(redirected from hyperpolarizing)
Also found in: Medical.
Related to hyperpolarizing: depolarizing


tr.v. hy·per·po·lar·ized, hy·per·po·lar·iz·ing, hy·per·po·lar·iz·es
To cause an increase in polarity, as across a biological membrane.
American Heritage® Dictionary of the English Language, Fifth Edition. Copyright © 2016 by Houghton Mifflin Harcourt Publishing Company. Published by Houghton Mifflin Harcourt Publishing Company. All rights reserved.


(ˌhaɪpəˈpəʊləˌraɪz) or


vb (tr)
(Biology) biology physics to cause increased polarization
Collins English Dictionary – Complete and Unabridged, 12th Edition 2014 © HarperCollins Publishers 1991, 1994, 1998, 2000, 2003, 2006, 2007, 2009, 2011, 2014
References in periodicals archive ?
In vertebrates, closure of cation-permeable CNG channels hyperpolarizes rods and cones in response to light, whereas in scallops, the opening of CNG [K.sup.+] channels underlies the hyperpolarizing response.
[3,4] Endothelium plays a major role in the regulation of vascular tone through the release of several vasorelaxing and vasoconstricting factors such as prostacyclin, nitric oxide (NO), and endothelium-derived hyperpolarizing factor.
The exact mechanism is still unknown, but certain research papers have suggested that slow deep breathing stretches the lung tissue which, in turn, produces inhibitory signals by the action of slow adapting receptors and hyperpolarizing currents.
The mechanisms involved in endothelial dysfunction caused by HHcy include inhibition of nitric oxide, endothelium-derived hyperpolarizing factor, regulation of prostanoids, activation of angiotensin II receptor 1, oxidative stress and endothelin-1 activation.15 Literature from this part of the world appears scarce.
A significant number of mediators that are produced by the endothelial layer are vasoconstrictors, angiotensin II and endothelin I, and vasodilators, nitric oxide (NO), endothelial hyperpolarizing factor, and prostacyclin [10].
The cones contact both depolarizing bipolar cells (DBCs) and hyperpolarizing bipolar cells (HBCs) through sign-inverting (−) synapses (ON synapse) and sign-preserving (+) synapses (OFF synapse), respectively.
On the other hand, the activation and inactivation V 1/2 values of the two channels had a reduction towards a hyperpolarizing shift caused by CGA under PGE2 pretreatment.
However, the experiments performed to elucidate whether the endothelium-derived hyperpolarizing factor EDHF could play a role in the vasorelaxant effect to clobenzorex, as previously reported for acetyl-choline (32,33), are discussed below.
It is known that cardiorenal regulation may involve several endogenous mediators, including prostaglandins, NO, and the endothelium-derived hyperpolarizing factor, synergistically acting in a complex hemodynamic and neurohumoral interaction [20].
For example, ECs secrete numerous bioactive substances to modulate vascular tone, such as nitric oxide (NO), prostaglandin [I.sub.2] ([PGI.sub.2]), and endothelium-derived hyperpolarizing factor (EDHF), which are regarded as endothelium-derived relaxing factors (EDRFs) as well as endothelin 1 (ET-1), thromboxane [A.sub.2] ([TXA.sub.2]), angiotensin II (Ang II), and uridine adenosine tetraphosphate ([UP.sub.4]A), which belong to endothelium-derived contracting factors (EDCFs).
These mediators can be divided into two types: (1) vasodilators, such as endothelium-derived relaxing factors (EDRFs), nitric oxide (NO), prostacyclin (PGI2) [8], and endothelium-derived hyperpolarizing factors (EDHFs) [13-16], and (2) vasoconstrictors, which include endothelin-1, reactive oxygen species (ROS), platelet-activating factor (PAF) [8], and arachidonic acid (AA) cyclooxygenase-derived metabolites [17].
To investigate the mechanisms involved in CGA-induced relaxation, the contribution of nitric oxide synthase (NOS), cyclooxy-genase (COX) and the endothelium-derived hyperpolarizing factor (EDHF) was assessed in endothelium-intact aortic rings preincubated with the NOS inhibitor, N[omega]-nitro-L-arginine methyl ester (L-NAME, [10.sup.-4] mol/l), the COX inhibitor indomethacin ([10.sup.-5] mol/l) or the calcium-dependent potassium channels inhibitors apamin and charybdotoxin ([10.sup.-7]7 mol/l) for 60 min.