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  • Title: Increased circulating vasopressin may account for ethanol-induced hypertension in rats.
    Author: Resstel LB, Scopinho AA, Lopes da Silva A, Antunes-Rodrigues J, Corrêa FM.
    Journal: Am J Hypertens; 2008 Aug; 21(8):930-5. PubMed ID: 18464746.
    Abstract:
    BACKGROUND: Long-term ethanol intake has been reported to evoke both hypertension and increase of systemic vasopressin levels in rats. METHODS: In this work, we investigated the involvement of systemic vasopressin in the hypertension evoked in rats by long-term ethanol (20% vol/vol) intake for 2 weeks, by systemic treatment with the V1-vasopressin receptor antagonist dTyr(CH2)5(Me)AVP (50 microg/kg). Moreover, plasma arginine-vasopressin (AVP) content was quantified using an AVP radioimmunoassay and the expression of vasopressin mRNA in the supraoptic (SON) and paraventricular (PVN) nuclei was measured using real-time PCR. RESULTS: Mild hypertension was observed after 2 weeks of ethanol treatment when compared with control animals. Moreover, an increase in both the expression of vasopressin mRNA and the vasopressin blood content was observed in ethanol-treated rats in comparison to the control group. Basal blood pressure levels of ethanol-treated animals were significantly reduced by IV treatment with the V1-vasopressin receptor antagonist dTyr(CH2)5(Me)AVP. However, dTyr(CH2)5(Me)AVP had no effect on the blood pressure of control animals. CONCLUSIONS: The results indicate that mild hypertension is already observed at an early phase of ethanol consumption in rats. Because the content of circulating vasopressin was increased in ethanol-treated rats and their basal blood pressure returned to control levels after IV treatment with a V1-vasopressin receptor antagonist, it is proposed that increased circulating vasopressin content may mediate the hypertension observed in ethanol-treated rats.
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