The interaction between renin angiotensin system and sympathetic nervous system in the renal vasculature of normal and hypertensive rats
| dc.contributor.author | H. Abdulla, Mohammed | |
| dc.date.accessioned | 2014-11-03T02:10:42Z | |
| dc.date.available | 2014-11-03T02:10:42Z | |
| dc.date.issued | 2009 | |
| dc.description | Master | en_US |
| dc.description.abstract | Interactions between the renin-angiotensin system (RAS) and sympathetic nervous system (SNS) have recently been the subject of much interest. This study was aimed to examine the adrenergic interactions of intrarenal arterially administered angiotensin II and a set of adrenergic agonists in normal and hypertensive rats. Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) were subjected to 7 days treatment with either losartan (10mg/kg/day), carvedilol (5mg/kg/day) or losartan plus carvedilol (10mg/kg/day+5mg/kg/day), in day 8, rats were anesthetized and renal vasoconstrictor/ vasodilator study was performed. A group of rats was subjected to acute unilateral renal denervation of the left kidney. The changes in the renal vascular responses were determined in terms of reductions or elevations in renal blood flow caused by renal nerve stimulation (RNS), noradrenaline (NA), phenylephrine (PE), methoxamine (ME), angiotensine II (Ang II), dopamine (Dop) and isoprenaline (Isop). The mean arterial pressure (MAP) and renal blood flow (RBF) were continuously monitored throughout the experiment. The data were represented as means±S.E.M. and were analyzed with one- and two-way ANOVA with a significance level of 5%. Baseline values of MAP and RBF remained consistent throughout the study except in few groups. Data showed augmented renal responsiveness to the vasoactive agents after denervation. Moreover, there was a significant (P<0.05) fall in the vascular responses to Ang II and adrenergic agonists after losartan treatment in SHR. Data from rats treated with carvedilol showed significant (P<0.05) reductions in the vasoconstrictor responses to Ang II along with all the adrenergic agonists given. Losartan plus carvedilol treated SHR showed a significant (P<0.05) reduction in the renal vascular responsiveness to Ang II, NA, PE and Dop. While, significant enhancement (P<0.05) in responses to NA, PE and ME was observed in WKY rats. In losartan, carvedilol and losartan plus carvedilol treated denervated SHR, there was a significant (P<0.05) blunting of the responses to neural stimuli and vasoactive agents as compared to untreated denervated SHR. These data suggest an enhanced sensitivity of α1-adrenoceptors to adrenergic agonists and possible enhancement of AT1 receptors functionality in the renal vasculature of these rats. Moreover, renal vasoconstriction induced by Ang II is contributed to by adrenergic action which is not dependent on intact renal innervation. The use of losartan plus carvedilol has no additional depressant effect for renal responses to Ang II while it has aggravating effect for these responses to adrenergic agonists and this indeed indicates a positive cross talk between RAS and SNS. | en_US |
| dc.identifier.uri | http://hdl.handle.net/123456789/216 | |
| dc.language.iso | en | en_US |
| dc.subject | Biological Science | en_US |
| dc.subject | Renin angiotensin system | en_US |
| dc.subject | Sympathetic nervous system | en_US |
| dc.subject | Rats | en_US |
| dc.title | The interaction between renin angiotensin system and sympathetic nervous system in the renal vasculature of normal and hypertensive rats | en_US |
| dc.type | Thesis | en_US |