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Effects of des-aspartate-angiotensin I on the actions of angiotensin III in the renal and mesenteric vasculature of normo- and hypertensive rats.
Regul Pept. 2004 Aug 15; 120(1-3):15-22.RP

Abstract

An earlier study showed that des-aspartate-angiotensin I (DAA-I) attenuated the pressor action of angiotensin III in aortic rings of the spontaneously hypertensive rat (SHR) but not the normotensive Wistar Kyoto (WKY) rat. The present study investigated similar properties of DAA-I in isolated perfused kidneys and mesenteric beds of WKY and SHR. In the renal vasculature, angiotensin III induced a dose-dependent pressor response, which was more marked in the SHR than WKY in terms of significant greater magnitude of response and lower threshold. DAA-I attenuated the pressor action of angiotensin III in both the WKY and SHR. The attenuation in SHR was much more marked, occurring at doses as low as 10(-15) M DAA-I, while effective attenuation was only seen with 10(-9) M in WKY. The effects of DAA-I was not inhibited by PD123319 and indomethacin, indicating that its action was not mediated by angiotensin AT2 receptors and prostaglandins. However, the direct pressor action of angiotensin III in the SHR but not the WKY was attenuated by indomethacin suggesting that this notable difference could be due to known decreased response of renal vasculature to vasodilator prostaglandins in the SHR. Pressor responses to angiotensin III in the mesenteric vascular bed was also dose dependent, but smaller in magnitude compared to the renal response. The responses in the SHR, though generally smaller, were not significantly different from those of the WKY. This trend is in line with the similar observations with angiotensin III and II by other investigators. In terms of the effect of DAA-I, indomethacin and PD123319 on angiotensin III action, similar patterns to those of the renal vasculature were observed. This reaffirms that in the perfused kidney and mesenteric bed, where the majority of the vessels are contractile, femtomolar concentrations of DAA-I attenuates the pressor action of angiotensin III. The attenuation is not indomethacin sensitive and does not involve the angiotensin AT2 receptor. The findings suggest that DAA-I possesses protective vascular actions and is involved in the pathophysiology of hypertension.

Authors+Show Affiliations

Department of Pharmacology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15177916

Citation

Mustafa, M R., et al. "Effects of Des-aspartate-angiotensin I On the Actions of Angiotensin III in the Renal and Mesenteric Vasculature of Normo- and Hypertensive Rats." Regulatory Peptides, vol. 120, no. 1-3, 2004, pp. 15-22.
Mustafa MR, Dharmani M, Kunheen NK, et al. Effects of des-aspartate-angiotensin I on the actions of angiotensin III in the renal and mesenteric vasculature of normo- and hypertensive rats. Regul Pept. 2004;120(1-3):15-22.
Mustafa, M. R., Dharmani, M., Kunheen, N. K., & Sim, M. K. (2004). Effects of des-aspartate-angiotensin I on the actions of angiotensin III in the renal and mesenteric vasculature of normo- and hypertensive rats. Regulatory Peptides, 120(1-3), 15-22.
Mustafa MR, et al. Effects of Des-aspartate-angiotensin I On the Actions of Angiotensin III in the Renal and Mesenteric Vasculature of Normo- and Hypertensive Rats. Regul Pept. 2004 Aug 15;120(1-3):15-22. PubMed PMID: 15177916.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of des-aspartate-angiotensin I on the actions of angiotensin III in the renal and mesenteric vasculature of normo- and hypertensive rats. AU - Mustafa,M R, AU - Dharmani,M, AU - Kunheen,N K, AU - Sim,M K, PY - 2003/07/16/received PY - 2003/12/23/accepted PY - 2004/6/5/pubmed PY - 2005/1/12/medline PY - 2004/6/5/entrez SP - 15 EP - 22 JF - Regulatory peptides JO - Regul Pept VL - 120 IS - 1-3 N2 - An earlier study showed that des-aspartate-angiotensin I (DAA-I) attenuated the pressor action of angiotensin III in aortic rings of the spontaneously hypertensive rat (SHR) but not the normotensive Wistar Kyoto (WKY) rat. The present study investigated similar properties of DAA-I in isolated perfused kidneys and mesenteric beds of WKY and SHR. In the renal vasculature, angiotensin III induced a dose-dependent pressor response, which was more marked in the SHR than WKY in terms of significant greater magnitude of response and lower threshold. DAA-I attenuated the pressor action of angiotensin III in both the WKY and SHR. The attenuation in SHR was much more marked, occurring at doses as low as 10(-15) M DAA-I, while effective attenuation was only seen with 10(-9) M in WKY. The effects of DAA-I was not inhibited by PD123319 and indomethacin, indicating that its action was not mediated by angiotensin AT2 receptors and prostaglandins. However, the direct pressor action of angiotensin III in the SHR but not the WKY was attenuated by indomethacin suggesting that this notable difference could be due to known decreased response of renal vasculature to vasodilator prostaglandins in the SHR. Pressor responses to angiotensin III in the mesenteric vascular bed was also dose dependent, but smaller in magnitude compared to the renal response. The responses in the SHR, though generally smaller, were not significantly different from those of the WKY. This trend is in line with the similar observations with angiotensin III and II by other investigators. In terms of the effect of DAA-I, indomethacin and PD123319 on angiotensin III action, similar patterns to those of the renal vasculature were observed. This reaffirms that in the perfused kidney and mesenteric bed, where the majority of the vessels are contractile, femtomolar concentrations of DAA-I attenuates the pressor action of angiotensin III. The attenuation is not indomethacin sensitive and does not involve the angiotensin AT2 receptor. The findings suggest that DAA-I possesses protective vascular actions and is involved in the pathophysiology of hypertension. SN - 0167-0115 UR - https://www.unboundmedicine.com/medline/citation/15177916/Effects_of_des_aspartate_angiotensin_I_on_the_actions_of_angiotensin_III_in_the_renal_and_mesenteric_vasculature_of_normo__and_hypertensive_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0167011503003185 DB - PRIME DP - Unbound Medicine ER -