Cardiovascular effects of @entity1 @entity461 and XXXX -related peptide.

@entity1 @entity1831 @entity101 @entity4293 @entity5463 @entity35 @entity551 @entity461
@entity461 ( @entity461 ) is @entity551 in mammals and is a potent coronary vasodilator. @entity4293 ( @entity4293 ) has been reported to have similar vascular activity. In the present study, the effects of @entity1 @entity461 ( @entity461 ) and @entity1 @entity4293 (hPTHrp) were compared in various in vivo and in vitro assays. In vivo studies included blood pressure measurement and coronary blood flow determination with labeled microspheres in anesthetized and cannulated normotensive @entity35 . Isolated @entity35 tail artery and portal vein helical strips were used in studying tension development in vitro. In the blood pressure assay, @entity4293 was several times more potent than @entity461 . @entity4293 was also significantly more potent than @entity461 in relaxing tail artery precontracted with @entity5463 ( @entity1831 ). @entity4293 and @entity461 both inhibited the spontaneously contracting portal vein, but again @entity4293 was significantly more potent. @entity4293 (1 microgram/kg) produced a greater increase in coronary blood flow as compared with the same dose of @entity461 . These data suggest that @entity4293 is more potent than @entity461 in its cardiovascular actions. It is possible that @entity4293 is the endogenous vasodilating ligand, and the structural similarity between @entity461 and @entity4293 may explain the pharmacological action of @entity461 . It is therefore unlikely that @entity461 or @entity4293 may be involved in the genesis or maintenance of @entity101 . Because the parathyroid gland seems to be involved in some forms of essential @entity101 , factor(s) other than @entity461 or @entity4293 may be responsible.
