Does arterial myogenic tone determine blood flow distribution in vivo?

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Abstract
Blood flow distribution at rest and during exercise is intricately controlled by centrally driven neuroeffector mechanisms and circulating hormones (particularly epinephrine), local autacoids, and metabolites, all superimposed on the inherent or “myogenic” reactivity of the arterial smooth muscle. During exercise, the cardiac output of a trained athlete can increase ∼5-fold, and these mechanisms serve to coordinate a huge (∼20-fold) increase in the amount of blood routed to the exercising muscle ([3][1]). The dramatic nature of this increase is illustrated by the fact that the proportion of the cardiac output diverted to skeletal muscle can change from 20% to ∼80%! Importantly, and to the benefit of the individual, despite this enormous increase in the flow of blood to muscle, brain blood flow is not compromised ([3][1]). But to what extent do the inherent characteristics of the arteries of the brain and musculature explain these distinct changes? As cerebral arteries are not particularly responsive to the sympathetic nerves surrounding them, myogenic reactivity is thought to be a fundamental determinant of the constant flow of blood to the brain and, as a consequence, has been extensively studied. The most direct studies have assessed how changes in intraluminal pressure links to smooth muscle contraction/relaxation in isolated arteries, where reflex and most local influences are absent and steady-state conditions can be achieved. It is technically extremely difficult to make intracellular recordings from the very small (40 mmHg (at which pressure active tone is higher than in cremaster arteries), and resting membrane potential more depolarized than −53 mV. From rough calculations based on Knot et al. ([20][26]), iberiotoxin causes increases in cerebral myogenic tone to a level similar to that in the cremaster arteries (∼60% passive diameter). However, quantifying this relationship precisely will require a more systematic study, to include membrane potential recording at different pressures in the presence of iberiotoxin, and excluding the potential variables that might be associated with gender, age, etc., of rats. Thus it appears that the differential activation of BKCa reported in cerebral arteries cannot in itself explain the inherent differences in myogenic response seen in muscle arteries (especially at lower pressures). However, there are obviously a host of other candidates that may have an influence, for example, the relative formation of intracellular 20-HETE and other cytochrome P -450 metabolites; the role of other K channels such as KATP channels; the mechanisms for Ca2+ signaling, including the ability of Ca2+ sparks to activate BKCa channels and thus dilation; plus other mechanisms controlling diameter that are not necessarily influenced by membrane potential (reviewed in Refs. [5][28] and [16][4]). However, from a purely empirical standpoint, the fact that blood vessels within themselves have evolved differentially to help regulate their inherent basal tone and in so doing help to match blood flow delivery to survival in distinct settings is an intriguing level of complexity. The late Neela Kotecha, through her elegant and technically demanding studies, did much to unravel these complexities. 1. [↵][29] Berg BR , Cohen KD, and Sarelius IH. Direct coupling between blood flow and metabolism at the capillary level in striated muscle. Am J Physiol Heart Circ Physiol 272: H2693–H2700, 1997. [OpenUrl][30][Abstract/FREE Full Text][31] 2. [↵][32] Brenner R , Perez GJ, Bonev AD, Eckman DM, Kosek JC, Wiler SW, Patterson AJ, Nelson MT, and Aldrich RW. Vasoregulation by the β1 subunit of the calcium-activated potassium channel. Nature 407: 870–876, 2000. [OpenUrl][33][CrossRef][34][Medline][35] 3. [↵][36] Chapman CB and Mitchell JH. The physiology of exercise. Sci Am 212: 88–96, 1965. 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