Original ArticleMouse Hepatic Portal Venoconstrictive Response to Vasoconstrictors Is Much Weaker Than That in RatZhao, Zhan-Sheng MD, PhD*; Shibamoto, Toshishige MD, PhD*; Tsutsumi, Mikihiro MD, PhD†; Cui, Sen MD, PhD*; Zhang, Wei M*; Takano, Hiromichi PhD*; Kurata, Yasutaka MD, PhD*Author Information From the Departments of *Physiology II and †Gastroenterology, Kanazawa Medical University, Uchinada Ishikawa, Japan. Dr Z-S. Zhao is now with the Department of Endocrinology, Hebei Medical University, China. Dr H. Takano is now with the Department of Physiology, Nagoya City University School of Medicine, Japan. Received for publication March 14, 2009; accepted July 13, 2009. Dr Z-S. Zhao and Dr W. Zhang were supported by postdoctoral fellowships for foreign researchers of Kanazawa Medical University in 2006 and 2007, respectively. The authors report no conflicts of interest. Reprints: Toshishige Shibamoto, MD, PhD, Professor and Chairman of Physiology, Department of Physiology II, Kanazawa Medical University, Uchinada Ishikawa 920-0293, Japan (e-mail: firstname.lastname@example.org). Journal of Cardiovascular Pharmacology: November 2009 - Volume 54 - Issue 5 - p 421-426 doi: 10.1097/FJC.0b013e3181bad2a6 Buy Metrics Abstract We previously reported that the portal venous pressure (PPV) response of perfused mouse livers to various vasoactive agents was much weaker than that of other mammals such as rat, rabbit, and guinea pigs. The purpose of this study was to determine the responsiveness of PPV in in vivo BALB/c mouse to intraportal injections of the 3 major vasoconstrictors of angiotensin II, norepinephrine, and endothelin-1 in comparison with that in Sprague-Dawley rats. In anesthetized spontaneously breathing animals, PPV, systemic arterial pressure, and central venous pressure were directly and continuously measured. The above-mentioned vasoconstrictors were injected into the portal vein as a bolus repetitively at the doses ranging 0.01-100 nmol/kg. A dose-dependent increase in systemic arterial pressure in response to each vasoconstrictor was observed similarly in both mice and rats. All vasoconstrictors also caused a dose-dependent increase in PPV in both species, but the peak levels in mouse did not reach higher than 7 mm Hg, whereas it reached as high as 15-24 mm Hg in rats. Immunostaining for α-smooth muscle actin revealed that smooth muscles were distributed substantially in portal venules of rat but scarcely in that of mouse. In conclusion, PPV response to various vasoconstrictors was limited in anesthetized BALB/c mice, as compared with the anesthetized Sprague-Dawley rats, presumably due to small amount of vascular smooth muscle in mouse portal venules. © 2009 Lippincott Williams & Wilkins, Inc.