Abstract:
:Hypotensive effects of oral sodium nitrite have been reported as alternative sources of nitric oxide (NO) formation in animals and human beings. Reductions in NO bioavailability were observed in lead-induced hypertension. However, no previous study has examined whether a single daily dose of sodium nitrite prevents the reductions in the NO bioavailability in lead-induced hypertension. Then, we expanded previous reports and evaluated the effects of sodium nitrite in 7-day lead-treated rats. Wistar rats were divided into four experimental groups: Pb+sodium nitrite group received intraperitoneally (i.p.) 1st dose 8 µg/100 g of lead acetate and a subsequent dose of 0.1 µg/100 g, and daily treatment with sodium nitrite (45 mg/kg/day) or water (Pb group) by gavage for 7 days; Sodium nitrite group received i.p. 1st dose 8 µg/100 g of sodium acetate and a subsequent dose of 0.1 µg/100 g, and daily treatment with sodium nitrite (45 mg/kg/day) or water (saline group) by gavage for 7 days. Similar and higher whole-blood lead levels (11.5 ± 1.2 and 13.2 ± 0.7 µg/dL) were found in lead-exposed rats treated with either water or sodium nitrite (Pb or Pb+sodium nitrite, respectively; both p < 0.05 versus control groups). We found lower NO markers such as plasma nitrite and nitrite + nitrate (NOx) levels (both p < 0.05 versus controls) in lead-exposed rats compared with normotensive (sodium acetate)-treated controls (Pb group versus saline group; p < 0.05). Lead induced increases in systolic blood pressure (from 130 ± 2 to 164 ± 6 mmHg in Pb group; p < 0.05); however, both lead-induced decreases in NO markers and hypertension (Pb+sodium nitrite group versus Pb group; both p < 0.05) were prevented by a single daily dose of sodium nitrite. In conclusion, these findings are consistent with the idea that impaired NO bioavailability contributes to the maintenance of elevated blood pressure in lead-induced hypertension. Additionally, our results show that sodium nitrite exerts antihypertensive effects in lead-induced hypertension and provide evidence that sodium nitrite prevents the impairment of NO, thus, reaffirming the relevance of nitrite as alternative source of recycling back to NO.
journal_name
Basic Clin Pharmacol Toxicoljournal_title
Basic & clinical pharmacology & toxicologyauthors
Gonçalves-Rizzi VH,Nascimento RA,Possomato-Vieira JS,Dias-Junior CAdoi
10.1111/bcpt.12480subject
Has Abstractpub_date
2016-03-01 00:00:00pages
225-30issue
3eissn
1742-7835issn
1742-7843journal_volume
118pub_type
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