Anomalous antidiuretic activity of antidiuretic hormone antagonists

Kinter, Lewis B.; Caltabiano, S; Huffman, William F.

doi:10.1016/0006-2952(93)90427-x

Cited by 18 publications

(12 citation statements)

References 28 publications

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“…Furthermore, it has been postulated that the vasodilation and associated release o f coagulation and fibrinolysis factors occurring in response to arginine vasopressin and DD-arginine vasopressin administration is neither mediated by V \ nor by V2 receptors because studies in rat aortae and in conscious dogs have revealed an absence o f inhibition both by V] and by Vo antagonists [22,23]. T he most plausible reason for this confusion seems to be the variability in the pharmacological profile of agonists and/or antagonists that has been suggested to exist among species, between in vitro and in vivo studies and among different vascular beds [6][7][8].…”

Section: Discussionmentioning

confidence: 99%

“…The vascular effects of Vo receptor antagonists have only recently been examined in a human in vivo study, which appeared to confirm that in the hum an forearm V 2 receptors are involved in the vasodilatory effect of arginine vasopressin [5]. However, these conclusions need to be considered with caution, because most V2 receptor antagonists show partial Vj receptor antagonism and their putative specificity has been based mainly on their aquaretic potencies in animals [6][7][8]. However, studies in patients with X-linked nephrogenic diabetes insipidus have provided convincing evidence for involvement of the V2 receptor in the vasodilatory actions of DD-arginine vasopressin [25].…”

Section: Discussionmentioning

confidence: 99%

“…A less well-known effect o f arginine vasopressin is vasodilation, which has been found to occur in response to high local concentrations o f the horm one [1][2][3][4][5]. Attempts to assess the type of receptor mediating this va so dilatory action have yielded contradictory results, with discrepancies between in i>u>o and in vitro studies, among diflerent species and among vascular beds [6][7][8]. h i vivo studies using Vj receptor antagonists have indicated that the vasodilation occur ring in response to high doses of arginine vasopressin is mediated by Vo receptors [1,3,[9][10][11][12][13], an observation w hich is in accord with the vasodilatory effect of the V 2 receptor agonist l-desam ino-8 -U (DD)-arginine vasopressin [1], Furthermore, recent investigations have suggested a role for endothelium-derived nitric oxide in the vasodilator response to arginine vasopressin [4,[14][15][16][17].…”

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confidence: 99%

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Effects of arginine vasopressin and 1-desamino-8-D arginine vasopressin on forearm vasculature of healthy subjects and patients with a V2 receptor defect

Lieburg

Knoers

Monnens³

et al. 1995

Journal of Hypertension

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Objectives: To assess which vasopressin receptor subtype mediates the vasodilation occurring in response to arginine vasopressin and 1-desamino-8-D (DD)-argtnine vasopressin and whether nitric oxide is involved in these effects.Materials and methods: Vasoactive effects of arginine vasopressin and DD-arginine vasopressin on forearm vasculature were studied in healthy subjects and in patients with congenital nephrogenic diabetes insipidus with a vasopressin type 2 (V 2) receptor gene defect. Venous occlusion plethysmography was used to assess the forearm blood flow responses to the infusion of arginine vasopressin and its analogue into the brachial artery, in the presence and the absence of the nitric oxide synthase inhibitor L-NG-monomethyl-arginine (l-NMMA).Results: In healthy subjects (n-10), DD-arginine vasopressin (0.1, 1 and 10 or 5, 10 and 20ng/min per dl) induced a dose-related increase in forearm biood flow, but did not affect forearm blood flow in the patients with nephrogenic diabetes insipidus (n = 3). In two healthy subjects, seven increasing doses of arginine vasopressin (0.25-12 ng/min per dl) induced an initial decrease in forearm blood flow and then a gradual increase. In one of the patients, the same arginine vasopressin doses produced a persistent decrease in forearm blood flow. In the healthy subjects, infusion of l-NM MA reduced forearm blood flow significantly (n = 10). Subsequent administration of DD-arginine vasopressin during l-N M M A infusion produced a slight reduction in the forearm blood flow increase compared with DD-arginine vasopressin alone, but this was significant only for the absolute forearm blood flow increase induced by 10 ng/min per dl in all subjects. Infusion of arginine vasopressin in the presence of l-NM MA did not increase forearm blood flow significantly.Conclusions: In human forearm vasculature, extrarenal V 2 receptors mediate the vasodilation induced by DD-arginine vasopressin or high doses of arginine vasopressin, whereas these receptors are not necessary for arginine vasopressininduced vasoconstriction. The DD-arginine vasopressin-induced vasodilation seems to be mediated predominantly by a mechanism other than endothelial nitric oxide release, whereas arginine vasopressin-induced vasodilation seems to involve nitric oxide release only.journal of Hypertension 1995, 13:1695-1700 9

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Effects of arginine vasopressin and 1-desamino-8-D arginine vasopressin on forearm vasculature of healthy subjects and patients with a V2 receptor defect

Lieburg

Knoers

Monnens³

et al. 1995

Journal of Hypertension

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“…Marked species heterogeneity exists for peptide V, receptor antagonists in vivo which has complicated their development as selective water diuretics (Kinter et al 1993). The description of OPC-3 1260 was particularly interesting as this was the first non-peptide V, antagonist to increase freewater clearance in humans (Ohnishi et al 199.5).…”

Section: Congestive Heart Failurementioning

confidence: 99%

Vasopressin receptor antagonism — a therapeutic option in heart failure and hypertension

Burrell

Risvanis

Johnston

et al. 2000

Experimental Physiology

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The precise role of vasopressin in the pathophysiology of cardiovascular disease is controversial, but this peptide hormone is important for several reasons. Firstly, circulating concentrations of vasopressin are elevated in heart failure and some forms of hypertension. Secondly, there is evidence that vasopressin is synthesized not only in the hypophysial-pituitary axis but also in peripheral tissues including the heart where it acts as a paracrine hormone. Thirdly, vasopressin has vasoconstrictor, mitogenic, hyperplastic and renal fluid retaining properties which, by analogy with angiotensin 11, may have deleterious effects when present in chronic excess. Finally, the availability of orally active non-peptide vasopressin receptor antagonists allows vasopressin receptor antagonism to be considered as a therapeutic option in cardiovascular disease. Experimental Physiology (2000) 85S, 259s-265s. VasopressinVasopressin is a major hormonal system in the body responsible for blood pressure homeostasis and for salt and water balance (Johnston, 1985; Phillips et al. 199%). Vasopressin belongs to a family of vasoactive and mitogenic peptides and has multiple actions including inhibition of diuresis, contraction of vascular smooth muscle, trophic actions, platelet aggregation, stimulation of Von Willebrand factor, liver glycogenolysis and central regulation of blood pressure and the baroreflex (Johnston, 1985; Phillips et al. 1 9 9 5~; Sampey et al. 1999). Vasopressin exerts its actions through binding to typical heptahelical transmembrane G-proteincoupled receptors with distinct second messenger systems; the V,, (vascular, hepatic) and V,, (anterior pituitary) receptors through phosphatidylinosilol hydrolysis to mobilize calcium, and the V, (kidney) receptor through adenylyl cyclase. In addition to its classical vasopressor action via the VIA receptor, vasopressin mediates vasodilatation through renal V,-like receptors (Naitoh et al. 1993; Burrell et al. 1994a). To date more than ten related complementary DNAs have been cloned and sequenced (Bichet, 1996) including rat and human vasopressin V,, receptors, human V,, receptor, rat and human V, receptors and sheep VIA receptors (Hutchins et al. 1995). These receptors are strikingly similar in both size and amino acid sequence. Vasopressin and cardiovascular disease

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“…Several peptide V 2 R antagonists have been developed, but they are plagued by several shortcomings including agonist properties, species specificity, poor receptor sub-type selectivity and lack of oral bioavailability [18,19]. These limitations set the stage for the development of orally active non-peptide V 2 R selective antagonists.…”

Section: Medical Needmentioning

confidence: 99%

Aquaretics

Thibonnier¹

1999

Emerging Drugs

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Anomalous antidiuretic activity of antidiuretic hormone antagonists

Cited by 18 publications

References 28 publications

Effects of arginine vasopressin and 1-desamino-8-D arginine vasopressin on forearm vasculature of healthy subjects and patients with a V2 receptor defect

Effects of arginine vasopressin and 1-desamino-8-D arginine vasopressin on forearm vasculature of healthy subjects and patients with a V2 receptor defect

Vasopressin receptor antagonism — a therapeutic option in heart failure and hypertension

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