Effects of renal denervation on endogenous ouabain in spontaneously hypertensive rats

Lai, Xiaomei; Wen, Haixia; Yang, Tingting; Qin, Fei; Zhong, Xiaoge; Pan, Yajin; Jie, Yu; Jing, Huang; Li, Jianling

doi:10.1590/acb371102

Cited by 3 publications

(3 citation statements)

References 45 publications

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“…While writing our manuscript, Lai et al published their results regarding the effects of renal denervation on endogenous ouabain in spontaneously hypertensive rats [ 50 ]. The similarities and differences between the two studies are as follows: the similarity between Lai's paper and this paper is that we both proved that RDN exerted an antihypertensive effect on hypertension associated with ouabain.…”

Section: Discussionmentioning

confidence: 99%

“…The major difference between the two studies is the hypertensive rat model: spontaneously hypertensive rats versus ouabain-induced hypertensive rats. Lai et al explored the influence of RDN on ouabain secretion in spontaneously hypertensive rats, and they found RDN could inhibit ouabain secretion in this rat model thus reducing blood pressure [ 50 ]. However, we have explored the effect of RDN on ouabain-induced hypertensive rats.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Renal Denervation on Ouabain‐Induced Hypertension in Rats

Tang,

Hu,

et al. 2024

International Journal of Hypertension

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Background. Ouabain, a Na+, K+‐ATPase inhibitor, is elevated in hypertensive patients. Evidence suggests ouabain contributes to hypertension mainly through activation of the sympathetic nervous system (SNS). Renal nerves play a vital role in the regulation of SNS activity, so we hypothesize that renal denervation may attenuate the development of ouabain‐induced hypertension. Methods and Results. Forty Sprague‐Dawley rats were divided into following groups (n = 10 each): control group (sham surgery plus intraperitoneal saline injection), RDN group (renal denervation (RDN) plus intraperitoneal saline injection), ouabain group (sham surgery plus intraperitoneal ouabain injection), and ouabain + RDN group (RDN plus intraperitoneal ouabain injection). After eight weeks, compared with the control group, rats in the ouabain group exhibited elevated blood pressure (P < 0.05), increased plasma epinephrine, norepinephrine, angiotensin II, and aldosterone levels (P < 0.05). These indexes could be significantly ameliorated by RDN. RDN also reduced the thickening of aortic tunica media and downregulated the expression of proliferating cell nuclear antigen (PCNA) in the thoracic aorta induced by ouabain. Masson staining and echocardiography showed that myocardial fibrosis and increased left ventricular mass in the ouabain group could be attenuated by RDN. Conclusions. The present study reveals that renal nerves play an important role in the development of ouabain‐induced hypertension. RDN could inhibit the pressor effect and the myocardial remodeling induced by ouabain potentially via inhibiting catecholamine release and vascular smooth muscle cell proliferation. Clinical studies are needed to explore whether RDN may exhibit better antihypertensive effects on hypertensive patients with high plasma ouabain levels as compared to those with normal plasma ouabain levels.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of Renal Denervation on Ouabain‐Induced Hypertension in Rats

Tang,

Hu,

et al. 2024

International Journal of Hypertension

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“…Importantly, rostafuroxin lowered BP in a number of salt/volume-sensitive forms of hypertension ( Table 4 ) but not in spontaneously hypertensive rats (SHR) ( 458 ); digoxin was not tested in this model. Another group, however, reported that serum EO (RIA) was elevated in SHR versus control Wistar-Kyoto (WKY) rats and that renal denervation in SHR lowered the EO to the level in WKY, but BP was not measured ( 430 ).…”

Section: The Physiology and Pathophysiology Of Cts-nka Interactionsmentioning

confidence: 99%

Sensational site: the sodium pump ouabain-binding site and its ligands

Blaustein,

Hamlyn

2024

American Journal of Physiology-Cell Physiology

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Cardiotonic steroids (CTS), used by certain insects, toads, and rats for protection from predators, became, thanks to Withering's trailblazing 1785 monograph, the mainstay of heart failure (HF) therapy. In the 1950's and 60's we learned that the CTS receptor was part of the sodium pump (NKA) and that the Na+/Ca2+ exchanger was critical for the acute cardiotonic effect of digoxin- and ouabain-related CTS. This "settled" view was upended by seven revolutionary observations. First, sub-nanomolar ouabain sometimes stimulates NKA whilst higher concentrations are invariably inhibitory. Second, endogenous ouabain (EO) was discovered in the human circulation. Third, in the DIG clinical trial, digoxin only marginally improved outcome in HF patients. Fourth, cloning of NKA in 1985 revealed multiple NKA α and β subunit isoforms that, in the rodent, differ in their sensitivities to CTS. Fifth, the NKA is a cation pump and a hormone receptor/signal transducer. EO binding to NKA activates, in a ligand- and cell-specific manner, several protein kinase and Ca2+-dependent signaling cascades that have widespread physiological effects and can contribute to hypertension and HF pathogenesis. Sixth, all CTS are not equivalent: e.g., ouabain induces hypertension in rodents while digoxin is anti-hypertensinogenic ("biased signaling"). Seventh, most common rodent hypertension models require a highly ouabain-sensitive α2 NKA and the elevated blood pressure is alleviated by EO immunoneutralization. These numerous activities are enabled by NKA's intricate structure. We have just begun to understand the endocrine role of the endogenous ligands and the broad impact of the ouabain binding site on physiology and pathophysiology.

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Molecular Basis of Na, K–ATPase Regulation of Diseases: Hormone and FXYD2 Interactions

Cordeiro,

Leite Fontes,

Meyer-Fernandes

2024

IJMS

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The Na, K–ATPase generates an asymmetric ion gradient that supports multiple cellular functions, including the control of cellular volume, neuronal excitability, secondary ionic transport, and the movement of molecules like amino acids and glucose. The intracellular and extracellular levels of Na+ and K+ ions are the classical local regulators of the enzyme’s activity. Additionally, the regulation of Na, K–ATPase is a complex process that occurs at multiple levels, encompassing its total cellular content, subcellular distribution, and intrinsic activity. In this context, the enzyme serves as a regulatory target for hormones, either through direct actions or via signaling cascades triggered by hormone receptors. Notably, FXYDs small transmembrane proteins regulators of Na, K–ATPase serve as intermediaries linking hormonal signaling to enzymatic regulation at various levels. Specifically, members of the FXYD family, particularly FXYD1 and FXYD2, are that undergo phosphorylation by kinases activated through hormone receptor signaling, which subsequently influences their modulation of Na, K–ATPase activity. This review describes the effects of FXYD2, cardiotonic steroid signaling, and hormones such as angiotensin II, dopamine, insulin, and catecholamines on the regulation of Na, K–ATPase. Furthermore, this review highlights the implications of Na, K–ATPase in diseases such as hypertension, renal hypomagnesemia, and cancer.

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Effects of renal denervation on endogenous ouabain in spontaneously hypertensive rats

Cited by 3 publications

References 45 publications

Effects of Renal Denervation on Ouabain‐Induced Hypertension in Rats

Effects of Renal Denervation on Ouabain‐Induced Hypertension in Rats

Sensational site: the sodium pump ouabain-binding site and its ligands

Molecular Basis of Na, K–ATPase Regulation of Diseases: Hormone and FXYD2 Interactions

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