Evidence for a dual innervation affecting local blood flow in the hypothalamus of the conscious rabbit.

We have attempted to evaluate the role of adrenergic nerves which arise from the superior cervical ganglia or which are intracerebral throughout their course, in the control of local cerebral blood flow (CBF). Hypothalamic blood flow (HBF) was measured in the conscious rabbit by the 133Xe-clearance technique. Stimulation of the upper brainstem, using 5-Hz, 3-V, 1-msec, square wave pulses, increased by HBF by a mean of 7.6 ml/100 g per min (P less than 0.005). This effect was abolished by the intrahypothalamic injection of the beta-adrenoreceptor blocker, propranolol, and by chemical sympathectomy of the hypothalamus or of the upper brainstem with 6-hydroxydopamine, but was not altered by bilateral cervical ganglionectomy. Intrahypothalamic injection of 0.1 mug of tyramine caused a mean decrease in HBF of 15.6 ml/100 g per min (P less than 0.001). This effect of intrahypothalamic injection of tyramine was abolished by bilateral cervical sympathectomy but not by chemical sympathectomy of the upper brainstem. These results support the idea that local CBF, at least in the hypothalamus, is mediated by two distinct pathways. The first consists of the sympathetic nerves which arise in the cervical ganglia, and which activate intrahypothalamic alpha-receptors to cause constriction. The second is an entirely intracerebral noradrenergic pathway which stimulates beta-receptors to cause vasodilation.

Adrenoceptors in intracerebral resistance vessels.

1. The effects of tyramine and isoprenaline on hypothalamic blood flow (HBF) were measured in conscious rabbits. 2. Injections of small doses of tyramine caused an increase in HBF while larger doses caused a decrease in HBF. 3. Isoprenaline injections also produced an increase in HBF. 4. The vasodilatation induced by isoprenaline and the small dose of tyramine was blocked by propranolol. 5. The vasoconstriction induced by the larger doses of tyramine was abolished by phenoxybenzamine. 6. Chemical sympathectomy of the hypothalamus with 6-hydroxydopamine and depletion of biogenic amines by reserpine also abolished tyramine-induced vasocoonstriction. 7. These results suggest the presence of alpha- and beta-adrenoceptors in cerebral resistance vessels, and that these receptors may be activated by released (endogenous) noradrenaline.