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Prostaglandin F 2α (PGF 2α ) (3–300 pmol) administered to the dog mandibular gland via the glandular artery produced salivation and an increase in blood flow rate in a dose-related manner. The salivary responses to PGF 2α and to electrical stimulation of the chorda-lingual nerve were abolished by intra-arterial infusion of 1 -hyoscymine (30 nmol/min), whereas the vascular responses to both were not affected. The salivary and vasodilator responses to PGF 2α were not affected by intra-arterial infusion of hexamethonium (0.6–2 μmol/min) which abolished those to stimulation of the chordalingual nerve. These results support the prevous conclusion that PGF 2α produces the two responses by exciting the parasympathetic ganglion or postganglionic neurons in the dog mandibular gland.

Prostaglandin E 2 (PGE 2 ) (0.1–300 nmol) and acetylcholine (ACh) (0.3–300 nmol) were injected into the glandular artery through which the mandibular gland of the dog was perfused with blood at a constant pressure of about 100 mm Hg. Either substance produced salivary secretion and an increase in blood flow rate in a dose-related manner. The effects of PGE 2 were far more powerful and long-lasting than those of ACh. The potency of PGE 2 was about 1/300 that of prostaglandin F 2α on a molar basis in producing the two effects. During complete nerve-block attained by intra-arterial infusion of tetrodotoxin (0.3 nmol/min) the sialogenous action of PGE 2 was abolished, although not completely, whereas the vasodilator effect remained in larger part. Both sialogenous and vasodilator effects of ACh were not affected by tetrodotoxin. These results indicate that the sialogenous effect of PGE 2 was due in most part to a neural, probably parasympathetic, excitant action, whereas the vasodilator action was due in larger part to a direct one on the vasculature.

Prostaglandin F2α (PGF2α) (1–100 ng) and acetylcholine (ACh) (0.3–30 μg) injected selectively into the artery supplying the submaxillary gland of the dog produced salivation and an increase in blood flow. Both salivary and vascular responses to PGF2α developed slowly and lasted long as compared with those to ACh. On a weight basis PGF2α was about 1000 times more potent than ACh in producing salivation. Upon repeated injections of PGF2α most glands developed moderate desensitization to PGF2α but not to ACh. Both salivary and vascular responses to PGF2α were abolished by infusion of tetrodotoxin ( or 0.1 or 0.2 μg/min), whereas those to ACh remained virtually unchanged. These results indicate that in the dog submaxillary gland PGF2α causes salivation and vasodilation exclusively through excitation of the parasympathetic postganglionic neurons.

1. The blood flow to the splenic artery of dogs anaesthetized with sodium pentobarbitone was measured under constant pressure perfusion with the animal's own blood led from the femoral artery. 2. Immediately after release of occlusion there was a rapid increase of inflow rate above the pre-occlusion level which then oscillated up and down. In a majority of cases such oscillatory responses continued for a while but progressively diminished during a period of about 6 min. 3. This post-occlusive oscillatory response was not modified by either neural or autonomic receptor blocking agents such as tetrodotoxin, guanethidine, phentolamine, propranolol, atropine and methysergide. 4. In the cases with a relatively short-lasting response, the selective administration of adenosine into the splenic artery caused a distinct enhancement of the oscillation. 5. These results suggest that adenosine may play an important role in the post-occlusive oscillatory response of the splenic circulation.

1. Effects of L-dopa and dopamine on the secretion of pancreatic juice were investigated in preparations of the isolated blood-perfused canine pancreas.2. Dopamine (1-10 mug) given intra-arterially caused a profuse flow of juice.3. The secretory activity of dopamine (3 mug) was approximately equal to that of secretin (0.1 unit).4. L-Dopa (10-100 mug) given by a single intra-arterial injection was ineffective, but infusion at 100 mug/min for 10 min caused a marked increase of secretion after a delay of a few minutes.5. Intravenous administration of either L-dopa (3 mg/kg) or dopamine (10-100 mug/kg) elicited a marked increase of pancreatic secretion, but was definitely less effective than intra-arterial injection.6. Dopamine-induced secretion was not modified by atropine, phentolamine, propranolol, guanethidine or tetrodotoxin.7. It is concluded that dopamine acts directly on the exocrine cells in the pancreas.

Responses of the dog submaxillary gland and its vascular bed to various compounds administered into the glandular branch of the facial artery were investigated under the constant perfusion pressure. Cholinergic drugs such as acetylcholine, bethaneehol, methacholine, carbachol, pilocarpine, physostigmine and neostigmine; ganglionic stimulants such as nicotine, DMPP, lobeline, TMA and McN-A-343; β-adrenergic stimulant such as isoproterenol; and biogenic amines such as histamine and 5-hydroxytryptamine, produced a salivary secretion and dilation of the glandular vascular bed. Adrenergic drugs catehcholamine releaser such as epinephrine, norepinephrine, dopamine, phenylephrine, tyramine and methoxamine, caused a salivary secretion and vasoconstriction. Although either vasoconstrictors such as angiotensin II, lys-vaso-pressin, oxytocin, TEA, cocaine and ergotamine, or vasodilators such as bradykinin, kallikrein, secretin, panereozymin, gastrin, adenosine, AMP, ADP, ATP, uridine, UMP, UDP, UTP, DPN, TPN, nitroglycerin, papaverine, dipyridamole, verapamil, hydralazine, caffeine, theophilline, theobromine, morphine, procaine and tolazoline, produced prominent vascular effects, they exerted no effect on the salivary secretion. There is no evidence on the direct relation between secretagogue and vasodilating effects of drugs which are administered selectively into the submaxillary glandular artery.

The perfusion of the sinus node artery in dogs in situ was performed. The selective administration of nicotine and DMPP into the sinus node artery induced a biphasic response, i.e., a negative chronotropic response followed by a positive one. Both compounds produced similar negative chronotropic responses, but positive responses were more markedly induced by DMPP than by nicotine. These negative chronotropic responses were blocked by atropine, hexamethonium and tetrodotoxin. The positive response to nicotine was blocked by propranolol and tetrodotoxin. DMPP-induced positive chronotropic effect was blocked by propranolol but never by tetrodotoxin. It is suggested that the positive chronotropic action of DMPP is different from that of nicotine on the sino-atrial node and is similar to that of tyramine.

The effect of McN-A-343 was studied by direct administration into the sinus node artery of dogs vagotomized at the mid-cervical level. McN-A-343 blocked sinus bradycardia caused by electrical stimulation of the right vagus, while bradycardia induced by administration of acetylcholine or nicotine into the sinus node artery was not modified.

It was demonstrated in both in vivo and in vitro experiments on the renal circulation that dipyridamole produced the potentiation of vascular responses not only to adenosine but also to norepinephrine. The potentiation of these responses was observed when concentrations of dipyridamole were relatively low. As the concentration of dipyridamole was elevated, the potentiation was rather decreased and finally abolished. Furthermore, in in vitro experiments, higher concentrations of dipyridamole blocked the action of norepinephrine. These results cast doubt on the mode of dipyridamole action, which has been interpreted as inhibition of deamination of adenosine.