CRF1 and CRF2 receptors in the bed nucleus of stria terminalis differently modulate the baroreflex function in unanesthetized rats

• Published in: The European journal of neuroscience Vol. 46; no. 2; pp. 1805 - 1812
• Main Authors: Oliveira, Leandro A., Almeida, Jeferson, Gomes‐de‐Souza, Lucas, Benini, Ricardo, Crestani, Carlos C.
• Format: Journal Article
• Language: English
• Published: Chichester Wiley Subscription Services, Inc 01-07-2017
• Subjects: Baroreceptors; bed nucleus of stria terminalis; Blood pressure; Bradycardia; cardiovascular system; Corticotropin-releasing hormone; corticotropin‐releasing factor; Heart rate; Intravenous administration; Intravenous infusion; Microinjection; Neurotransmission; Phenylephrine; Pressure drop; Rats; Reflexes; Rodents; Sodium; Sodium nitroprusside; Stria terminalis; Tachycardia; urocortin
• ISSN: 0953-816X; 1460-9568
• DOI: 10.1111/ejn.13622

The baroreflex is an important blood pressure regulating mechanism. The bed nucleus of stria terminalis (BNST) modulates the baroreflex function. However, the local BNST neurochemical mechanisms involved in control of baroreflex responses are not completely understood. Therefore, in this study, we investigated the involvement of corticotropin‐releasing factor (CRF) receptors within the BNST in baroreflex control of heart rate in unanesthetized rats. For this, we evaluated effects of bilateral microinjection into the BNST of either the selective CRF1 receptor antagonist CP376395 (5 nmol/100 nL) or the selective CRF2 receptor antagonist antisauvagine‐30 (5 nmol/100 nL) in bradycardiac response evoked by blood pressure increases caused by intravenous infusion of phenylephrine as well as tachycardiac response to blood pressure decrease caused by intravenous infusion of sodium nitroprusside. Bilateral microinjection of CP376395 into the BNST decreased the baroreflex bradycardiac response without affecting the reflex tachycardia. Conversely, BNST treatment with antisauvagine‐30 decreased heart rate response during blood pressure drop without affecting the reflex bradycardia. Overall, these findings provide evidence of an involvement of CRF neurotransmission within the BNST in baroreflex activity. Nevertheless, data indicate that local CRF1 and CRF2 receptors differently modulate the baroreflex control of heart rate.
Activation of CRF1 and CRF2 receptors within the bed nucleus of stria terminalis (BNST) differently modulates the baroreflex function. BNST CRF1 receptor plays a facilitatory role on bradycardiac response evoked by arterial pressure increase, without affecting the tachycardia to blood pressure decrease. Conversely, activation of CRF2 receptor within the BNST mediates the baroreflex tachycardiac response, without affecting the reflex bradycardiac response.