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β3-adrenoceptors inhibit stimulated norepinephrine release in spontaneously hypertensive rats

Overview of attention for article published in Frontiers in Physiology, December 2014
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Title
β3-adrenoceptors inhibit stimulated norepinephrine release in spontaneously hypertensive rats
Published in
Frontiers in Physiology, December 2014
DOI 10.3389/fphys.2014.00499
Pubmed ID
Authors

Torill Berg

Abstract

Here, the influence of β3-adrenoceptors on catecholamine release in normotensive and spontaneously hypertensive rats was analyzed. Blood pressure was recorded through a femoral artery catheter, and cardiac output by ascending aorta flow. Time from onset of flow to maximum rise in flow indicated inotropy. Total peripheral vascular resistance (TPR) was calculated. Norepinephrine release was stimulated with tyramine, which allowed presynaptic release-control to be reflected as changes in the plasma norepinephrine concentration. β3-adrenoceptor agonist (BRL37344) reduced baseline vascular resistance, the tyramine-stimulated norepinephrine overflow and the positive inotropic response to tyramine in hypertensive but not normotensive rats. β3-adrenoceptor antagonist (SR59230A) reduced tyramine-stimulated norepinephrine release in both strains and the secretion of epinephrine in hypertensive rats. SR59230A reduced tyramine-induced tachycardia in normotensive rats, and prevented down-regulation of the tyramine-induced rise in resistance in hypertensive rats. It was concluded that the contradicting results obtained by agonist vs. antagonist, could be explained by their interaction with two different β-adrenoceptors: The BRL37344-dependent inhibition of stimulated norepinephrine release and positive inotropic response to tyramine was compatible with stimulation of β3-adrenoceptor coupling to inhibitory G-protein. This was observed only in hypertensive rats during stimulated, high levels of circulating catecholamines. The effect of BRL37344 on baseline vascular resistance was compatible with activation of β3-adrenoceptor coupling to endothelial nitric oxide synthase. The inhibitory effect of SR59230A on tyramine-stimulated norepinephrine release in both strains, the increased TPR-response to tyramine in hypertensive rats and tachycardia in normotensive rats may result from inhibition of the low-affinity-state β1-adrenoceptor, also known as the putative β4-adrenoceptor.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 6 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 6 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 1 17%
Student > Bachelor 1 17%
Researcher 1 17%
Student > Master 1 17%
Unknown 2 33%
Readers by discipline Count As %
Pharmacology, Toxicology and Pharmaceutical Science 2 33%
Nursing and Health Professions 1 17%
Agricultural and Biological Sciences 1 17%
Medicine and Dentistry 1 17%
Unknown 1 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 19 December 2014.
All research outputs
#20,246,428
of 22,774,233 outputs
Outputs from Frontiers in Physiology
#9,337
of 13,560 outputs
Outputs of similar age
#295,965
of 353,125 outputs
Outputs of similar age from Frontiers in Physiology
#73
of 104 outputs
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