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Am J Physiol Heart Circ Physiol 281: H60-H66, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 1, H60-H66, July 2001

Parathyroid hormone-related protein-(1-34) inhibits intrinsic pump activity of isolated murine lymph vessels

Risuke Mizuno1, Nobuyuki Ono2, and Toshio Ohhashi1,3

1 First Department of Physiology, Shinshu University School of Medicine, Matsumoto; 2 Department of Electronics and Control Engineering, Nagano National College of Technology, Nagano, 381-8550; and 3 Institute of Organ Transplants, Reconstructive Medicine, and Tissue Engineering, Shinshu University Graduate School of Medicine, Matsumoto 390-8621, Japan

Parathyroid hormone-related protein (PTHrP) was originally found as a tumor-derived vasoactive factor and has also been known to produce significant relaxation of vascular smooth muscles. Thus effects of PTHrP-(1-34), a PTH receptor-binding domain, on spontaneous lymphatic pump activity was investigated in isolated pressurized lymph vessels of mice. Low concentrations (1 × 10-10 and 3 × 10-10 M) of PTHrP-(1-34) dilated lymph vessels and reduced the frequency of pump activity, whereas high concentrations (1 × 10-9 to 1 × 10-8 M) of PTHrP-(1-34) caused dilation with cessation of the lymphatic pump activity. Nomega -nitro-L-arginine methyl ester (L-NAME; 3 × 10-5 M) but not indomethacin (1 × 10-5 M) significantly reduced the PTHrP-(1-34)-induced inhibitory responses of the lymphatic pump activity. In the presence of L-NAME (3 × 10-5 M) and L-arginine (1 × 10-3 M), the L-NAME-induced inhibition in the PTHrP-(1-34)-mediated responses was significantly reduced. Glibenclamide (1 × 10-6 M) significantly suppressed the inhibitory responses of the lymphatic pump activity induced by PTHrP-(1-34) and S-nitroso-N-acetyl-penicillamine. The PTHrP-(1-34)-mediated inhibitory responses were significantly reduced by treatment with PTHrP-(7-34) (1 × 10-7 M). These results suggest that PTHrP-(1-34) inhibits spontaneous pump activity of the isolated lymph vessels via PTH receptors and that production and release of endogenous nitric oxide and activation of ATP-sensitive K+ channels in the lymph vessels contribute to the PTHrP-(1-34)-mediated inhibitory responses of the lymphatic pump activity.

mice; nitric oxide; ATP-sensitive K+ channel


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