Age-dependent effect of ouabain on renal Na+,K+-ATPase

Silva, E.; Serrão, Paula; Soares-da-Silva, Patrı́cio

doi:10.1016/j.lfs.2011.02.012

Cited by 4 publications

(3 citation statements)

References 38 publications

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“…In most studies, ouabain administration started at an approximate age of 6–7 weeks ( Table S1 – S3 ). At this age, arterial pressure is not stable in rats and continues to increase at a rate of 2–3 mmHg/week [9] , [16] , [17] . It is possible that a “time window” exists when blood pressure and its regulatory mechanisms are not fully developed and can be modified by ouabain.…”

Section: Discussionmentioning

confidence: 99%

Wistar Rats Resistant to the Hypertensive Effects of Ouabain Exhibit Enhanced Cardiac Vagal Activity and Elevated Plasma Levels of Calcitonin Gene-Related Peptide

2014

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Ouabain is a cardiac glycoside produced in the adrenal glands and hypothalamus. It affects the function of all cells by binding to Na+/K+-ATPase. Several lines of evidence suggest that endogenous ouabain could be involved in the pathogenesis of essential (particularly, salt-sensitive) hypertension. However, information regarding the postulated hypertensive effect of the long-term administration of low-dose exogenous ouabain is inconsistent. This study was designed to help settle this controversy through the use of telemetric monitoring of arterial blood pressure and to elucidate the ouabain-induced alterations that could either promote or prevent hypertension. Ouabain (63 and 324 µg/kg/day) was administered subcutaneously to male Wistar rats. Radiotelemetry was used to monitor blood pressure, heart rate and measures of cardiovascular variability and baroreflex sensitivity. The continuous administration of ouabain for 3 months did not elevate arterial blood pressure. The low-frequency power of systolic pressure variability, urinary excretion of catecholamines, and cardiovascular response to restraint stress and a high-salt diet as well as the responsiveness to α1-adrenergic stimulation were all unaltered by ouabain administration, suggesting that the activity of the sympathetic nervous system was not increased. However, surrogate indices of cardiac vagal nerve activity based on heart rate variability were elevated. Molecular remodeling in mesenteric arteries that could support the development of hypertension (increased expression of the genes for the Na+/Ca2+ exchanger and Na+/K+-ATPase α2 isoform) was not evident. Instead, the plasma level of vasodilatory calcitonin gene-related peptide (CGRP) significantly rose from 55 (11, SD) in the control group to 89 (20, SD) pg/ml in the ouabain-treated rats (PTukey's = 18.10−5). These data show that long-term administration of exogenous ouabain does not necessarily cause hypertension in rodents. The augmented parasympathetic activity and elevated plasma level of CGRP could be linked to the missing hypertensive effect of ouabain administration.

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Section: Discussionmentioning

confidence: 99%

Wistar Rats Resistant to the Hypertensive Effects of Ouabain Exhibit Enhanced Cardiac Vagal Activity and Elevated Plasma Levels of Calcitonin Gene-Related Peptide

2014

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“…Terminology to describe various developmental milestones in rodents is not consistent across publications (Jackson et al, 2017[ 49 ]; Picut and Ziejewski, 2018[ 86 ]). Male Wistar rats at PND 28 (Kosaka et al, 1987[ 53 ]) or 42 (Cunha et al, 2001[ 20 ]), male Sprague Dawley rats at PND 36-37 (Ku et al, 2016[ 54 ]), male Fisher rats at PND 30 (Swamy and Abraham, 1987[ 109 ]) or 45-60 (Delp et al, 1998[ 23 ]), and male WKY rats at PND 35 (Silva et al, 2011[ 100 ]) have been considered to be juvenil. 9-week old male Wistar rats (Kosaka et al, 1987[ 53 ]), 8-week old male Sprague Dawley (Ku et al, 2016[ 54 ]), 4-month old male Fisher rats (Swamy and Abraham, 1987[ 109 ]), 2-month old female Wistar rats (Pestronk et al, 1980[ 82 ]), 6-week old female Sprague Dawley rats (Meyer et al, 2006[ 66 ]), and 3-6-month-old Fisher 344 rats (Delp et al, 1998[ 23 ]; Stanley and Shetty, 2004[ 105 ]; Rao et al, 2005[ 90 ]), have been considered young adults.…”

Section: Addressing Rat Developmental Stages In the Literaturementioning

confidence: 99%

The laboratory rat: age and body weight matter

Ghasemi

Jeddi

Kashfi

2021

EXCLI Journal; 20:Doc1431; ISSN 1611-2156

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“…Furthermore, this and another study from the same group that used Sprague-Dawley rats as the normotensive model (12) only addressed the acute effects of clonidine. Recent studies suggest that different rat strains are associated to differences in renal handling of electrolytes (26,27). In this view, in the present study we evaluated the sub-acute effect of clonidine and have used the WKY rat as the control strain not only to better understand the effect of clonidine on renal sodium handling in SHR, but also to provide a background to evaluate the possible influence of hypertension on this mechanism.…”

Section: Discussionmentioning

confidence: 99%

Effect of Clonidine on Renal Sodium Handling in Spontaneously Hypertensive Rats

Vieira-Coelho

Moura

2012

J Pharmacol Sci

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Abstract. Up-regulation of kidney α 2 -adrenoceptor expression has been implicated in the development of hypertension in spontaneously hypertensive rats (SHR). This study was carried out to evaluate renal sodium excretion in response to clonidine administration in SHR and control normotensive Wistar-Kyoto (WKY) rats. SHR and WKY rats (12-week-old) were placed in metabolic cages for 4 days: the first 2 days in control conditions and the following 2 days under oral clonidine treatment (100 μg/kg body weight). Clonidine produced a similar reduction in systolic blood pressure values in SHR and WKY rats, although SHR remained hypertensive. At the end of the study SHR and WKY rats presented similar noradrenaline plasma levels. However, noradrenaline kidney tissue levels were significantly higher in SHR compared to WKY rats. Under control conditions, SHR presented lower urine flow compared to WKY rats. Clonidine produced a significant decrease in urine flow in WKY rats but not in SHR. Furthermore, clonidine also produced a significant reduction in urinary sodium, potassium, and creatinine excretion in WKY rats, but had no effect in SHR. In conclusion, in SHR the reduction in systolic blood pressure and sympathetic activity produced by clonidine was not accompanied by a decrease in urine volume and sodium excretion.

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Age-dependent effect of ouabain on renal Na+,K+-ATPase

Cited by 4 publications

References 38 publications

Wistar Rats Resistant to the Hypertensive Effects of Ouabain Exhibit Enhanced Cardiac Vagal Activity and Elevated Plasma Levels of Calcitonin Gene-Related Peptide

Wistar Rats Resistant to the Hypertensive Effects of Ouabain Exhibit Enhanced Cardiac Vagal Activity and Elevated Plasma Levels of Calcitonin Gene-Related Peptide

The laboratory rat: age and body weight matter

Effect of Clonidine on Renal Sodium Handling in Spontaneously Hypertensive Rats

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