Cross-talk with β2-adrenoceptors enhances ligand affinity properties from endothelial alpha1D-adrenoceptors that mediates carotid relaxation

Objectives Our main objectives were to investigate the affinity properties of endothelial and muscular α1D-adrenoceptors and to characterize the cross-talk between endothelial α1D- adrenoceptors and β2-adrenoceptors in rat carotid. Methods Relaxation and contraction concentration-response curves for phenylephrine (α1-adrenergic agonist) were obtained in carotid rings in absence or presence of increasing concentrations of BMY7378 (α 1D-adrenergic antagonist), combined or not with increasing concentration of ICI-118,551 (β2-adrenergic antagonist). Schild analysis was used to estimate the affinity constant from pA2 values of BMY7378. Key Findings BMY7378 produced an unsurmountable antagonism on phenylephrine-induced relaxation but a surmountable antagonism on phenylephrine-induced contraction. BMY7378 potency was higher in inhibiting the relaxation than the contraction induced by phenylephrine because the rightward shifts induced by BMY7378 were greater in the relaxation. The apparent pA 2 value for BMY7378 in phenylephrine-induced relaxation was greater than in contraction. When combined with ICI-118,551, BMY7378 yielded a surmountable antagonism on phenylephrine-induced relaxation and presented a pA2 value similar to that obtained in phenylephrine-induced contraction. Conclusions Endothelial α1D-adrenoceptors, which mediates rat carotid relaxation, present high ligand affinity because of the cross-talk with β2-adrenoceptors, which explains the higher potency of phenylephrine in inducing relaxation than contraction and the atypical unsurmountable antagonism produced by BMY7378 on phenylephrine-induced relaxation. © 2013 Royal Pharmaceutical Society.

Horner-s Syndrome following common carotid artery translocation in a horse: case report

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Evaluation of clinical and inflammatory markers of subclinical carotid atherosclerosis in postmenopausal women

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

L-Carnitine supplementation impairs endothelium-dependent relaxation in mesenteric arteries from rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Manutenção da prática de atividade física e indicadores hemodinâmicos, metabólicos e inflamatório em adultos: análise transversal e coorte de 12 meses

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Systemic blood flow relations in conscious South American rattlesnakes

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Pseudoaneurysm of the internal carotid artery presenting with massive (recurrent) epistaxes: a life-threatening complication of craniofacial trauma

Vascular lesions can be serious complications resulting of blunt or penetrating trauma(1,2). Internal carotid artery lesion is one of most serious and relatively frequent in all mechanisms of craniofacial trauma. Several clinical manifestations can occur as central neurologic and cranial nerves deficits as well as several degrees of bleeding (from mild symptomatic to fatal). Recurrent and massive epistaxis can occur after trauma due to pseudaoneurysms of the external and internal carotid artery (ICA)(3,4). Considering its life-threatening course, the assisting physician has a relatively narrow time to detect and treat these lesions.We present two cases of recurrent and massive epistaxis secondary to ICA pseudoaneurysm following blunt and perforating trauma. Evolution was fatal in the first case with delayed treatment and uneventfully in the second which was treated by occlusion of the pseudoaneurysm and ICA via endovascular intervention.