ArticlePloS one2012
Activation of thiazide-sensitive co-transport by angiotensin II in the cyp1a1-Ren2 hypertensive rat.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Integrated renal and sympathetic mechanisms underlying the development of sex- and age-dependent hypertension and the salt sensitivity of blood pressure.GeroScience · 2024Article
- Sex differences in dietary sodium evoked NCC regulation and blood pressure in male and female Sprague-Dawley, Dahl salt-resistant, and Dahl salt-sensitive rats.American journal of physiology. Renal physiology · 2024Article
- Aldosterone Antagonism Is More Effective at Reducing Blood Pressure and Excessive Renal ENaC Activity in AngII-Infused Female Rats Than in Males.Hypertension (Dallas, Tex. : 1979) · 2023Article
- Article
- Sympathetic Regulation of the NCC (Sodium Chloride Cotransporter) in Dahl Salt-Sensitive Hypertension.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Electrolyte and transporter responses to angiotensin II induced hypertension in female and male rats and mice.Acta physiologica (Oxford, England) · 2020Article
- Spironolactone mitigates, but does not reverse, the progression of renal fibrosis in a transgenic hypertensive rat.Physiological reports · 2020Article
- Sympathetic regulation of NCC in norepinephrine-evoked salt-sensitive hypertension in Sprague-Dawley rats.American journal of physiology. Renal physiology · 2019Article
- Mechanism of Thiazide Diuretic Arterial Pressure Reduction: The Search Continues.Frontiers in pharmacology · 2019Review
- Angiotensin II-induced hypertension in rats is only transiently accompanied by lower renal oxygenation.Scientific reports · 2018Article
- Renal and Blood Pressure Response to a High-Salt Diet in Mice With Reduced Global Expression of the Glucocorticoid Receptor.Frontiers in physiology · 2018Article
- Responses of distal nephron NaAmerican journal of physiology. Renal physiology · 2017Article
- Renal disease pathophysiology and treatment: contributions from the rat.Disease models & mechanisms · 2016Review
- Norepinephrine-evoked salt-sensitive hypertension requires impaired renal sodium chloride cotransporter activity in Sprague-Dawley rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Inhibition of the purinergic P2X7 receptor improves renal perfusion in angiotensin-II-infused rats.Kidney international · 2015Article
- Pressure natriuresis and the renal control of arterial blood pressure.The Journal of physiology · 2014Review
- Glucocorticoids and renal Na+ transport: implications for hypertension and salt sensitivity.The Journal of physiology · 2014Review
- Chronic angiotensin II infusion drives extensive aldosterone-independent epithelial Na+ channel activation.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Effect of P2X4 and P2X7 receptor antagonism on the pressure diuresis relationship in rats.Frontiers in physiology · 2013Article
- Evolving concepts on regulation and function of renin in distal nephron.Pflugers Archiv : European journal of physiology · 2013Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Transgenic rats with inducible expression of the mouse Ren2 gene were used to elucidate mechanisms leading to the development of hypertension and renal injury. Ren2 transgene activation was induced by administration of a naturally occurring aryl hydrocarbon, indole-3-carbinol (100 mg/kg/day by gastric gavage). Blood pressure and renal parameters were recorded in both conscious and anesthetized (butabarbital sodium; 120 mg/kg IP) rats at selected time-points during the development of hypertension. Hypertension was evident by the second day of treatment, being preceded by reduced renal sodium excretion due to activation of the thiazide-sensitive sodium-chloride co-transporter. Renal injury was evident after the first day of transgene induction, being initially limited to the pre-glomerular vasculature. Mircoalbuminuria and tubuloinsterstitial injury developed once hypertension was established. Chronic treatment with either hydrochlorothiazide or an AT1 receptor antagonist normalized sodium reabsorption, significantly blunted hypertension and prevented renal injury. Urinary aldosterone excretion was increased ≈ 20 fold, but chronic mineralocorticoid receptor antagonism with spironolactone neither restored natriuretic capacity nor prevented hypertension. Spironolactone nevertheless ameliorated vascular damage and prevented albuminuria. This study finds activation of sodium-chloride co-transport to be a key mechanism in angiotensin II-dependent hypertension. Furthermore, renal vascular injury in this setting reflects both barotrauma and pressure-independent pathways associated with direct detrimental effects of angiotensin II and aldosterone.
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