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Pulmonary Vascular and Airway Responses to Systemic Vasoconstrictors in Anesthetized BALB/c Mice

Wang, Mofei MD*,†; Shibamoto, Toshishige MD, PhD*; Shinomiya, Shohei MD, PhD; Yamamoto, Yuki BA*; Kurata, Yasutaka MD, PhD*; Kuda, Yuhichi MS*; Tanida, Mamoru PhD*; Toga, Hirohisa MD, PhD

Journal of Cardiovascular Pharmacology: April 2015 - Volume 65 - Issue 4 - p 325–334
doi: 10.1097/FJC.0000000000000199
Original Article
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Abstract: There is no systematic study in which the effects of vasoactive substances were investigated on pulmonary vascular resistance (PVR) in in vivo mouse by directly measuring cardiac output and the inflow and outflow pressures in the pulmonary circulation. We determined the responses of PVR, total peripheral resistance (TPR), and airway pressure (AWP) to angiotensin II, endothelin-1, vasopressin, phenylephrine, and thromboxane A2 analog U46619 in anesthetized BALB/c mice. Pulmonary arterial pressure, left atrial pressure (LAP), and aortic blood flow were measured. TPR increased dose-dependently in response to consecutive administration of all vasoconstrictors except vasopressin which reduced TPR at the highest dose of 100 nmol/kg. At high doses of vasoconstrictors, pulmonary arterial pressure and AWP increased due to increased LAP, as demonstrated by the separate LAP elevation experiments. When LAP transiently increased at high doses, PVR did not increase but decreased. Nonetheless, enodothelin-1, angiotensin II, and U46619 increased PVR. Vasopressin at 100 nmol/kg increased AWP without LAP elevation. In conclusion, the high doses of the vasoconstrictors studied here exert indirectly a transient pulmonary vasodilatory and AWP increasing actions due to pulmonary congestion evoked by strong systemic vasoconstriction. Nevertheless, enodothelin-1, angiotensin II, and U46619 cause pulmonary vasoconstriction, and vasopressin constricts airway in anesthetized BALB/c mice.

*Department of Physiology II, Kanazawa Medical University, Uchinada, Ishikawa, Japan;

Department of Colorectal surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, China; and

Department of Respiratory Medicine, Kanazawa Medical University, Uchinada, Ishikawa, Japan.

Reprints: Toshishige Shibamoto, MD, PhD, Department of Physiology II, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan (e-mail: shibamo@kanazawa-med.ac.jp).

Supported by a Grant from Kanazawa Medical University (SR2012-04, S2013-1, and PR2012-14).

The authors report no conflicts of interest.

Received March 05, 2014

Accepted November 20, 2014

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