BackgroundThe literature did not evidence yet with which age spontaneously hypertensive rats (SHR) start to present baroreflex reduction. We endeavored to evaluate the baroreflex function in eight-week-old SHR.MethodsMale Wistar Kyoto (WKY) normotensive rats and SHR aged eight weeks were studied. Baroreflex was calculated as the variation of heart rate (HR) divided by the mean arterial pressure (MAP) variation (ΔHR/ΔMAP) tested with a depressor dose of sodium nitroprusside (SNP, 50 μg/kg) and with a pressor dose of phenylephrine (PHE, 8 μg/kg) in the right femoral venous approach through an inserted cannula in the animals. Significant differences for p < 0.05.ResultsBaseline MAP (p < 0.0001) and HR (p = 0.0028) was higher in SHR. Bradycardic peak was attenuated in SHR (p < 0.0001), baroreflex gain tested with PHE was also reduced in the SHR group (p = 0.0012). PHE-induced increase in MAP was increased in WKY compared to SHR (p = 0.039). Bradycardic reflex responses to intravenous PHE was decreased in SHR (p < 0.0001).ConclusionEight weeks old SHR already presents impairment of the parasympathetic component of baroreflex.
The antihypertensive drugs moxonidine and clonidine are α2-adrenoceptor and imidazoline (I1) agonists. Previous results from our laboratory have shown that moxonidine can act in the commissural nucleus of the solitary tract (commNTS). In addition, some studies have shown that GABA or glutamate receptor blockade in the RVLM blunted the hypotension produced by these antihypertensive agents in spontaneously hypertensive rats. Therefore, in the present study we verify whether the cardiovascular and sympathetic effects produced by moxonidine in the commNTS are dependent on GABAergic or glutamatergic mechanisms. Mean arterial pressure (MAP) and splanchnic sympathetic nerve activity (sSNA) were recorded in urethane-anesthetized, and artificially-ventilated male Wistar rats (250-350 g). Injection of the GABAA antagonist bicuculline (25 pmol/50 nL) into the commNTS reduced the hypotension as well as the sympathoinhibition elicited by moxonidine. Prior injection of the glutamate receptor antagonist kynurenic acid (2.5 nmol/50 nL) into the commNTS was not effective in reducing the hypotension and sympathoinhibition elicited by moxonidine. Therefore, we conclude that the hypotensive and sympathoinhibitory effects elicited by microinjection of moxonidine into the commNTS are dependent on GABA receptors, but not ionotropic glutamate receptors.
This article describes data set of the profile of patients diagnosed with Diabetic Nephropathy (DN) undergoing hemodialysis and followed-up by Hemodialysis Service in medical centers in Goiânia, Go, Brazil. These data describe specifically the demographic, clinical, and lifestyle variables of 101 patients. In addition, these data provide detailed clinical associations about the profile of patients diagnosed with DN and which are made publicly available to enable critical or extended analyzes. For further interpretation of the data presented in this article, see the research article: Do GST polymorphisms influence in the pathogenesis of diabetic nephropathy? (Lima et al., 2018).
Objective: To review the literature and synthesize evidence on pathophysiological interactions attributed to the simultaneous occurrence of COVID-19 and preeclampsia. Methods: A systematic review was conducted from November (2021) to January (2022) to retrieve observational studies published on the PubMed, LILACS, SciELO Brazil and Google Scholar databases. The search was based on the descriptors [(eclampsia OR preeclampsia) AND (COVID-19)]. Quantitative studies that pointed to pathophysiological interactions were included. Literature reviews, studies with HIV participants, or with clinical approach only were excluded. The selection of studies was standardized and the evaluation was performed by pairs of researchers. Results: In this review, 155 publications were retrieved; 16 met the inclusion criteria. In summary, the physiological expression of angiotensin-converting enzyme-2 (ACE-2) receptors is physiologically increased in pregnant women, especially at the placental site. Studies suggest that the coronavirus binds to ACE-2 to enter the human cell, causing deregulation of the renin-angiotensin-aldosterone system and in the ratio between angiotensin-II and angiotensin-1-7, inducing manifestations suggestive of preeclampsia. Furthermore, the cytokine storm leads to endothelial dysfunction, vasculopathy and thrombus formation, also present in preeclampsia. Conclusion: The studies retrieved in this review suggest that there is a possible overlap of pathophysiological interactions between COVID-19 and preeclampsia, which mainly involve ACE-2 and endothelial dysfunction. Given that preeclampsia courses with progressive clinical and laboratory alterations, a highly quality prenatal care may be able to detect specific clinical and laboratory parameters to differentiate a true preeclampsia superimposed by covid-19, as well as cases with hypertensive manifestations resulting from viral infection.
The sympathoinhibition elicited by moxonidine has been attributed to activation of α2‐adrenergic/imidazoline receptors in the rostral ventrolateral medulla (RVLM) and, more recently, in the nucleus of the solitary tract (NTS). In the present study, we aimed to determine the role of the γ‐aminobutyric acid (GABA) mechanisms in the commissural NTS (cNTS) in mediating anti‐hypertensive effects of moxonidine in anesthetized normotensive rats. Mean arterial pressure (MAP) and splanchnic sympathetic nerve activity (sSNA) were recorded in urethane anaesthetized and artificially ventilated male Wistar rats (280–320 g, n = 5–7). Injections of moxonidine (2.5 and 5 nmol/50 nl) into the cNTS reduced resting MAP (105 ± 3 and 95 ± 5 mmHg, vs. pre‐injection: 117 ± 4 mmHg) and resting sSNA (92 ± 1 and 82 ± 3% of the control). The pre‐treatment with the GABA‐A antagonist bicuculline (25 pmol/50 nl) in the cNTS blocked the hypotension (Δ = −2 ± 3 mmHg, vs. moxonidine: Δ = −22 ± 4 mmHg) and sympathoinhibition (Δ = −1 ± 2%, vs. moxonidine: Δ = −18 ± 3%; p<0.05) elicited by moxonidine‐injected (5 nmol/50 nl) in the cNTS. These current data suggest that GABAergic mechanisms in the cNTS are essential for the sympathoinhibition and hypotension of moxonidine.Financial support: FAPESP; CNPq; CAPES.
ResumoIntrodução: A hipertensão arterial é uma doença que atinge grande parte da população mundial. Seu tratamento consiste na modificação de hábitos de vida, os quais incluem dieta, diminuição de peso e cessação do tabagismo, entre outros. A atividade física é uma das recomendações de destaque, sustentada pelos seus positivos efeitos sobre a manutenção dos níveis pressóricos dentro dos limites de normalidade. Objetivo:Caracterizar a resposta hipotensora pós-exercício sobre indivíduos com hipertensão. Método: Trata-se de uma revisão de literatura realizada por meio do levantamento bibliográfico de 1990 a 2011 junto às bases eletrônicas de dados MEDLINE, ScIELO, Cochrane e Lilacs. Foram selecionados artigos a partir das palavras-chave hipertensão, exercício físico e pressão alta. Resultados: Após a realização de uma sessão de atividade física ocorre a redução da hipertensão arterial, denominada hipotensão pós-exercício. Porém, esse fenômeno dependerá de fatores relacionados como o tipo, a intensidade e a duração do exercício. Conclusão: A realização de atividade e/ou exercício físico é importante no tratamento não farmacológico para a redução da pressão arterial, contudo, ainda não está definido qual o melhor tipo de exercício.Palavras-chave: pressão arterial; hipertensão; terapia por exercício. AbstractIntroduction: Hypertension is a disease that affects a large part of the world population, in which the treatment consists in changing habits of life,
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