Role of nitric oxide in the arterial pressure and renal adaptations to long-term changes in sodium intake
| Autor: | L. Hu, Manning Rd, J. F. Reckelhoff |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
medicine.medical_specialty
Vasopressin Time Factors Physiology Acclimatization Sodium chemistry.chemical_element Blood Pressure Kidney Nitric Oxide Plasma renin activity Renal Circulation Nitric oxide Excretion chemistry.chemical_compound Dogs Heart Rate Reference Values Physiology (medical) Internal medicine Renin medicine Animals Nitrite Infusions Intravenous Aldosterone Nitrites Nitrates Hemodynamics Sodium Dietary Diet Sodium-Restricted Arginine Vasopressin NG-Nitroarginine Methyl Ester Blood pressure Endocrinology chemistry Regional Blood Flow Vascular Resistance Glomerular Filtration Rate |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 272:R1162-R1169 |
| ISSN: | 1522-1490 0363-6119 |
| DOI: | 10.1152/ajpregu.1997.272.4.r1162 |
| Popis: | The goals of this study were to determine whether long-term nitric oxide (NO) synthesis inhibition in dogs results in an increase in the sodium sensitivity of arterial pressure and whether changes in plasma renin activity or the plasma concentrations of arginine vasopressin (AVP) and aldosterone play an important role in this hypertension. Studies were conducted in a control group and groups that received NO inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) at 10 or 25 microg x kg(-1) x min(-1). Each group was challenged with normal, low, and high sodium intake for periods of 5 days each. Urinary nitrate + nitrite excretion (UNOx) more than doubled in the control group during high sodium intake. In both L-NAME groups, UNOx decreased significantly, there was a hypertensive shift in the relation between urinary sodium excretion and arterial pressure, and urinary sodium excretion remained normal even in the high-sodium intake period. L-NAME infusion did not change the sodium sensitivity of arterial pressure or plasma renin activity, plasma aldosterone, and plasma AVP. In conclusion, the data suggest that, in dogs, increases in NO synthesis are not necessary to excrete a chronic sodium load, and decreases in NO do not increase the sodium sensitivity of arterial pressure. |
| Databáze: | OpenAIRE |
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