Abstract
Stimulation of the renal nerves to the perfused toad kidney produced an increase in intravascular pressure. This response was always abolished by bretylium, indicating that it was mediated by adrenergic nerves. The response was usually reduced by tubocurarine, indicating that some of the fibres in the renal nerve trunks were preganglionic. The vasoconstrictor response was abolished by treatment with yohimbine or phenoxybenzamine, but was only partially reduced by phentolamine. It is postulated that adrenaline released from nerve terminals acts primarily on "junctional" adrenoceptors which are not antagonised by phentolamine. However, part of the vasoconstrictor response appears to be due to occupation of nearby "extra-junctional" receptors by neurally-released adrenaline: only this part of the response can be antagonised by phentolamine. The vasoconstrictor response was enhanced by propranolol in both summer and winter. This indicates that neurally-released adrenaline can occupy beta-adrenoceptors, to antagonise the effects of alpha-receptor occupation, at both times of the year. In this respect, the beta-receptors mediating the effects of renal nerve stimulation are different from those acted upon by perfused adrenaline. A non-adrenergic vasodilatation was sometimes revealed after abolition of the vasoconstrictor response, but the nature of the nerve fibres mediating this response could not be determined.
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