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1 Department of Cell Biology and Physiology, Vascular Physiology Group, University of New Mexico Health Sciences Center, Albuquerque, NM, USA
* To whom correspondence should be addressed. E-mail: bwalker{at}salud.unm.edu.
Chronic obstructive pulmonary diseases as well as prolonged residence at high altitude can result in generalized airway hypoxia eliciting an increase in pulmonary vascular resistance (PVR). We hypothesized that a portion of the elevated PVR following chronic hypoxia (CH) is due to the development of myogenic tone. Isolated pressurized small pulmonary arteries from control (PB 
630 Torr) and CH (4 wk, PB = 380 Torr) rats were loaded with fura 2-AM and perfused with warm (37°C) aerated (21%-O2, 6%-CO2, balance-N2) physiological saline solution. Vascular smooth muscle (VSM) [Ca2+]i and diameter responses to increasing intraluminal pressure were determined. Diameter and VSM cell [Ca2+]i responses to KCl were also determined. In a separate set of experiments VSM cell membrane potential (Em) responses to increasing luminal pressure were determined in arteries from control and CH rats. VSM Em in arteries from CH animals were depolarized relative to control at each pressure step. VSM cells from both groups exhibited a further depolarization in response to step increases in intraluminal pressure. However, arteries from both control and CH rats distended passively to increasing intraluminal pressure and VSM cell [Ca2+]i was not affected. KCl elicited a dose-dependent vasoconstriction that was nearly identical between control and CH groups. Whereas KCl administration resulted in a dose dependent increase in VSM cell [Ca2+]i in arteries taken from control animals, this stimulus elicited only a slight increase in VSM cell [Ca2+]i in arteries from CH animals. We conclude that the pulmonary circulation of the rat does not demonstrate pressure-induced vasoconstriction.
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