The main objective of our study was to determine whether angiotensins
cause vasoconstriction of mammary arterial segments in vitro. Once thi
s action was established, its specificity was determined. Mammary arte
rial sections were obtained from lactating cattle at slaughter. Vessel
sections were placed in a gravity-fed, closed, perfusion apparatus, a
nd flow was measured by a transit-time flow sensor mounted in-line. Tr
eatments were administered by injection into a leurlock port located p
roximal to the sensor. Angiotensins I, II, and III induced a dose-depe
ndent vasoconstriction of arterial segments at concentrations of 5 x 1
0(-10) to 5 x 10(-6) M. Angiotensin II receptor antagonists, Saralisin
and (Sarl, Thr8)-angiotensin II (5 x 10(-8) M)), inhibited vasoconstr
iction induced by angiotensins I, II, and III. The angiotensin-convert
ing enzyme inhibitor, Captopril (5 x 10(-8) M), inhibited angiotensin
I vasoconstriction, thereby showing that the vasoconstriction by angio
tensin I was mediated through its conversion to angiotensin II. These
data demonstrated that the mammary artery of lactating cows is respons
ive to the angiotensin family. Furthermore, mammary arteries contain a
ngiotensin-converting enzyme and specific receptors for angiotensin II
. This system may be important in the normal physiological regulation
of mammary gland blood flow of lactating cows.