To elucidate the microvascular mechanisms of change in tumor blood flow due to vasopressors (angiotensin II, epinephrine, methoxamine), we analyzed the site of vascular resistance (VR) increased by each vasopressor. Arteriolar vessels within a transparent rat chamber were classified centripetally (a2-a5) according to Strahler's nomenclature. Vessels that feed into the tumor microcirculation were a2 modified by the tumor (starting vessels). Under angiotensin II (A II)-induced hypertension, the pressure of all arteriolar vessels increased roughly in proportion to the increase in mean arterial blood pressure. The greatest pressure drop and hence the most resistance due to A II occurred across the a2. During epinephrine-induced hypertension, there were major pressure drops between a4 and a3, and between a3 and a2. The amount of contraction of arteriolar vessels due to methoxamine was much smaller than that due to epinephrine, and the pressure increase in a4 and a3 was also small. From the facts described above, we may conclude as follows: A II creates greater vascular resistance of a2 vessels to blood flow and also greater perfusion pressure of a5-a3 vessels, resulting in increased blood inflow into a starting vessel which then becomes a passive vessel. Epinephrine causes an increase in the resistance of a3, a4 and probably upstream from a4 arterioles to blood flow. Thus, tissue blood flow in subcutis and tumor almost always decreases together. The fact that tissue blood flow in normal subcutis and tumor did not change significantly under methoxamine-induced hypertension is probably due to the results that methoxamine had little effects on the vascular resistance of smaller arterioles to blood flow.