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SUMMARY Peripheral resistance was examined in the microcirculat ion of the rat cremaster muscle using a network-conserved parameter, power dissipation. Previous studies of peripheral resistance used network-sensitive parameters, and their interpretation is limited by tacit assumptions about the structure of the peripheral vasculature. Power dissipation is directly linked to the resistive process, providing a measure of resistance based on the actual hemodynamics of the network. The dissipation parameter was quantified with the usual vascular parameters of velocity and vessel segment length; 991 segment lengths were measured in 12 normotensive Wistar-Kyoto rats and 16 spontaneously hypertensive rats. Arterial power dissipation was significantly elevated over a wide range of vessel segments; blood flow ranged from 0.08 to 80 nl/sec. Since the largest vessels showed the greatest power dissipation, the organ resistance elevation seen in hypertension in the cremaster apparently is mediated by the larger vessels in the high flow range. Vessel segment length and number of dissipative vessels were unchanged. The increase in power dissipation was due to a network-averaged reduction in mean vessel diameter. Power dissipation also increased significantly in the fastest flowing venous microvessels (>25 nl/sec), also due to a reduction in vessel segment diameter. (Hypertension 8: 184-191, 1986) KEYWORDS networks hypertension • microcirculation • peripheral resistance • vascular I RESISTANCE changes associated with hypertenj^T sion are manifested in the most distal circula-A^L . tory ramifications, the microcirculation. It is somewhat ironic that in large vascular tubes, where resistance is well defined and easily calculated, there is only a small contribution of the conduits to the resistive process. Although the smaller vessels are the predominant determinants of total peripheral resistance, they are interwoven in a vascular mesh that makes it difficult to examine or describe how individual elements interact to produce resistance. In a network of interconnecting vessels the concept of resistance has only limited application. In a strict sense, resistance is a relationship between flow and pressure. If there is more than one entrance to allow flow in or more than one exit to allow flow out, then it is difficult, it not impossible, to define resistance in a meaningful way. Thus, there is little significance in resistance terms unless the network has a single entrance and exit. Un-

SUMMARY This study investigated the microvascular changes that affect vascular resistance in the rat small intestine during two-kidney, one clip renal hypertension 4 weeks after renal artery stenosis. To study the intestinal microcirculation, a loop of the small intestine was exteriorized with intact circulation and innervation and a section of the bowel wall was prepared for observation with an intravital video microscopy system. Microvascular diameter, pressure, and flow velocity were measured for first, second, and third branch order arterioles and venules, using an image shearing monitor, servo-null micropipette system, and an optical Doppler velocimeter, respectively. The diameters of the first order arterioles and venules were significantly (p < 0.05) reduced in hypertensive rats; however, diameters were unaltered in smaller second and third order arterioles and venules as compared with normotensive vessels. In hypertensive rats, mean arterial pressure was significantly (p < 0.05) elevated (47%) and pressures also were elevated significantly (p < 0.05) throughout the microcirculation, although by a proportionally smaller amount. Total network flow (i.e., first order arteriole flow) was significantly (p < 0.05) reduced (40%) in hypertensive rats, but volume flows in individual second and third order arterioles were similar to flows measured in normotensive rats. Calculated total network resistance was increased (124%) in hypertensive rats. Thus, the intestinal microcirculation in rats with two-kidney, one clip renal hypertension is disturbed by elevated pressure and decreased total flow. The presence of normal flows in individual second and third order arterioles without any demonstrable difference in their diameters suggests that the predominant cause of elevated resistance across this segment of the intestinal microcirculation is a reduction in the number of perfused small arterioles. (Hypertension 8: 66-75, 1986) KEY WORDS • microvascular pressures • microvascular flows • microvascular diameters • vascular resistance • splanchnic circulation • two-kidney, one clip Goldblatt hypertension T HE microvascular characteristics that determine vascular resistance in hypertension have received increased attention over the last decade. This is principally because the microcirculation is a primary site of peripheral resistance and is controlled by neural and hormonal mechanisms of blood pressure regulation, which are well known to be altered in various forms of experimental hypertension.