Salt-Sensitive Hypertension Resulting From Nitric Oxide Synthase Inhibition is Associated with Loss of Regulation of Angiotensin II in the Rat
| Autor: | V. Z. C. Ye, G. Hodge, K. A. Duggan |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Male
medicine.medical_specialty Sodium Angiotensinogen chemistry.chemical_element Blood Pressure Peptidyl-Dipeptidase A Rats Inbred WKY Plasma renin activity Renin-Angiotensin System chemistry.chemical_compound Internal medicine Renin Renin–angiotensin system medicine Animals Enzyme Inhibitors Sodium Chloride Dietary Aldosterone biology Angiotensin II General Medicine Rats Nitric oxide synthase NG-Nitroarginine Methyl Ester Endocrinology Blood pressure Losartan chemistry Hypertension biology.protein Angiotensin I Nitric Oxide Synthase hormones hormone substitutes and hormone antagonists medicine.drug |
| Zdroj: | Experimental Physiology. 87:1-8 |
| ISSN: | 0958-0670 |
| DOI: | 10.1113/eph8702322 |
| Popis: | In the Dahl salt-sensitive hypertensive rat, a diet containing L-arginine, the natural substrate for nitric oxide synthase, abrogates the hypertension. We postulated that nitric oxide synthase inhibition might induce a salt-sensitive form of hypertension and that this salt sensitivity might be linked to a loss of the regulatory effect of sodium ingestion on angiotensin II (Ang II) and angiotensinogen. Male Wistar-Kyoto rats were randomised to a diet containing 0.008 %, 2.2 % or 4.4 % sodium chloride and to treatment with the NO synthase inhibitor L-NAME (10 mg kg(-1) day(-1)) in the drinking water, or drinking water alone (Controls) for 4 weeks. Blood pressure was measured by tail cuff plethysmography twice weekly. After 4 weeks, the rats were anaesthetised and truncal blood collected for determination of angiotensinogen, renin, angiotensin I (Ang I), Ang II and aldosterone concentrations as well as angiotensin-converting enzyme (ACE) activity. Systolic blood pressure increased with increasing dietary sodium intake in the L-NAME-treated rats (P < 0.05). Plasma renin and aldosterone concentrations decreased with increasing dietary sodium intake in both Control and L-NAME-treated rats. Ang I and ACE activity were unchanged by increasing dietary sodium intake. In contrast, the plasma concentration of Ang II and angiotensinogen increased with increasing dietary sodium (P < 0.05 and P < 0.005, respectively). Treatment with the Ang II receptor blocker, losartan, reversed the blood pressure increase. We conclude that treatment with L-NAME induces an increase in blood pressure that is at least in part salt sensitive. Further, the salt-sensitive component appears to be Ang II-dependent, as it was associated with increasing plasma Ang II levels and could be reversed by treatment with an Ang II receptor antagonist. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text