Salt and Nitric Oxide Inhibition Induced Hypertension: The Role of Prostacycline and 8-Isoprostane

Abstract

Renal prostacycline (PGI(2)) and oxidative stress are known to be important factors that effect the natriurezis and diuresis. 8-iso prostaglandin F(2)α± (8-isoprostane), a member of F(2)-isoprostanes, is formed from the nonenzymatic reaction of arachidonic acid and oxygen radicals in vivo and in vitro, and also it is a marker of oxidative stress in vivo. The aim of this study is to determine the role of renal PGI(2) and 8-isoprostane in a salt and nitric oxide (NO) inhibition-induced hypertension model. Rats were distributed equally among four groups (n = 6 per group). Control rats were given normal salt diet (0.32%); high-salt (HS) rats were given high salt diet (3.2%); NG-nitro-L-arginine (L-NNA) rats were given normal salt diet and 25 mg/kg L-NNA; HS+L-NNA rats were given high salt diet and 25 mg/kg L-NNA. Rats were placed in individual metabolic cages for 17 days. Systolic blood pressure (SBP) was measured at days initial, 7th and 14th .Urinary 8-isoprostane and PGI(2) levels were analyzed. Salt- loading alone did not change SBP values. The average SBP in L-NNA and HS+L-NNA groups were shown to significantly enhance compared to initial and day 7th in the same groups, respectively. The levels of 8-isoprostane in the HS+L-NNA group was significantly enhanced compared to the other groups. L-NNA or HS diet alone did not change the levels of 8-isoprostane compared to the control group. L-NNA alone did not change PGI(2) levels in urine compared to the control. PGI(2) levels in the HS, and the HS+L-NNA group was significantly higher compared to the control group. This study concluded that NOS inhibition plus salt-loading induced oxidative stress and increased renal PGI(2). Also, it is suggested that augmented oxidative stress may aggravate the hypertension. But the renal synthesis of PGI(2) is increased in order to augment the diuresis and natriuresis without the effect of blood pressure (BP).

Comparative Effectıveness of Novokinin, Perindopril and Losartan on Blood Pressure, Adma, Nadph Oxidase and Rho Kinase at Renal Tissue in L-Name and Salt Induced Hypertension

“…The blood pressure was numerically higher by the 28th day, but there was no significant difference between the 14th and 28th days. These results were similar with previous study [17][18][19]. Treatments of the losartan, perindopril or novokinin to L-NAME and salt administration groups lowered the blood pressure significantly.…”

Assessment of lifestyle effect on oxidative stress biomarkers in free‐living elderly in rural Japan

“…Reports about gender and oxidative stress are controversial; our findings are consistent with a previous report that reported no gender differences in urinary 8‐isoprostane, 19 but are inconsistent with the study by Sakano et al ., which found higher levels of 8‐isoprostane in men and a negative association between urinary 8‐isoprostane and age 17 . 8‐Isoprostane was found to correlate positively with systolic blood pressure in females, meaning that increased levels of 8‐isoprostane might contribute to the development or progression of hypertension 20 . 8‐Isoprostane is believed to be high in patients with hypertension.…”

“…17 8-Isoprostane was found to correlate positively with systolic blood pressure in females, meaning that increased levels of 8-isoprostane might contribute to the development or progression of hypertension. 20 8-Isoprostane is believed to be high in patients with hypertension. However, in the present study, levels of 8-isoprostane were not different between hypertensive participants and normotensive participants.…”

Novel Concepts in the Genesis of Hypertension: Role of LOX-1

“…It is well known that hypertension is associated with increased vascular oxidative stress, although there is an ongoing debate whether oxidative stress is a cause or a result of hypertension [1,2,19]. Oxidative stress has been demonstrated in patients with essential/spontaneous hypertension, renovascular hypertension, malignant hypertension, and pre-eclampsia, as well as in experimental models such as Ang II-mediated hypertension, Dahl saltsensitive hypertension, lead-induced hypertension, obesityassociated hypertension, mineralocorticoid hypertension, aldosterone-provoked hypertension, nitric oxide synthase inhibitor-induced hypertension and cyclosporine-induced hypertension [20][21][22][23][24][25][26][27][28][29][30][31][32]. Oxidative stress may contribute to the generation and/or maintenance of hypertensive state via a number of possible mechanisms.…”