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Altered β(1−3)-adrenoceptor influence on α(2)-adrenoceptor-mediated control of catecholamine release and vascular tension in hypertensive rats

α(2)- and β-adrenoceptors (AR) reciprocally control catecholamine release and vascular tension. Disorders in these functions are present in spontaneously hypertensive rats (SHR). The present study tested if α(2)AR dysfunctions resulted from altered α(2)AR/βAR interaction. Blood pressure (BP) was rec...

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Autor principal: Berg, Torill
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4403294/
https://www.ncbi.nlm.nih.gov/pubmed/25941491
http://dx.doi.org/10.3389/fphys.2015.00120
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author Berg, Torill
author_facet Berg, Torill
author_sort Berg, Torill
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description α(2)- and β-adrenoceptors (AR) reciprocally control catecholamine release and vascular tension. Disorders in these functions are present in spontaneously hypertensive rats (SHR). The present study tested if α(2)AR dysfunctions resulted from altered α(2)AR/βAR interaction. Blood pressure (BP) was recorded through a femoral artery catheter and cardiac output by an ascending aorta flow probe. Total peripheral vascular resistance (TPR) was calculated. Norepinephrine release was stimulated by a 15-min tyramine-infusion, which allows presynaptic release-control to be reflected as differences in overflow to plasma. Surgical stress activated some secretion of epinephrine. L-659,066 (α(2)AR-antagonist) enhanced norepinephrine overflow in normotensive controls (WKY) but not SHR. Nadolol (β(1+2)) and ICI-118551 (β(2)), but not atenolol (β(1)) or SR59230A [β((3)/1L)] prevented this increase. All βAR antagonists allowed L-659,066 to augment tyramine-induced norepinephrine overflow in SHR and epinephrine secretion in both strains. Inhibition of cAMP-degradation with milrinone and β(3)AR agonist (BRL37344) enhanced the effect of L-659,066 on release of both catecholamines in SHR and epinephrine in WKY. β(1/2)AR antagonists and BRL37344 opposed the L-659,066-dependent elimination of the TPR-response to tyramine in WKY. α(2)AR/βAR antagonists had little influence on the TPR-response in SHR. Milrinone potentiated the L-659,066-dependent reduction of the TPR-response to tyramine. Conclusions: β(2)AR activity was a required substrate for α(2)AR auto inhibition of norepinephrine release in WKY. β(1+2)AR opposed α(2)AR inhibition of norepinephrine release in SHR and epinephrine secretion in both strains. βAR-α(2)AR reciprocal control of vascular tension was absent in SHR. Selective agonist provoked β(3)AR-G(i) signaling and influenced the tyramine-induced TPR-response in WKY and catecholamine release in SHR.
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spelling pubmed-44032942015-05-04 Altered β(1−3)-adrenoceptor influence on α(2)-adrenoceptor-mediated control of catecholamine release and vascular tension in hypertensive rats Berg, Torill Front Physiol Neurology α(2)- and β-adrenoceptors (AR) reciprocally control catecholamine release and vascular tension. Disorders in these functions are present in spontaneously hypertensive rats (SHR). The present study tested if α(2)AR dysfunctions resulted from altered α(2)AR/βAR interaction. Blood pressure (BP) was recorded through a femoral artery catheter and cardiac output by an ascending aorta flow probe. Total peripheral vascular resistance (TPR) was calculated. Norepinephrine release was stimulated by a 15-min tyramine-infusion, which allows presynaptic release-control to be reflected as differences in overflow to plasma. Surgical stress activated some secretion of epinephrine. L-659,066 (α(2)AR-antagonist) enhanced norepinephrine overflow in normotensive controls (WKY) but not SHR. Nadolol (β(1+2)) and ICI-118551 (β(2)), but not atenolol (β(1)) or SR59230A [β((3)/1L)] prevented this increase. All βAR antagonists allowed L-659,066 to augment tyramine-induced norepinephrine overflow in SHR and epinephrine secretion in both strains. Inhibition of cAMP-degradation with milrinone and β(3)AR agonist (BRL37344) enhanced the effect of L-659,066 on release of both catecholamines in SHR and epinephrine in WKY. β(1/2)AR antagonists and BRL37344 opposed the L-659,066-dependent elimination of the TPR-response to tyramine in WKY. α(2)AR/βAR antagonists had little influence on the TPR-response in SHR. Milrinone potentiated the L-659,066-dependent reduction of the TPR-response to tyramine. Conclusions: β(2)AR activity was a required substrate for α(2)AR auto inhibition of norepinephrine release in WKY. β(1+2)AR opposed α(2)AR inhibition of norepinephrine release in SHR and epinephrine secretion in both strains. βAR-α(2)AR reciprocal control of vascular tension was absent in SHR. Selective agonist provoked β(3)AR-G(i) signaling and influenced the tyramine-induced TPR-response in WKY and catecholamine release in SHR. Frontiers Media S.A. 2015-04-20 /pmc/articles/PMC4403294/ /pubmed/25941491 http://dx.doi.org/10.3389/fphys.2015.00120 Text en Copyright © 2015 Berg. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neurology
Berg, Torill
Altered β(1−3)-adrenoceptor influence on α(2)-adrenoceptor-mediated control of catecholamine release and vascular tension in hypertensive rats
title Altered β(1−3)-adrenoceptor influence on α(2)-adrenoceptor-mediated control of catecholamine release and vascular tension in hypertensive rats
title_full Altered β(1−3)-adrenoceptor influence on α(2)-adrenoceptor-mediated control of catecholamine release and vascular tension in hypertensive rats
title_fullStr Altered β(1−3)-adrenoceptor influence on α(2)-adrenoceptor-mediated control of catecholamine release and vascular tension in hypertensive rats
title_full_unstemmed Altered β(1−3)-adrenoceptor influence on α(2)-adrenoceptor-mediated control of catecholamine release and vascular tension in hypertensive rats
title_short Altered β(1−3)-adrenoceptor influence on α(2)-adrenoceptor-mediated control of catecholamine release and vascular tension in hypertensive rats
title_sort altered β(1−3)-adrenoceptor influence on α(2)-adrenoceptor-mediated control of catecholamine release and vascular tension in hypertensive rats
topic Neurology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4403294/
https://www.ncbi.nlm.nih.gov/pubmed/25941491
http://dx.doi.org/10.3389/fphys.2015.00120
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