ArticlePhysiological reports2019
Interactions between renal vascular resistance and endothelium-derived hyperpolarization in hypertensive rats in vivo.
Article in Physiological reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Impact of aging on vascular ion channels: perspectives and knowledge gaps across major organ systems.American journal of physiology. Heart and circulatory physiology · 2023Review
- A hybrid approach to full-scale reconstruction of renal arterial network.Scientific reports · 2023Article
- Microvascular dysfunction and kidney disease: Challenges and opportunities?Microcirculation (New York, N.Y. : 1994) · 2021Review
- Interactions between renal vascular resistance and endothelium-derived hyperpolarization in hypertensive rats in vivo.Physiological reports · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelium derived signaling mechanisms play an important role in regulating vascular tone and endothelial dysfunction is often found in hypertension. Endothelium-derived hyperpolarization (EDH) plays a significant role in smaller renal arteries and arterioles, but its significance in vivo in hypertension is unresolved. The aim of this study was to characterize the EDH-induced renal vasodilation in normotensive and hypertensive rats during acute intrarenal infusion of ACh. Our hypothesis was that the increased renal vascular resistance (RVR) found early in hypertension would significantly correlate with reduced EDH-induced vasodilation. In isoflurane-anesthetized 12-week-old normo- and hypertensive rats blood pressure and renal blood flow (RBF) was measured continuously. RBF responses to acute intrarenal ACh infusions were measured before and after inhibition of NO and prostacyclin. Additionally, RVR was decreased or increased using inhibition or activation of adrenergic receptors or by use of papaverine and angiotensin II. Intrarenal infusion of ACh elicited a larger increase in RBF in hypertensive rats compared to normotensive rats suggesting that endothelial dysfunction is not present in 12-week-old hypertensive rats. The EDH-induced renal vasodilation (after inhibition of NO and prostacyclin) was similar between normo- and hypertensive rats. Reducing RVR by inhibition of α
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