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Reproduction in Domestic Animals

Reproduction in Domestic Animals

Reproduction in Domestic Animals

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Regulation of Luteal Function 61bov<strong>in</strong>e CL. These data suggest that NO produced bytwo NOS isoforms is <strong>in</strong>volved <strong>in</strong> structural and functionalchanges that occur <strong>in</strong> the bov<strong>in</strong>e CL through thewhole oestrous cycle. Luteolytic or luteotropic actionsof NO on the bov<strong>in</strong>e CL is strictly dependent on thestage of CL, and cell <strong>in</strong>teractions (cell-to-cell contact)and composition (Jaroszewski et al. 2003a; Klipperet al. 2004; Weems et al. 2004; Rosiansky-Sultan et al.2006). Nitric oxide donor (S-NAP) stimulated PGE 2secretion by steroidogenic CL cells <strong>in</strong> the early and midlutealphases (Skarzynski et al. 2000). Dur<strong>in</strong>g developmentand ma<strong>in</strong>tenance of the CL, PGE 2, which is bothluteotropic and antiluteolytic, stimulated NO production(Boiti et al. 2000). Nitric oxide donors and ET-1<strong>in</strong>creased PGE 2 secretion by bov<strong>in</strong>e CL slices <strong>in</strong> vitro ondays 13–14 of the cycle without any effect on P4secretion (Weems et al. 2004). Therefore, <strong>in</strong>creased NOproduction dur<strong>in</strong>g early stages of the cycle and pregnancyis likely to play a role <strong>in</strong> CL development andangiogenesis (Skarzynski et al. 2000; Weems et al. 2004;Vonnahme et al. 2005; Rosiansky-Sultan et al. 2006).In the late luteal phase PGF 2a might simulate a shearstress-like reaction of endothelial CL cells result<strong>in</strong>g <strong>in</strong>compensative NO release dur<strong>in</strong>g the first steps ofluteolysis – up to 2–4 h after PGF 2a treatment (Li et al.2002; Skarzynski et al. 2003b; Acosta et al. 2007). Intralutealadm<strong>in</strong>istration of a NOS <strong>in</strong>hibitor (L-NAME)dur<strong>in</strong>g the late luteal phase <strong>in</strong>creased P4 secretion andprolonged the functional lifespan of bov<strong>in</strong>e CL (Jaroszewskiand Hansel 2000; Sasahara et al. 2007). Whenan analogue of PGF 2a (aPGF 2a , cloprostenol) was<strong>in</strong>jected on day 15 of the cycle <strong>in</strong> comb<strong>in</strong>ation withL-NAME, the luteolytic effect of aPGF 2a was counteractedby the NOS <strong>in</strong>hibitor (Fig. 4; Jaroszewski et al.2003b; Skarzynski et al. 2003b). Nitric oxide has beenfound as the most potent <strong>in</strong>hibitor of P4 secretion<strong>in</strong> vitro (Skarzynski et al. 2003b; Korzekwa et al. 2004,2006) and <strong>in</strong> vivo (Sasahara et al. 2007). Moreover, aNO donor (Sperm<strong>in</strong>e NONOate) strongly stimulatedproduction of PGF 2a and LTC 4 by bov<strong>in</strong>e CL both<strong>in</strong> vitro and <strong>in</strong> vivo, show<strong>in</strong>g that NO is <strong>in</strong>volved <strong>in</strong> theprocess of luteal regression by bov<strong>in</strong>e CL (Fig. 3;Progesterone (ng/ml)129630L-NAME/aPGF (n = 5)Sal<strong>in</strong>e/aPGF(n = 6)L-NAME/Sal<strong>in</strong>e (n = 4)Sal<strong>in</strong>e/sal<strong>in</strong>e (n = 4)aPGF0 3 6 9 12 15 18 0 4Day of the estrous cycle– EstrusEstrusFig. 4. The effect of 2 h <strong>in</strong>fusion of sal<strong>in</strong>e or nitric oxide synthase<strong>in</strong>hibitor-L-NAME (400 mg ⁄ h) and <strong>in</strong>jection of sal<strong>in</strong>e or PGF 2aanalogue, cloprostenol (aPGF; 100 lg; Bioestrophan, Biowet, GorzowWielkopolski, Poland) at 30 m<strong>in</strong> of <strong>in</strong>fusion on progesterone concentrations<strong>in</strong> peripheral blood plasma of heifers on day 15 of the oestrouscycle. Different subscript letters <strong>in</strong>dicate significant differences(p

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