Quantities of immunoreactive estrone and estradiol in blood plasma, urine, and milk were measured during the estrous cycle and pregnancy of cows. The objectives were to develop a radioimmunoassay procedure for quantifying estrogen in milk and urine and to compare changes in milk estrogen with those in blood plasma and urine. Concentrations of estrone and estradiol in milk varied during the estrous cycle. Relative concentrations of estradiol in blood plasma and milk were not different, but average estrone concentrations in milk were four times greater than those in blood plasma. Concentration of total estrogen (estradiol plus estrone) exceeded 1 ng/ml in colostrum and milk from cows milked prepartum, and was correlated with total estrogen in blood plasma and urine before and after calving. Blood plasma estrone was correlated only with milk estrone whereas blood plasma estradiol was correlated with urinary estradiol, milk estrone, and milk estradiol during the estrous cycle. These results raise possibilities that mammary gland of the lactating cow may concentrate preferentially estrone or convert estradiol to estrone. However, estimated excretion of estrogen through the milk represents no more than a fraction of 1% of the total excreted during the estrous cycle, and the proportion becomes less as gestation progresses up to at least 7 mo.
1 Calcitonin gene-related peptide (CGRP) potently enhances mucosal blood flow in the rat stomach. The aim of this study was to examine whether CGRP also dilates extramural arteries supplying the stomach and whether the vasodilator action of CGRP involves nitric oxide (NO). 2 Rat CGRP-x (0.03-1 nmol kg-', i.v.) produced a dose-dependent increase in blood flow through the left gastric artery (LGA) as determined by an ultrasonic transit time technique in urethane-anaesthetized rats. Blockade of NO synthesis by NG-nitro-L-arginine methyl ester (L-NAME, 20 and 60 ymol kg-', i.v.) significantly reduced basal blood flow (BF) in the LGA and attenuated the hyperaemic activity of CGRP by a factor of 2.8-4. D-NAME tended to enhance basal BF in the LGA but had no influence on the dilator activity of CGRP. The ability of vasoactive intestinal polypeptide to increase left gastric arterial blood flow remained unaltered by L-NAME. 3 L-NAME (20 and 60 ymol kg-', i.v.) evoked a prompt and sustained rise of mean arterial blood pressure (MAP) and caused a slight decrease in the hypotensive activity of CGRP. In contrast, D-NAME induced a delayed and moderate increase in MAP and did not influence the hypotensive activity of CGRP. 4 Rat CGRP-o dilated the isolated perfused bed of the rat LGA precontracted with methoxamine and was 3 times more potent in this respect than rat CGRP-P. The dilator action of rat CGRP-x in this preparation was not affected by L-NAME or D-NAME (40 pM).5 L-NAME (601tmol kg-', i.v.) reduced gastric mucosal blood flow as assessed by laser Doppler flowmetry and diminished the hyperaemic activity of rat CGRP-a in the gastric mucosa by a factor of 4.5, whereas D-NAME was without effect. 6 These data show that CGRP is a potent dilator of mucosal and extramural resistance vessels in the rat stomach. Its dilator action involves both NO-dependent and NO-independent mechanisms.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.