Open AccessUrotensin II-induced increase in myocardial distensibility is modulated by angiotensin II and endothelin-1
Author(s) -
AP Fontes-Sousa,
Pires Al,
Monteiro-Cardoso Vf,
Leite-Moreira Af
Publication year - 2009
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931524
Subject(s) - losartan , urotensin ii , medicine , angiotensin ii , endocrinology , chemistry , angiotensin ii receptor type 1 , endothelin receptor , endothelin 1 , renin–angiotensin system , receptor , blood pressure
Endogenous regulators, such as angiotensin-II (AngII),endothelin-1 (ET-1) and urotensin-II (U-II) are released fromvarious cell types and their plasma levels are elevated in severalcardiovascular diseases. The present study evaluated a potentialcrosstalk between these systems by investigating if themyocardial effects of U-II are modulated by AngII or ET-1.Effects of U-II (10-8, 10-7, 10-6 M) were tested in rabbit papillarymuscles in the absence and in the presence of losartan (selectiveAT1 receptor antagonist), PD-145065 (nonselective ET-1receptors antagonist), losartan plus PD-145065, AngII or ET-1.U-II promoted concentration-dependent negative inotropic andlusitropic effects that were abolished in all experimentalconditions. Also, U-II increased resting muscle length up to1.008±0.002 L/Lmax. Correcting it to its initial value resulted in a19.5±3.5 % decrease of resting tension, indicating increasedmuscle distensibility. This effect on muscle length was completelyabolished in the presence of losartan and significantly attenuatedby PD-145065 or losartan plus PD-145065. This effect wasincreased in the presence of AngII, resulting in a 27.5±3.9 %decrease of resting tension, but was unaffected by the presenceof ET-1. This study demonstrated an interaction of the U-IIsystem with the AngII and ET-1 systems in terms of regulation ofsystolic and diastolic function.