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Dietary Nitrate Reduces Blood Pressure in Rats With Angiotensin II-Induced Hypertension via Mechanisms That Involve Reduction of Sympathetic Hyperactivity
Karolinska Inst, Dept Physiol & Pharmacol, Stockholm, Sweden;Univ Fed Paraiba, Ctr Biotechnol, Joao Pessoa, Paraiba, Brazil.
Karolinska Inst, Dept Physiol & Pharmacol, Stockholm, Sweden;Univ Fed Paraiba, Ctr Biotechnol, Joao Pessoa, Paraiba, Brazil.
Univ Fed Paraiba, Ctr Biotechnol, Joao Pessoa, Paraiba, Brazil.
Karolinska Inst, Dept Physiol & Pharmacol, Stockholm, Sweden.ORCID iD: 0000-0002-6002-6670
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2019 (English)In: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 73, no 4, p. 839-848Article in journal (Refereed) Published
Abstract [en]

Several experimental and clinical studies have shown that dietary nitrate supplementation can increase nitric oxide bioavailability. In the oral cavity, commensal bacteria reduce nitrate to nitrite, which is subsequently absorbed into the circulation where reduction to nitric oxide by enzymatic systems occur. Although it is well-known that boosting the nitrate-nitrite-nitric oxide pathway can improve cardiovascular, renal, and metabolic functions and that sympathoexcitation contributes to the development of the same disorders, the potential effects of dietary nitrate on sympathetic activity remain to be elucidated. In this study, we hypothesized that treatment with inorganic nitrate could prevent the increase in sympathetic nerve activity in an experimental model of Ang II (angiotensin II)-induced hypertension. Multiple in vivo approaches were combined, that is, Wistar rats orally treated with the nitric oxide synthase inhibitor L-NAME (N(G)-nitro-L-arginine methyl ester, 0.5 g/L) and implanted with subcutaneous osmotic minipump for continuous delivery of Ang II (120 ng/kg per minute; 14 days). Simultaneously, rats were supplemented with sodium nitrate (10 mmol/L) or placebo (sodium chloride; 10 mmol/L) in the drinking water. Blood pressure, heart rate, and renal sympathetic nerve activity were recorded. In placebo-treated rats, Ang II+ L-NAME treatment-induced arterial hypertension, which was linked with reduced spontaneous baroreflex sensitivity and increased renal sympathetic nerve activity, as well as upregulation of AT 1 Rs (Ang II type-1 receptors) in the rostral ventrolateral medulla. Supplementation with nitrate normalized the expression of AT 1 Rs in rostral ventrolateral medulla and reduced sympathetic nerve activity, which was associated with attenuated development of hypertension. In conclusion, chronic dietary nitrate supplementation blunted the development of hypertension via mechanisms that involve reduction of sympathetic outflow.

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2019. Vol. 73, no 4, p. 839-848
Keywords [en]
angiotensin II, blood pressure, hypertension, kidney, nitric oxide, sodium nitrate, sympathethic activity
National Category
Physiology
Identifiers
URN: urn:nbn:se:uu:diva-387561DOI: 10.1161/HYPERTENSIONAHA.118.12425ISI: 000469351200012PubMedID: 30712424OAI: oai:DiVA.org:uu-387561DiVA, id: diva2:1330083
Funder
Swedish Research Council, 2016-01381Swedish Heart Lung Foundation, 20180568 20170124Available from: 2019-06-25 Created: 2019-06-25 Last updated: 2019-06-25Bibliographically approved

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