مشروع البحث: PARAVENTRICULAR NUCLEUS V1b RECEPTORS MEDIATE INTRANUCLEAR VASOPRESSIN-INDUCED SYMPATHETIC NERVE ACTIVITY IN CONSCIOUS
| dc.contributor.advisor | جامعة واين ستيت | |
| dc.date.accessioned | 2024-12-11T14:10:22Z | |
| dc.date.available | 2024-12-11T14:10:22Z | |
| dc.description | blockade completely abolished AVP induced changes in both MAP and HR. Furthermore, we investigated whether peripheral AVP levels increased after microinjection of AVP into the PVN due to either stimulation of AVP release from magnocellular neurons into systemic circulation, or AVP leakage from the injection site to the periphery. In a separate group of rats, we observed that plasma AVP levels 10 minutes after AVP microinjection into the PVN were not significantly different from baseline levels or from saline-injected controls. Finally, to exclude the possibility of leakage of centrally injected AVP into the periphery, arterial blood samples were taken in anesthetized rats before and after PVN microinjection with AVP. Leakage was < 0.3%. These data support the concept that in conscious unrestrained rats under basal conditions microinjection of AVP into the PVN produces significant increases in mean | |
| dc.description.abstract | ABSTRACT Studies have shown that V1b receptors mediate the pituitary vasopressin (AVP) effects in regulating hypothalamic pituitary axis (HPA) activity during stress; nevertheless, the role of V1b receptors in cardiovascular system regulation has not been studied. Dendritically released AVP in the PVN may act as a neurotransmitter/neuromodulator. Dendritically released AVP may play a role in regulating efferent outputs from the paraventricular nucleus of the hypothalamus (PVN) to caudal cardiovascular regulatory sites controlling hemodynamics and sympathetic nerve activity. Given the evidence that the PVN of the hypothalamus is involved in autonomic control of cardiovascular function, we hypothesized that dendritic release of AVP will increase MAP, HR and RSNA by acting upon V1b receptors. We found that unilateral microinjection of AVP into the PVN of conscious Sprague Dawley rats significantly increased MAP, HR and RSNA. Pretreatment of the PVN with the selective V1b receptor antagonist, nelivaptan, blocked the pressor, tachycardic and RSNA responses to AVP. We further evaluated whether these responses to AVP were due to sympathetic nerve activation or peripheral AVP effects. We found that ganglionic | |
| dc.identifier | 343 | |
| dc.identifier.uri | https://dspace.academy.edu.ly/handle/123456789/846 | |
| dc.subject | arterial pressure, heart rate and RSNA that are mediated by V1b receptors due to increased sympathetic outflow and not due to AVP release into the periphery | |
| dc.title | PARAVENTRICULAR NUCLEUS V1b RECEPTORS MEDIATE INTRANUCLEAR VASOPRESSIN-INDUCED SYMPATHETIC NERVE ACTIVITY IN CONSCIOUS | |
| dspace.entity.type | Project | |
| project.endDate | 2013 | |
| project.funder.name | علم وظائف الاعضاء | |
| project.investigator | WAFA M. ELWERFALI | |
| project.startDate | 2012 |