotensin blockade. Catecholamine depletion decreased blood pressure and stimulated vasopressin levels in all rats, but significantly more so in the anephric ones. Subsequent injection of an antagonist to the vasopressor effect of vasopressin produced a lasting fall of blood pressure in anephric rats, but only transient fall in those with intact kidneys. Infusion of teprotide -an angiotensin converting enzyme inhibitor -in the latter animals also produced transient blood pressure fall, but if this were followed by injection of the vasopressin antagonist, the pressure remained low for several hours. Blood pressure levels were closely correlated with those of plasma catecholamines throughout these maneuvers. Catecholamine levels were inversely correlated with those of plasma vasopressin, which were far greater in anephric rats through both stimulation and accumulation. Plasma renin activity was increasingly stimulated by falling blood pressure after each maneuver in rats with intact kidneys. Thus, it appears that in the resting state the sympathetic nervous system is more involved in the maintenance of blood pressure, whereas vasopressin and renin are important backup mechanisms. The present experiments were designed to evaluate the contribution of each one of these three vasopressor systems to the maintenance of normal blood pressure. Catecholamine depletion and bilateral nephrectomy were intended to produce conditions comparable -albeit extreme -to those likely to be encountered in the therapy of human hypertension, e.g., treatment with sympatholytic agents and advanced renal failure. Under these conditions, we studied the interaction and relationships of catecholamines, vasopressin, and the renin-angiotensin system.

show abstract

“…The natural hormones are subjected to rapid enzymatic degradation in vivo. Four sites of cleavage have been identified, the most important of which appear to be at posi tions 7-8 and 8-9 in the linear portion of the peptide; the disulfide bond and positions 1-2 are also sites of modification by a variety of enzymes in kidney, brain, liver and uterus [24], The kidney and liver are the major sites of metabolic clearance.…”

Section: Vasoactive Drugsmentioning

confidence: 99%

Clinical Pharmacology of Active Variceal Bleeding

Scarpignato¹

1992

Dig Dis

View full text Add to dashboard Cite

Although the mechanism initiating and maintaining variceal hemorrhage is not completely understood, there has been general agreement in recent years on the concept that variceal rupture occurs when the tension on the wall of the varices reaches a critical value (the rupture point) that leads to the leakage of the elastic components of the wall. If this hypothesis is true, the aim of pharmacological treatment should be to reduce variceal wall tension or to prevent any abrupt increase in this parameter. Some vasoconstrictor drugs are currently used in order to achieve these goals and in the attempt to stop the acute bleeding episode. All these agents decrease either portal pressure and azygos blood flow. Vasopressin although effective, has significant cardiac and gastrointestinal adverse effects that discourage its use. Combination with nitroglycerin reduces its adverse effects while maintaining or even enhancing the reduction in portal pressure. Glypressin, which acts as a slow-release preparation of vasopressin, has a longer duration of action and can be administered as single intravenous injections instead of continuous infusion. However, the similarity of effects of these drugs on systemic circulation leads to an overlapping spectrum of untoward effects. Somatostatin and the synthetic octapeptide octreotide display similar pharmacological effects on splanchnic hemodynamics but have a better tolerability profile. Thanks to its longer duration of action and ease of administration, octreotide could become the drug of choice for the early, pre-hospital management of bleeding varices. A different approach to the pharmacological treatment of variceal bleeding may be the use of compounds, like metoclopramide and domperidone, that increase the lower esophageal sphincter pressure (LESP), thereby reducing the inflow of blood flow into the submucous venous plexus of the esophagus and hence into the esophageal varices. However, more studies are needed before these compounds be considered a real alternative to the above established drugs.

show abstract

Metabolism of Neurohypophyseal Hormones: Considerations from a Molecular Viewpoint1

Cited by 21 publications

References 0 publications

Resistance of 1-deamino-(8-D-arginine)-vasopressin to in vitro degradation as compared with arginine vasopressin.

Resistance of 1-deamino-(8-D-arginine)-vasopressin to in vitro degradation as compared with arginine vasopressin.

Interaction of the sympathetic nervous system with vasopressin and renin in the maintenance of blood pressure.

Clinical Pharmacology of Active Variceal Bleeding

Contact Info

Product

Resources

About