Key result
In the isolated human uterine artery, atrial natriuretic peptide inhibited the smooth muscle contractile activity elicited by angiotensin II, decreasing both maximum contractile response and pD2.
ANP specifically antagonizes the contractile effect of Angiotensin II in the human uterine artery, which may be relevant to the pathogenesis of pre-eclampsia.
May implicate ANP-Ang II interaction in pre-eclampsia; leaves open any mechanistic or therapeutic role.
The regulatory peptides angiotensin II (Ang II) and atrial natriuretic peptide (ANP) are believed to play important roles in the pathogenesis of pre-eclampsia. The interactions between Ang II, ANP and noradrenaline (NA) were studied in vitro on the human uterine artery. Both Ang II and NA contracted the isolated vessel in a concentration-dependent way. At high doses a decrease in the contractile force induced by Ang II but not NA was encountered. ANP inhibited the smooth muscle activity elicited by Ang II, resulting in a dextroshift of the concentration-response curve, and a decrease in both Emax (the maximum contractile response) and pD2 (the negative logarithm of the agonist concentration inducing 50% of the Emax) for Ang II. The results might indicate a specific antagonism between Ang II and ANP, probably at the post-receptor level. ANP did not induce any significant change in pD2 of the concentration-response curve for NA. Only at the highest dose of ANP (10(-7) M) was Emax depressed. Thus, the results only indicate a weak antagonistic relationship between NA and ANP in the human uterine artery.
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Poulsen et al. (1994) studied Pre-eclampsia (in vitro human uterine artery model). Atrial natriuretic peptide (ANP) vs. Angiotensin II and noradrenaline alone was evaluated on Smooth muscle contractile activity. In the isolated human uterine artery, atrial natriuretic peptide inhibited the smooth muscle contractile activity elicited by angiotensin II, decreasing both maximum contractile response and pD2.
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