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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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Detalles Bibliográficos
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
Descripción
Sumario: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.