ArticleAmerican journal of physiology. Heart and circulatory physiology2010
Sympathetic nerves and the endothelium influence the vasoconstrictor effect of low concentrations of ouabain in pressurized small arteries.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Sensational site: the sodium pump ouabain-binding site and its ligands.American journal of physiology. Cell physiology · 2024Review
- The vascular Na,K-ATPase: clinical implications in stroke, migraine, and hypertension.Clinical science (London, England : 1979) · 2023Review
- Effects of renal denervation on endogenous ouabain in spontaneously hypertensive rats.Acta cirurgica brasileira · 2023Article
- The Na,K-ATPase-Dependent Src Kinase Signaling Changes with Mesenteric Artery Diameter.International journal of molecular sciences · 2018Article
- Salt, aldosterone and extrarenal NaPlacenta · 2017Review
- Silencing salusin-β attenuates cardiovascular remodeling and hypertension in spontaneously hypertensive rats.Scientific reports · 2017Article
- Salt Sensitivity: Challenging and Controversial Phenotype of Primary Hypertension.Current hypertension reports · 2016Review
- Endogenous cardiotonic steroids in kidney failure: a review and an hypothesis.Advances in chronic kidney disease · 2015Review
- Ouabain-digoxin antagonism in rat arteries and neurones.The Journal of physiology · 2014Article
- Article
- Nanomolar ouabain augments Ca2+ signalling in rat hippocampal neurones and glia.The Journal of physiology · 2013Article
- Activation of c-SRC underlies the differential effects of ouabain and digoxin on Ca(2+) signaling in arterial smooth muscle cells.American journal of physiology. Cell physiology · 2013Article
- Salt sensitivity, endogenous ouabain and hypertension.Current opinion in nephrology and hypertension · 2013Review
- Nanomolar ouabain increases NCX1 expression and enhances Ca2+ signaling in human arterial myocytes: a mechanism that links salt to increased vascular resistance?American journal of physiology. Heart and circulatory physiology · 2012Article
- How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension.American journal of physiology. Heart and circulatory physiology · 2012Review
- Increased arterial smooth muscle Ca2+ signaling, vasoconstriction, and myogenic reactivity in Milan hypertensive rats.American journal of physiology. Heart and circulatory physiology · 2012Article
- Article
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5 authors at 1 institution in 1 country.
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Abstract
We hypothesized that in salt-dependent forms of hypertension, endogenous ouabain acts on arterial smooth muscle to cause enhanced vasoconstriction. Here, we tested for the involvement of the arterial endothelium and perivascular sympathetic nerve terminals in ouabain-induced vasoconstriction. Segments of rat mesenteric or renal interlobar arteries were pressurized to 70 mmHg at 37 degrees C and exposed to ouabain (10(-11)-10(-7) M). Removal of the endothelium enhanced ouabain-induced vasoconstriction by as much as twofold (at an ouabain concentration of 10(-9) M). A component of the ouabain-induced vasoconstriction is due to the enhanced spontaneous release of norepinephrine (NE) from nerve terminals in the arterial wall. The alpha(1)-adrenoceptor blocker prazosin (10(-6) M) decreased ouabain-induced vasoconstrictions by as much as 50%. However, neither the contraction induced by sympathetic nerve activity (SNA) nor the NE release evoked by SNA (measured directly by carbon fiber amperometry) was increased by ouabain (<10(-7) M). Nevertheless, the converse case was true: after brief bursts of SNA, vasoconstrictor responses to ouabain were transiently increased (1.75-fold). This effect may be mediated by neuropeptide Y and Y(1) receptors on smooth muscle. In arteries lacking the endothelium and exposed to prazosin, ouabain (10(-11) M and greater) caused vasoconstriction, indicating a direct effect of very "low" concentrations of ouabain on arterial smooth muscle. In conclusion, in intact arteries, the endothelium opposes ouabain (10(-11)-10(-7)M)-induced vasoconstriction, which is caused by both enhanced spontaneous NE release and direct effects on smooth muscle. Ouabain (<10(-7)M) does not enhance SNA-mediated contractions, but SNA enhances ouabain-induced contractions. The effects of endogenous ouabain may be accentuated in forms of hypertension that involve sympathetic nerve hyperactivity and/or endothelial dysfunction.
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