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A potential role for cerebrovascular nerves containing vasoactive intestinal polypeptide (VIP) was examined in 24 anesthetized, ventilated dogs. Cerebral blood flow (CBF) was measured by either the cerebral venous outflow or microsphere method. Plasma VIP concentration was measured by radioimmunoassay. Hypercapnia (5% and 10% CO2) and hypoxia (7% O2) produced significant increases in cerebral venous outflow, but had no affect on arterial or cerebral venous VIP concentrations. Measurements of VIP in cerebrospinal fluid (CSF) made during 5% and 8% CO2 breathing also were not different from control values. VIP produced large dose-dependent increases in common carotid artery and temporalis muscle blood flow when injected or infused intraarterially; however, VIP had no effect on total or regional cerebral blood flow (rCBF) within the brain when administered in a similar manner. Unilateral perfusion of the cerebral ventricles with VIP produced significant increases (range: 11-80%) in rCBF. These data are consistent with the possibility that local release of VIP from perivascular nerve endings could affect CBF. The unresponsiveness of canine cerebral vessels to blood-borne VIP may be due to the blood-brain barrier, since VIP dilates cerebral vessels when the barrier is bypassed by intraventricular infusion. These studies do not support the hypothesis that CBF changes induced during hypercapnia or hypoxia are mediated by VIP.

To examine the possible role of adenosine in the vasoactivity of acetate, acetate and adenosine were injected into the renal artery of the dog while measuring renal blood flow. Low (9-28 mg) doses of acetate produced vasodilation, but higher doses (28-94 mg), like adenosine, produced vasoconstriction followed by vasodilation. Theophylline, a competitive inhibitor of the vascular action of adenosine, inhibited the vasodilator action of adenosine but not that of acetate. Secondly, theophylline inhibited the vasoconstrictor effect of adenosine and acetate but the latter to a much lesser extent. These findings suggest that adenosine mediates the vasoconstriction effect of acetate in the canine kidney.