6533b853fe1ef96bd12ad77e

RESEARCH PRODUCT

V2-receptor–mediated relaxation of human renal arteries in response to desmopressin

Gloria SegarraPascual EmedinaCristina Benlloch DomènechPascual ChuanJosé M. VilaSalvador Lluch

subject

AdultMaleAgonistReceptors VasopressinVasopressinmedicine.medical_specialtymedicine.drug_classMuscle RelaxationIndomethacinIn Vitro TechniquesRenal AgentsMuscle Smooth VascularRenal ArteryIsometric ContractionArginine vasopressin receptor 2Internal medicineInternal MedicinemedicineHumansCyclooxygenase InhibitorsDeamino Arginine VasopressinEnzyme InhibitorsDesmopressinReceptorAgedVasopressin receptorbusiness.industryAntidiuretic Hormone Receptor AntagonistsMiddle AgedVasodilationNG-Nitroarginine Methyl EsterEndocrinologyCirculatory systemProstaglandinsFemaleNitric Oxide SynthasebusinessAntidiuretic Hormone Receptor Antagonistshormones hormone substitutes and hormone antagonistsmedicine.drug

description

The effects of deamino-8-D-arginine vasopressin (desmopressin), a V2 receptor antidiuretic agonist, were studied in isolated rings from branches of renal arteries obtained from 22 patients undergoing nephrectomy. The rings were suspended in organ bath chambers for isometric recording of tension. In precontracted rings with norepinephrine (10(-6) to 3 x 10(-6) mol/L), desmopressin (10(-11) to 3 x 10(-7) mol/L) caused endothelium-dependent relaxation (81%+/-4% reversal of the initial contraction in arteries with endothelium; 20%+/-4% in arteries without endothelium; P < .05). The relaxation to desmopressin in rings with endothelium was reduced significantly by indomethacin (10(-6) mol/L) and unaffected by the inhibitor of nitric oxide synthase NG-nitro-L-arginine methyl ester (10(-4) mol/L). Two V1 receptor antagonists (a peptidic and a nonpeptidic) had no effect on desmopressin-induced relaxation. However, V2 receptor antagonists (three peptidic and a nonpeptidic) reduced significantly (P < .05) the maximal response to desmopressin. The results of this study show that desmopressin exerts powerful endothelium-dependent relaxation of human renal arteries, probably through stimulation of V2-like receptors that may bring about the release of dilating prostaglandins.

https://doi.org/10.1016/s0895-7061(98)00230-1