Oxidative stress may explain how hypertension is maintained by normal levels of angiotensin II

Abstract

It is well known that essential hypertension evolves in most patients with near normal levels of plasma renin activity. However, these levels appear to be responsible for the high levels of arterial pressure because they are normalized by the administration of angiotensin II converting inhibitors or angiotensin receptor antagonist. In experimental animals, hypertension can be induced by the continuous intravenous infusion of small doses of angiotensin II that are not sufficient to evoke an immediate pressor response. However, this condition resembles the characteristics of essential hypertension because the high levels of blood pressure exist with normal plasma levels of angiotensin II. It is suggested that small amounts of angiotensin whose plasma levels are inappropriate for the existing size of extracellular volume stimulate oxidative stress which binds nitric oxide forming peroxynitrite. The latter compound oxidizes arachidonic acid producing isoprostaglandin F2a (an isoprostane) which is characterized by a strong antinatriuretic vasoconstrictor renal effect. In this chain of reactions the vasoconstrictor effects derived from oxygen quenching of nitric oxide and increased isoprostane synthesis could explain how hypertension is maintained with normal plasma levels of renin. Correspondence

Hubungan Kadar Timbal Dalam Darah Dengan Tekanan Darah Pada Tenaga Kerja Di Karoseri Semarang

“…31 Sejumlah kecil angiotensin dalam plasma darah akan merangsang stres oksidatif yang dapat mengikat nitrat oksida. 32 Hasil penelitian Sirivarasai J, dkk menyimpulkan bahwa ada hubungan sebab akibat antara paparan timbal dan peningkatan tekanan darah. Paparan timbal kadar rendah yang terkait dengan stres oksidatif dan defisiensi enzim katalase dapat berkontribusi terhadap hipertensi.…”

Nitrate Tolerance

“…6,7 The activation of the renin-angiotensin-aldosterone axis and the increased angiotensin II production during tolerance might mediate both processes. Furthermore, the recent demonstration that GTN treatment causes increased levels of isoprostanes, 8 given their direct vasoconstrictor and antinatriuretic effects, 9 provides an additional, redox-mediated explanation. Finally, changes in the redox state in the endothelial cellular milieu, and, in particular, changes in the availability of reduced thiol groups, might induce abnormalities in microvascular permeability.…”

Involvement of TP and EP3 Receptors in Vasoconstrictor Responses to Isoprostanes in Pulmonary Vasculature

“…In the pulmonary vein, 8-iso-PGE 2 can also act upon another type of excitatory receptor, likely EP 3 receptors or possibly a unique isoprostane receptor. This may represent an important mechanism during hypertension, which is characterized in part by production of large amounts of isoprostanes (Jankov et al, 2000;Romero and Reckelhoff, 2000).…”