The Interaction Of Renin Angiotensin And Sympathetic Nervous Systems On Renal Haemodynamics In Hypertension

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Date
2005-09
Authors
Wong, Kuan Yau
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Abstract
The renin angiotensin (RAS) and sympathetic nervous system (SNS) are closely interrelated and are involved in the maintenance of blood pressure and body fluid homeostasis. This study examined the role of the RAS and SNS at the peripheral levels in normo and hypertension in the control of renal haemodynamics and to assess any alterations in renal haemodynamics after chemical sympathectomy. For this purpose, WKY rats, SHR, 2K1C Goldblatt and DOCA-salt hypertensive rats were utilised. Chemical sympathectomy was carried out by the administration of 6-0HDA intraperitoneally to animals at a dose of 50mg/kg on day 1, 100 mg/kg on day 2 and 50mg/kg on days 5 and 8. Perindopril was given orally at a dose of 0.2 mg/kg for 7 days. In haemodynamics study, the animal was anaesthetized (60 mg/kg IP, sodium pentobarbitone), followed by cannulation of carotid artery & jugular vein and isolation of renal artery. Renal blood flow (RBF) was measured using electromagnetic flow probe. Arterial blood pressure was measured using pressure transducer. All data were recorded in computerized data acquisition system. Data was expressed as mean ± S.E.M and compared by 2 way ANOVA followed by Bonferroni post hoc with the significance level of 5%. A substantial change was observed in the sympathectomized rats in terms of haemodynamics. There was a marked reduction of blood pressure in sympathectomized hypertensive rats. However, there was no significant change in renal blood flow after sympathectomy. Without ACE inhibition, noradrenaline and phenylephrine were found to exert a significant difference (p<0.05) in peripheral and renal haemodynamics of both of normo- and hypertensive rats xix except in DOCA-salt models when administered peripherally and intrarenally. However, a significant change (p<O.05) was observed in blood pressure to peripheral methoxamine in both normo- and hypertensive rats. Moreover, when administered intrarenally it caused a significant reduction in RBF only, in both normo-and hypertensive rats. Angiotensin II, peripherally and intrarenally caused significant change (p<O.05) in peripheral and renal haemodynamics in normotensive rats only. Angiotensin II caused a significant change in RBF only in sympathectomized SHR and DOCA-salt hypertensive rats when administered intrarenally. With ACE inhibition, NA was found to exert a significant difference (p<O.05) in peripheral arid renal haemodynamics in 2K1C Goldblatt and DOCAsalt .h ype-rtensive animal when-administered intrarenally. PE did not cause any . significant change in pressor and renal vasoconstrictor responses in both normo and hypertensive animals except renal vasoconstrictor responses to intrarenal PE in 2K1C Goldblatt and DOCA salt. A meaningful change (p<O.05) was observed in RBF to MTX when administered peripherally and intrarenally in sympathectomized SHR. Ang II peripherally and intrarenally did not cause major changes in pressor responses in both sympathectomized WKY and SHR. However there was attenuation in renal vasoconstrictor responses to peripheral and intrarenal Ang II in sympathectomized DOCA-salt hyperten~ive animals. These results suggested that, u1-adrenoceptors and RAS are involved in mediating the pressor responses in both the peripheral and renal resistance vessels, thus indicating a complex interaction of SNS and RAS in hypertension.
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The renin angiotensin (RAS) and sympathetic nervous system (SNS) are , involved in the maintenance of blood pressure and body fluid homeostasis.
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