Vasopressin Does not Effect Hypertension Caused by Long-Term Nitric Oxide Inhibition
| Autor: | C. Loichot, Jean-Louis Imbs, C. Cazaubon, D. Nisato, W. De Jong, Mariette Barthelmebs, Michèle Grima |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Male
medicine.medical_specialty Vasopressin Indoles Pyrrolidines Time Factors Systole Vasopressins Blood Pressure Kidney Nitric Acid Nitroarginine Plasma renin activity Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound Heart Rate Internal medicine Internal Medicine medicine Albuminuria Animals Enzyme Inhibitors biology business.industry Heart Organ Size Rats Nitric oxide synthase Endocrinology medicine.anatomical_structure Blood pressure chemistry Hypertension biology.protein Vascular resistance Nitric Oxide Synthase medicine.symptom business Antidiuretic Hormone Receptor Antagonists Vasoconstriction |
| Zdroj: | Hypertension. 35:602-608 |
| ISSN: | 1524-4563 0194-911X |
| DOI: | 10.1161/01.hyp.35.2.602 |
| Popis: | Abstract —Nitric oxide attenuates both vasopressin-induced vasoconstriction and vasopressin release. We tested whether hypertension and renal dysfunction elicited by chronic inhibition of nitric oxide (NO) synthesis using N G -nitro- l -arginine (L-NNA) could be mediated in part by vasopressin V 1A receptors. Male rats were treated orally for 6 weeks with L-NNA (15 mg/kg per day), a nonpeptide V 1A receptor antagonist (2 S )-1-[(2 R ,3 S )-5-chloro-3-(2-chlorophenyl)-1-(3,4-dimethoxybenzene-sulfonyl)-3-hydroxy-2,3-dihydro-1 H -indole-2-carbonyl]-pyrrolidine-2-carboxamide (SR 49059, 30 mg/kg per day), or a combination of SR 49059 and L-NNA (same doses), or they received no treatment. Both drugs were added to the food. Measurements were performed in conscious rats (urine collection in metabolic cages, tail-cuff arterial pressure) and at the end of the study in anesthetized rats (clearance measurements). L-NNA produced sustained hypertension, decreased glomerular filtration rate, and increased renal vascular resistance, plasma renin activity, and urinary albumin excretion. SR 49059 had no effect per se on these parameters and also did not attenuate the hypertension and renal dysfunction induced by L-NNA. Surprisingly, SR 49059 potentiated L-NNA–induced hypertension at the end of the 6-week treatment. However, the blood pressure response and the renal and mesenteric vasoconstriction elicited by exogenous vasopressin were attenuated in rats treated with SR 49059. L-NNA did not change plasma vasopressin concentration or 24-hour urinary vasopressin excretion. Our findings suggest that activation of vasopressin V 1A receptors does not contribute to the hypertension and renal dysfunction induced by chronic NO synthesis inhibition. They also document unchanged plasma vasopressin concentration in NO-deficient hypertension. |
| Databáze: | OpenAIRE |
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