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The corticotropin-releasing properties of lysine vasopressin and that of a porcine pituitary extract were compared by means of injections into hypothalamic sites or into the adenohypophysis of dexamethasone-pretreated rats of both sexes. In all cases the doses used for central injections were below the minimal dose capable of causing an increase in adrenal secretion of corticosterone after intravenous injection, so that corticotropin (ACTH-like) effects or contamination by ACTH could be excluded as a cause of increased adrenal secretion of corticosterone after the central injections. Vasopressin provoked extensive release of ACTH when it was placed in the median eminence of the hypothalamus, as did the pituitary extract. When the 2 substances were tested by intra-adenohypophysial injection, the vasopressin caused much less ACTH release and the extract caused more ACTH release than observed after intrahypothalamic injections. Morphine abolished the ACTH release after vasopressin injections at either site, as well as after the injection of the extract into the median eminence. However, morphine failed to abolish, or even diminish extensively, the ACTH release observed after injection of the extract into the anterior pituitary. From these results it was concluded that the extract contained activity resembling that of a corticotropin-releasing factor, but that vasopressin did not have such activity at the doses used. The vasopressin apparently acted directly on the hypothalamus to cause release of endogenous corticotropin-releasing factor. (Endocrinology 79: 328, 1966)

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.