Luteinising hormone attenuates the vascular response to norepinephrine

Abstract

The present study examines the direct effect of luteinising hormone (LH) on the reactivity of the porcine uterine artery to norepinephrine (NE). Three-mmlong arterial segments collected during the luteal phase of the oestrous cycle were mounted in an organ bath for isometric tension recording. After 30 min of equilibration in optimal passive tone, one part of the vessels was treated with 10 ng/ml of LH in PBS (experimental), while a second part of the arterial segments was treated with 10 ng/ml of bovine serum albumin (BSA) in PBS (control). After 30 min of equilibration, NE was given to each organ bath in a cumulative concentration manner, ranging between 1 × 10 -8 mol/l to 3 × 10 -4 mol/l. NE caused a dose-dependent contraction of all experimental and control arteries. The addition of LH caused a rightward shift of the dose-response curve to NE. The corresponding EC 50 values were 2.17 (± 0.39) µmol/l in PBS-pretreated vessels and 3.35 (± 0.41) µmol/l in LH-pretreated vessels (P < 0.05). The results of the present study demonstrate that LH attenuates the vascular response to NE in third-order branches of the uterine artery. Therefore, it can be suggested that besides the known effect of LH-hCG on the formation of vasoactive eicosanoids, an additional mechanism is involved in the direct action of LH on blood flow in the uterine arteries in pigs.

Contractile effect of PGF2α and PGE2 on isolated branches of uterine and ovarian artery in different days of estrous cycle and early pregnancy in pigs

“…Arteries were prepared for isometric tension recording according to the method described previously (Skipor et al 2007). Randomly chosen arterial rings (n = 6, only uterine or only ovarian artery) were used for the first part of the experiment, while the remaining rings stayed in the Petri dish for a sec-ond part of the experiment, which was conducted 5 hours later (this delay did not influence the vessel reactivity).…”