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Analysis of angiotensin II-Induced rat urinary bladder contractions in the presence of angiotensin II receptors blockers.
Archives of Physiology and Biochemistry 2019 Februrary 11
OBJECTIVE: An application of a specific analysis on recordings obtained from urinary bladder (UB) preparations influenced with Angiotensin II (AngII) and AngII receptor (ATR) blockers was performed.
METHODS: UB preparations were divided as follows: group 1 stimulated with AngII only; group 2:PD123319 (ATR type-2 blocker)+AngII; group 3:Losartan (ATR type-1 blocker)+AngII. The averaged time and force parameters of the contractions were processed by a spline interpolation and graphic images of the different patterns of the contractile activity were obtained.
RESULTS: The speed of AngII-induced UB contraction, when PD123319 was administered, was significantly higher than those, registered by the application of AngII alone and Losartan + AngII. The presence of Losartan markedly delayed the speed of the overall AngII-induced contraction.
CONCLUSION: The study indicates the contribution of both ATR subtypes for the development of AngII-induced UB contraction. Our results showed that probably ATR mediate a reciprocal dynamic response to AngII in the bladder.
METHODS: UB preparations were divided as follows: group 1 stimulated with AngII only; group 2:PD123319 (ATR type-2 blocker)+AngII; group 3:Losartan (ATR type-1 blocker)+AngII. The averaged time and force parameters of the contractions were processed by a spline interpolation and graphic images of the different patterns of the contractile activity were obtained.
RESULTS: The speed of AngII-induced UB contraction, when PD123319 was administered, was significantly higher than those, registered by the application of AngII alone and Losartan + AngII. The presence of Losartan markedly delayed the speed of the overall AngII-induced contraction.
CONCLUSION: The study indicates the contribution of both ATR subtypes for the development of AngII-induced UB contraction. Our results showed that probably ATR mediate a reciprocal dynamic response to AngII in the bladder.
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