Abstract
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 α– and β–adrenoceptor effects. The study first confirmed previous findings of a β–adrenergic inhibitory component in the neural control of microvascular resistance which attenuated the a–adrenergic constriction. The results concerning the interaction between adrenergic and myogenic control mechanisms corroborated the conclusion that the sympathoadrenal system, via its β–adrenergic link, exerts effective inhibitory action on myogenic excitatory reactions. As regards the neural control, its –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 a–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 β–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 β–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.