“…However, Killam, Rosenfeld, Battaglia, Makowski & Meschia (1973) found that surgery and anaesthesia suppressed oestrogen-induced vasodilatation in ovariectomized ewes. The magnitude of oestrogen-induced vasodilatation in chronic preparations is clearly much greater in ovariectomized (Killam et al, 1973;Resnik, Killam, Battaglia, Makowski & Meschia, 1974;Resnik, Battaglia, Makowski & Meschia, 1975;Resnik & Brink, 1978, 1980 than in intact animals (Nuwayhid et al, 1975;present results), probably due to differences in tissue sensitivity resulting from endogenous steroid depletion and subsequent stimulation by repeated injections of oestradiol. Thus, the high flow observed in our study in pregnant animals cannot be attributed to anaesthesia, though it may be related to a reduction in sympathetic vascular tone arising from the procedure of confining flow to the middle uterine artery (Ladner, Brinkman, Weston & Assali, 1970;Bell, 1972).…”
Summary. Uterine blood flow and myometrial activity were measured simultaneously in anaesthetized sheep 15 days after a sterile (non-pregnant group) or fertile (pregnant) mating. During the peri-implantation period uterine blood flow was similar in both groups of animals, but spontaneous myometrial activity was greatly reduced in pregnant ewes. This 'block' of myometrial activity was associated with circulating levels of progesterone which were significantly higher (2\m=.\8\ m=+-\0\m=.\8ng/ml, mean \m=+-\ s.e.m.) than those in non-pregnant animals (0\m=.\4 \m=+-\0\m=.\3 ng/ml). Adenosine injected into the uterine artery produced uterine vasodilatation in both groups, but the log dose\p=n-\response was significantly less in pregnant than in non-pregnant animals (P < 0\m=.\001).Myometrial activity was stimulated by adenosine, particularly in the pregnant group (P < 0\m=.\001
“…However, Killam, Rosenfeld, Battaglia, Makowski & Meschia (1973) found that surgery and anaesthesia suppressed oestrogen-induced vasodilatation in ovariectomized ewes. The magnitude of oestrogen-induced vasodilatation in chronic preparations is clearly much greater in ovariectomized (Killam et al, 1973;Resnik, Killam, Battaglia, Makowski & Meschia, 1974;Resnik, Battaglia, Makowski & Meschia, 1975;Resnik & Brink, 1978, 1980 than in intact animals (Nuwayhid et al, 1975;present results), probably due to differences in tissue sensitivity resulting from endogenous steroid depletion and subsequent stimulation by repeated injections of oestradiol. Thus, the high flow observed in our study in pregnant animals cannot be attributed to anaesthesia, though it may be related to a reduction in sympathetic vascular tone arising from the procedure of confining flow to the middle uterine artery (Ladner, Brinkman, Weston & Assali, 1970;Bell, 1972).…”
Summary. Uterine blood flow and myometrial activity were measured simultaneously in anaesthetized sheep 15 days after a sterile (non-pregnant group) or fertile (pregnant) mating. During the peri-implantation period uterine blood flow was similar in both groups of animals, but spontaneous myometrial activity was greatly reduced in pregnant ewes. This 'block' of myometrial activity was associated with circulating levels of progesterone which were significantly higher (2\m=.\8\ m=+-\0\m=.\8ng/ml, mean \m=+-\ s.e.m.) than those in non-pregnant animals (0\m=.\4 \m=+-\0\m=.\3 ng/ml). Adenosine injected into the uterine artery produced uterine vasodilatation in both groups, but the log dose\p=n-\response was significantly less in pregnant than in non-pregnant animals (P < 0\m=.\001).Myometrial activity was stimulated by adenosine, particularly in the pregnant group (P < 0\m=.\001
“…The available evidence suggests that oestrogens mediate the increase in uterine blood flow occurring in pregnancy and during the oestrous cycle (Markee 1932, Greiss & Anderson 1970, Killam et al 1973, Rosenfeld 1989. The mechanism(s) responsible for oestrogen-induced elevated blood flow remain, despite much effort, unclear .…”
Section: Discussionmentioning
confidence: 99%
“…Increases in uterine blood flow by 17 -oestradiol are prevented by the NOS inhibitor nitro--arginine methyl ester, suggesting that nitric oxide is involved (Van Buren et al 1992, Rosenfeld et al 1996. However, other vasoactive substances, such as prostanoids and vasoactive polypeptides have also been implicated (Killam et al 1973, Clark et al 1981a. Here, we report that both ER and are expressed in uterine vessels and thus both receptors may be involved in the regulation of uterine blood flow by oestrogens.…”
The role of oestrogen receptor (ER) in vascular function remains unclear. With the use of a specific ER antibody we have now, using immunocytochemistry, visualized ER in different parts of the vascular tree. In about 70% of medial smooth muscle cells of female rat aorta, tail artery and uterine artery, nuclear immunoreactivity to ER was observed. In these vessels endothelial cells also expressed ER . Vascular expression of the ER subtype was lower than that of ER . In aorta and tail artery, no immunoreactivity towards ER was observed, while in uterine vessels occasional medial smooth muscle and endothelial cells expressed this ER subtype. ER and expression in uterine vessels was independent of the stage of the oestrous cycle, suggesting that variations in uterine blood flow occurring during the cycle are independent of ER density. The regional distribution of ER , as determined by immunocytochemistry, was supported by measurements of ER levels by enzyme immunoassay. In the uterine artery, the level of ER was several times higher (P<0·001) than that of aorta and tail artery (10·1 1·7 fmol/mg protein in the uterine artery vs 3·3 1·0 and 0·5 0·5 fmol/mg protein in aorta and tail artery respectively). Thus, a prominent nuclear expression of ER was observed in the vascular wall of several parts of the vascular tree, while ER predominantly was expressed in uterine vessels, suggesting that ER and may have different roles in vascular function.
“…Sensitization to ACh in a proportion of animals 1 h after intramuscular administration of 10 mg oestradiol-17ß has been observed (C. Coffey, unpublished observation). In the sheep the uterine dilator effect of oestrogens appears within 30-40 min after intra-arterial administration (Killam, Rosenfeld, Battaglia, Makowski & Meschia, 1973), although ACh receptors do not appear to be involved in this species (Nuwayhid, Brinkman, Woods, Martinek & Assali, 1975).…”
Summary. The guinea-pig uterine artery responded to acetylcholine (ACh) with vasodilatation only during pregnancy or after oestrogen treatment. Even with high doses (1 mg/day) oestradiol-17\g=b\ esters had to be administered for several days to effect sensitization to ACh, but oestradiol-17\g=b\ itself was active within a few hours. Oestriol was equipotent with oestradiol. Sensitization was prevented when protein synthesis was inhibited over the period of oestrogen administration, but was not dependent on the integrity of the cholinergic vasodilator nerve supply to the artery.
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