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Analysis of myogenic microvascular reactivity in terms of its recently described prominent dynamic component was performed before and during graded sympathetic stimulation and catecholamine infusion. Phenoxybenzamine and propranolol were used to differentiate between alpha- and beta-adrenoceptor effects. The study first confirmed previous findings of a beta-adrenergic inhibitory component in the neural control of microvascular resistance which attenuated the alpha-adrenergic constriction. The results concerning the interaction between adrenergic and myogenic control mechanisms corroborated the conclusion that the sympathoadrenal system, via its beta-adrenergic link, exerts effective inhibitory action on myogenic excitatory reactions. As regards the neural control, its beta-adrenergic component seemed to quite precisely compensate for the reinforcing effect on the myogenic constrictor response which results from increased vascular tone per se (in this case caused by alpha-adrenergic constriction), interpreted as a physical 'gain' effect inherent in the inverse fourth power relationship between radius and resistance. The latter complicating factor, which implies non-linearity in integrated peripheral resistance control, was thus revealed only after beta-blockade, but not on the vascular bed with intact adrenoceptors, where a given transmural pressure stimulus evoked an almost equally large myogenic constrictor response irrespective of the prevailing level of vascular tone. The beta-inhibitory action of blood-borne noradrenaline was similar to the neural one, whereas that of adrenaline was more effective, causing decline of myogenic reactivity below control.
Per‐Olof Grände (1979) studied this question.