Synthetic human parathyroid hormone-related peptide (hPTHrP)-(1-34) fragment was compared with parathyroid hormone (bovine sequence, 1-34; bPTH-(1-34) for inhibiting oxytocin or prostaglandin F2 alpha (PGF2 alpha)-induced contractions on rat uterus in vitro. bPTH exhibited a potent (ED50 = 7 x 10(-9) M) inhibition on oxytocin-induced contractions. Both bPTH-(1-34) and hPTHrP-(1-34) were devoided of any significant effect upon PGF2 alpha-induced uterine contractions. Human PTHrP also inhibited oxytocin-induced uterine contractions (ED50 = 77 x 10(-9) M) and this effect, like that of bPTH, was dose dependent. Human PTHrP-(140-173) fragment had no significant effect on oxytocin-induced uterine contractions. The inhibitory effect of hPTHrP-(1-34) disappeared after pretreatment with [Tyr]34-bPTH-(7-34)-NH2, a competitive reversible antagonist of bPTH-(1-34). Thus PTHrP might be involved in the control of myometrial activity.
The effects of dopamine on plasma renin-angiotensin-aldosterone system vasopressin levels and blood pressure were studied in anesthetized guinea-pig. The inhibition of the angiotensin converting enzyme with perindopril permitted assessment of the role of the renin-angiotensin system. In perindopril-treated guinea-pigs, the activity of angiotensin-converting enzyme was decreased by 90% with simultaneous increases in plasma renin activity and angiotensin I concentration; aldosterone and vasopressin levels, blood pressure and heart rate were not modified. Dopamine depressed mean arterial pressure by 30% and increased heart rate (8%) in controls. Dopamine infusion did not affect either plasma renin activity or angiotensin I concentration or angiotensin-converting enzyme activity in control animals. But in perindopril pretreated animals it further increased plasma renin activity (88%) and angiotensin I concentration (35%). Finally, in controls, dopamine infusion increased plasma vasopressin concentrations (91%) whereas this increase did not occur in perindopril treated animals.
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