Cardiovascular alterations at different stages of hypertension development during ethanol consumption: time-course of vascular and autonomic changes.

The aim of the present work was to establish a time-course correlation between vascular and autonomic changes that contribute to the development of hypertension during ethanol ingestion in rats. For this, male Wistar rats were subjected to the intake of increasing ethanol concentrations in their drinking water during four weeks. Ethanol effects were investigated at the end of each week. Mild hypertension was already observed at the first week of treatment, and a progressive blood pressure increase was observed along the evaluation period. Increased pressor response to phenylephrine was observed from first to fourth week. α1-Adrenoceptor protein in the mesenteric bed was enhanced at the first week, whereas ß2-adrenoceptor protein in the aorta was reduced after the second week. In the third week, ethanol intake facilitated the depressor response to sodium nitroprusside, whereas in the fourth week it reduced nitrate content in aorta and increased it plasma. The bradycardic component of the baroreflex was impaired, whereas baroreflex tachycardia was enhanced at the third and fourth weeks. AT1A receptor and C-type natriuretic peptide (CNP) mRNAs in the nucleus tractus solitarius were increased at the fourth week. These findings suggest that increased vascular responsiveness to vasoconstrictor agents is possibly a link factor in the development and maintenance of the progressive hypertension induced by ethanol consumption. Additionally, baroreflex changes are possibly mediated by alterations in angiotensinergic mechanisms and CNP content within the brainstem, which contribute to maintaining the hypertensive state in later phases of ethanol ingestion. Facilitated vascular responsiveness to nitric oxide seems to counteract ethanol-induced hypertension.

Effect of pain related of sex and estrous cycle on blood plasma glucose, free fatty acids and corticosterone in rats - doi: 10.4025/actascibiolsci.v34i4.10568

Sex differences related with pain have been studied and evidences suggesting influence of sex steroid hormones on the thresholds of pain. Experimental nociception has been test using formalin as a model of nociceptive stimulus. Association of stress, pain and metabolic and hormonal changes has not been explored. The aim of this study was to compare metabolic and hormonal changes between male rats and female rats in proestrus and estrus cycle after painful stimulus by formalin into the masseter muscle. Male and female Wistar rats (200-250 g b.w.) were submitted to an injection of formalin (F, 1.5%) or saline (S, 9.9%) into the masseter muscle and after 0 (N, control group without injection), 5, 15, 30 or 60 minutes they were decapitate and blood was collected to measure biochemical parameters. Plasma estradiol concentration (pg dL-1) was significantly higher in proestrus (106.3 ± 4.3, n = 45, p 0.05) group compared to the estrous group (89.4 ± 3.5, n = 43). Blood plasma concentration of glucose (mg dL-1) was increased after 5 and 15 minutes of injection of formalin or saline in the animals, but in the estrus group the increase was bigger than in the others. Free fatty acids levels increased in the estrous group after 5, 15 and 30 minutes and also the corticosterone levels and these concentrations wer significantly different (p 0.05) from either male or female animals i

Increased circulating vasopressin may account for ethanol-induced hypertension in rats.

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.