CONTROL OF PERIPHERAL CIRCULATION 
When the subjects were heated, the blood flow on the innervated 
forearm rose substantially above that in the forearm where cutan- 
eous nerves were blocked. This increase could not be explained by 
release of vasoconstrictor tone and indicated that forearm skin 
vessels had a vasodilator nerve supply. A clue to the way these 
vasoconstrictor and vasodilator fibres work together was obtained 
by experiments of the type illustrated in Figure 11. Forearm and 
hand blood flow were simultaneously measured and at the beginning 
of the experiment the subject was cold. When the subject was heated, 
the pattern of vasodilation in the forearm differed from that in the 
hand (Roddie, Shepherd, and Whelan, 1957b). The increase in fore- 
arm flow occurred in two phases. The first increase, a very small 
fraction of that attainable by heating, occurred synchronously with 
the precipitous increase in hand blood flow. This increase, like that 
in the hand, was not affected by atropinization of tissues (Fig. 12) 
and it is possibly due to release of vasoconstrictor tone. The second 
phase of the forearm vasodilation, which comprises the major 
part of that attainable by heating, occurred at a time when the hand 
blood flow had reached its maximum and when sweating in the fore- 
arm had commenced. Atropinization of the forearm delayed and 
reduced this phase, suggesting that the mechanism responsible was 
at least in part cholinergic. 
This close association of the second phase with the onset of 
sweating suggested that the vasodilation might be linked in some 
way with sweat gland activity, a situation analogous to that seen in 
the functional vasodilation in the submandicular salivary gland 
(Hilton and Lewis, 19 55). There is now evidence that the vasodila- 
tion in forearm skin during body heating may be due to products 
released during sweat gland excitation rather than to the excitation 
of specific vasodilator nerve fibres. Fox and Hilton (1956, 1958) 
found that sweat collected from the hand and forearm contained 
bra(fykinin-forming enzyme. They also found that the amount of 
bradykinin in the subcutaneous tissue spaces increased during body 
heating (Figs. 13 and 14). They suggested that bradykinin-forming 
enzyme was a normal product of sweat gland activity, and that it 
could escape from the gland to act on the protein in the subcutaneous 
tissue space to form bradykinin. They considered that the bradykinin 
thus formed might contribute to the cutaneous vasodilation. Be 
that as it may, it does not affect the general conclusion that the 
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