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Voltage-Sensitive K+ Channels Inhibit Parasympathetic Ganglion Transmission and Vagal Control of Heart Rate in Hypertensive Rats

Overview of attention for article published in Frontiers in Neurology, December 2015
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Title
Voltage-Sensitive K+ Channels Inhibit Parasympathetic Ganglion Transmission and Vagal Control of Heart Rate in Hypertensive Rats
Published in
Frontiers in Neurology, December 2015
DOI 10.3389/fneur.2015.00260
Pubmed ID
Authors

Torill Berg

Abstract

Parasympathetic withdrawal plays an important role in the autonomic dysfunctions in hypertension. Since hyperpolarizing, voltage-sensitive K(+) channels (K V) hamper transmitter release, elevated K V-activity may explain the disturbed vagal control of heart rate (HR) in hypertension. Here, the K V inhibitor 3,4-diaminopyridine was used to demonstrate the impact of K V on autonomic HR control. Cardiac output and HR were recorded by a flow probe on the ascending aorta in anesthetized, normotensive (WKY), and spontaneously hypertensive rats (SHR), and blood pressure by a femoral artery catheter. 3,4-diaminopyridine induced an initial bradycardia, which was greater in SHR than in WKY, followed by sustained tachycardia in both strains. The initial bradycardia was eliminated by acetylcholine synthesis inhibitor (hemicholinium-3) and nicotinic receptor antagonist/ganglion blocker (hexamethonium), and reversed to tachycardia by muscarinic receptor (mAchR) antagonist (atropine). The latter was abolished by sympatho-inhibition (reserpine). Reserpine also eliminated the late, 3,4-diaminopyridine-induced tachycardia in WKY, but induced a sustained atropine-sensitive bradycardia in SHR. Inhibition of the parasympathetic component with hemicholinium-3, hexamethonium, or atropine enhanced the late tachycardia in SHR, whereas hexamethonium reduced the tachycardia in WKY. In conclusion, 3,4-diaminopyridine-induced acetylcholine release, and thus enhanced parasympathetic ganglion transmission, with subsequent mAchR activation and bradycardia. 3,4-diaminopyridine also activated tachycardia, initially by enhancing sympathetic ganglion transmission, subsequently by activation of norepinephrine release from sympathetic nerve terminals. The 3,4-diaminopyridine-induced parasympathetic activation was stronger and more sustained in SHR, demonstrating an enhanced inhibitory control of K V on parasympathetic ganglion transmission. This enhanced K V activity may explain the dysfunctional vagal HR control in SHR.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 12 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 12 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 4 33%
Student > Bachelor 2 17%
Student > Doctoral Student 1 8%
Student > Master 1 8%
Researcher 1 8%
Other 1 8%
Unknown 2 17%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 2 17%
Medicine and Dentistry 2 17%
Neuroscience 2 17%
Mathematics 1 8%
Environmental Science 1 8%
Other 2 17%
Unknown 2 17%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 16 July 2016.
All research outputs
#17,778,101
of 22,834,308 outputs
Outputs from Frontiers in Neurology
#7,061
of 11,712 outputs
Outputs of similar age
#264,226
of 388,741 outputs
Outputs of similar age from Frontiers in Neurology
#41
of 55 outputs
Altmetric has tracked 22,834,308 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 11,712 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.3. This one is in the 33rd percentile – i.e., 33% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 388,741 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 27th percentile – i.e., 27% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 55 others from the same source and published within six weeks on either side of this one. This one is in the 16th percentile – i.e., 16% of its contemporaries scored the same or lower than it.