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The effects of atrial natriuretic factor (ANF) on neural control of renin release and sodium excretion by the kidney were examined in pentobarbital-anesthetized dogs. Electrical stimulation of the renal nerves (RNS, 1 Hz) increased the renal secretion rate of renin (RSR) by 627 +/- 141 ng angiotensin I (ANG I)/min and that of norepinephrine (NESR) by 22.2 +/- 5.9 ng/min. Furthermore, urinary sodium excretion (UNaV) was decreased by 59 +/- 7%, with little change in either renal blood flow (RBF) or glomerular filtration rate (GFR). Intrarenal arterial infusion of ANF (alpha-human atrial natriuretic peptide; 10 ng.kg-1.min-1) increased basal UNaV about twofold but had no effect on basal RBF or GFR. The RNS-induced increase in RSR during ANF infusion (198 +/- 117 ng ANG I/min) was significantly lower than that before the infusion (P less than 0.05), whereas the RNS-induced changes in NESR (27.1 +/- 8.5 ng/min) and UNaV (51 +/- 11%) were unaffected. These results suggest that neural stimulation of renin release, but not of tubular sodium reabsorption, can be suppressed by exogenously administered ANF at a dose that does not affect glomerular filtration or renal neurotransmitter release.

In the welded joint having a pre-existing defect, the crack tip is subjected to thermal-strain and stress cycles by successive welding. Hot straining embrittlement and residual stress due to successive welding will influence the brittle fracture initiation of weldment.Two-dimensional finite element method analyse are carried out for obtaining thermal stress-strain cycles during welding and distribution of residual stresses-strains near the tip of a pre-existing crack.Appreciable difference in residual stress distribution is not observed between Before-Weld-Notch (BWN) and After-Weld-Notch (AWN) specimens. Much difference in the residual equivalent plastic strain is observed between BWN and AWN specimen. In BWN-specimen, there is a large concentration of plastic strain near crack tip during welding. This hot-straining causes considerable decrease in fracture toughness. In the welded joint of steel, the residual stress-strain distributions near crack tip is decided by the parameter TCmax/σY0, where TCmax is the maximum heating temperature at the crack tip and σY0 is the yield stress of materials at room temperature. The conventional formulae on residual stress distribution and residual equivalent plastic strain in the vicinity of a pre-existing crack are shown using the parameter TCmax/σY0.

Considerations have been conducted fundamentally on stresses·strains controlling parameter of cracked plate joined with two dissimilar materials, especially of which yield strengths are different each other, that is σIY, σIY. Attention mainly is paid to the joined plate with a crack of which tip, exists in the vicinity of joining surface of dissimilar materials. FEM analyses are applied for calculation of deformation behaviours under tension of two kinds of cracked plates: L-type specimen in which crack is perpendicular to the joining surface and P-type specimen in which crack is parallel to the ioinine surface.Mechanical heterogeneity remarkably influences on stresses.strains in the vicinity of the crack tip when plastic deformation spreads beyond the joining surface. On the analogy of linear elastic fracture mechanics theory, the parameter, F, which controls stresses. strains in the vicinity of the crack tip has been proposed. By using two parameters; strength ratio of two materials, Sr(=σIIY/σIY, and F[=σG/σIY)·√c/d], characteristics of stress.strain distributions of two kinds of cracked plates can be classified.

We studied the effect of E-64, a new thiol protease inhibitor derived from Aspergillus japonicus TPR-64, and of its synthesized analogue, E-64-d, on dystrophic mice ( C57BL 6J -dy ). The locomotor activity of normal mice increased markedly, reaching a plateau at 8 weeks of age. In dystrophic mice, it increased until they were 7 weeks old, thereafter, it decreased gradually. This decrease reflected the degradation of the hind legs. Serum activities of creatine phosphokinase were significantly greater in dystrophic than in normal mice. When 3-week-old dystrophic mice were injected with E-64 (1 mg/kg, i.p.) or E-64-d (40 to 60 mg/kg, p.o.), the decrease in their locomotor activity was retarded and their serum enzyme activities decreased significantly. In addition, the survival time of treated dystrophic mice was prolonged. The locomotor activity of normal mice and their serum enzyme levels were not affected by the administration of E-64-d. We posit that the new thiol protease inhibitors we tested retard the porgression of dystrophy in mice.

We studied the effect of mitochondrial protein synthesis inhibitors on the neurotrophic action of the nerve stump in mice. The sciatic nerve was cut as close to, or as far from the extensor digitorum longus muscles as possible. At 2 and 3 days after denervation, depolarization in the resting membrane potential of muscles with long nerve stumps (14-16 mm) was significantly smaller than in muscles with very short (less than 2 mm) nerve stumps. Chloramphenicol (100 mg/kg, p.o.), erythromycin (4 micrograms/kg, i.p.), ethidium bromide, (10 micrograms/kg, i.p.) or acridine (10 micrograms/kg, i.p.), administered for 2 or 3 days after denervation, increased depolarization in the resting membrane potential of muscles with long nerve stumps; muscles with very short nerve stumps were not affected by these drugs. The administration of chloramphenicol and erythromycin resulted in an earlier increase in the depolarization than ethidium bromide and acridine. Activities of cathepsin B and L of lysosomal proteases in the nerve stumps were enhanced by nerve degeneration; they were not affected by the administration of chloramphenicol or ethidium bromide. We suggest that proteins synthesized in mitochondria of the nerve may participate in trophic actions.

The results of stereotactic aspiration, conventional craniotomy, and conservative treatment were compared in 91 cases of putaminal hemorrhage, all involving a medium-sized hematoma (20-60 ml). The average interval between onset of symptoms and operation was 7.4 days for stereotactic aspiration and 11.5 hours for craniotomy. Patients with low neurological grades and low computed tomography (CT) classifications had better outcomes regardless of treatment. Among patients with a neurological grade of 3, the outcome was significantly poorer with conservative treatment than with stereotactic aspiration or conventional craniotomy (p < 0.05). Among grade 4a patients, conventional craniotomy yielded the best results (p < 0.05). Among those with CT classifications III and IVa, the outcome was significantly poorer with conservative treatment than with stereotactic aspiration or conventional craniotomy (p < 0.05).

We report that protein synthesis inhibitors exert an inhibitory effect on the trophic action of the nerve stump. The sciatic nerve innervating the extensor digitorum longus muscles of mice was cut either as close to, or as far from, the muscle as possible. Denervation changes in the muscle were evaluated using the resting membrane potential and dose-response curves obtained by plotting acetylcholine-induced contractures. Actinomycin D (2 micrograms/kg, i.p.), ethidium bromide (10 micrograms/kg, i.p.), cycloheximide (1 or 5 mg/kg, i.p.), or chloramphenicol (100 mg/kg, p.o.) administration was immediately after neurotomy and continued daily until the day preceding muscle removal. Although denervation changes occurred significantly later in muscles with a long rather than a short nerve stump, the administrated antibiotics, excluding cycloheximide, accelerated the manifestation of denervation changes in muscles with long nerve stumps without affecting those in muscles with short nerve stumps.

The metallurgical factors affecting the press formability of cold rolled high strength steels are discussed and the properties of the following 40 kgf/mm2 class tensile strength steels are examined: dual phase steel consisting of a ferrite-martensite structure, produced by rapid cooling in a continuous annealing line, which has a very low yield to tensile strength ratio and high n-value; rephosphorized steel, which is a batch-annealed aluminum-killed steel hardened with phosphorus and manganese, having a high r-value and a relatively low yield strength; and a recently developed steel of extra deep drawing quality and high strength which is characterized by its extremely high r-value, over 2.0, and low yield strength. This can be produced by continuous annealing of niobium-stabilized, extra low carbon, phosphorus-bearing steel. The formability and brittleness of the steels are also examined.

The dog renal inner medullary slices synthesized PGE 2 , TXA 2 and PGI 2 (measured as TXB 2 and 6-keto-PGF 1α ). When incubated with isoproterenol, the synthesis of PGE 2 and PGI 2 were stimulated dose-dependently. The effect of isoproterenol could be antagonized by β-adrenoceptor blocking drugs, propranolol or atenolol, but not by α-adrenoceptor blocking agent. Neither propranolol nor atenolol at concentrations that block this isoproterenol stimulation of PG synthesis suppress the increase in PG synthesis induced by arachidonic acid. These results indicate that in dog renomedullary slices isoproterenol — induced increase in PG synthesis is mediated via β-adrenergic receptors.

Effect of 3-4-dihydro-8-(2-hydroxy-3-isopropylaminopropoxy)-3-nitroxy-2H-1-b enzopyran (K-351) infused into the renal artery on renin release during graded renal nerve stimulation (RNS) was investigated in pentobarbital-anesthetized dogs. K-351 (20 micrograms/min) produced significant suppression of the RNS-induced renin release; the renin secretion responses to RNS at lower frequencies (0.5 and 1 Hz) were almost abolished, and those at the highest frequency (3 Hz) were attenuated. K-351 also suppressed an increase in renal vascular resistance during RNS at 3 Hz. The same extent of inhibition in the renin secretion response to RNS was also obtained during infusion of DL-propranolol (100 micrograms/min). Inhibitory effect of K-351, prazosin, or phentolamine on the renal vasoconstriction induced by RNS and norepinephrine (NE) injected into the renal artery, an approximately 50% reduction in renal blood flow, was also assessed. K-351 and prazosin exerted a greater inhibitory effect on RNS-than on NE-induced vasoconstriction, and the opposite was true of phentolamine. The potency of K-351 in reducing the vasoconstriction due to RNS or NE was roughly estimated to be 10-30 times less than that of prazosin. These results suggest that K-351 shares beta- and alpha-adrenoceptor blocking properties, which effectively contribute to the suppression of adrenergically induced renin release and renal vasoconstriction.

Somatostatin (SS) was produced in Escherichia coli (E. coli) as a 110 aminoacid fused protein, C-L-Met-SS, consisting of somatomedin C (Phe23Glu46) [1], human interferon-γ (Cys1-Leu59) [1], methionine and 14 aminoacids of SS. High-level expression of the fused protein, C-L-Met-SS, was achieved with pCLSStrpN2, a plasmid containing trp promoter. The fused protein, C-L-Met-SS, which was formed as a insoluble inclusion body in E. coli, was easily cleaved with cyanogen bromide to give reduced SS (SS(R)). The SS(R) was purified efficiently by gelfiltration chromatography, refolded under dilution, and further purified by reversed phase HPLC to give biologically active SS. The yield was 6.6 mg of the purified SS/20 L culture of E. Coli.

The reducing effect of desipramine (DMI) on the duration of immobility induced in rats by forced swimming was markedly potentiated after chronic injection of the lower dose, whereas the action of chronic amitriptyline (AMI) was similar to that of acute treatment. MHPG-SO4 in most of the brain regions, particularly that in the septal area, was increased by the forced swimming. Unlike the effect in the normal rats, acutely administered AMI and DMI did not reduce MHPG-SO4 in the brain regions other than the septal area in the forced swimming rats. Similar to the effect in the normal rats, chronic treatment with DMI increased MHPG-SO4 in the cortex, hippocampus and the thalamus in the forced swimming rats. In these rats, MHPG-SO4 in the septal area was still lowered by both drugs. These results indicate that 1) inhibitory effect of acutely administered AMI and DMI on the presynaptic noradrenergic neurons disappears in most of the brain regions after the forced swimming, 2) chronic treatment with DMI increases the noradrenergic activity in the cortex, hippocampus and thalamus and 3) both acute and chronic treatments with the drugs inhibit the forced swimming-induced increase in noradrenergic activity in the septal area. The relevance of these effects to the behavioral action of the drugs is discussed.

For the purpose of investigating the formation mechanism of the texture which is developed by ferrite (α)→austenite (γ)→ferrite (α) transformation, the effects of heating and cooling rates during phase transformation and specimen thickness on the transformation texture have been studied by using an extra low carbon sheet steel with the initial texture of {111}.The results obtained are summarized in the following:(1) A weak {100} and {111} texture was formed in the surface layer of the specimen transformed by rapid heating and rapid cooling.(2) By rapid heating and subsequent slow cooling, a texture with {110} orientations and orientations 20-30 deg shifted away from {100} was obtained in the surface layer.(3) Slow heating and slow cooling produced a distinct {100} texture in the surface layer.(4) There was a marked difference in texture between surface and midsection of thick specimen: In the midsection, the texture similar to that described in (1) was formed, independent of the heating and cooling rates. While, the specimen surface exhibited the texture as mentioned in (1) to (3) on each condition.(5) Those results were consistently explained on the assumptions that the orientation relationship between bcc and fcc follows the Kurdjumov-Sachs relation, and that during a slow progress of α→γ→α transformation the orientation change proceeds preferentially by operation of such variants that generate a larger elastic work in the normal direction of a sheet surface.

Effects of the volume fraction of γ phase on {111} texture development have been investigated by making use of several extra low carbon sheet steels which were intercritically annealed in alpha plus gamma two phase region. The results obtained are summarized in the following.(1) {111} texture developed with increase in volume fraction of γ phase. {111} component had two maxima; first at the γ fraction below 50% and second at the fraction above 60%.(2) The similar relation to (1) was obtained between the Lankford value and γ fraction.(3) The development of {111} annealing texture was stronger in a thinner specimen than in a thicker one, and on the surface than on the midsection.(4) During slow cooling after intercritical annealing, {111} component increased and {100} component decreased.(5) In the residual α phase, {111} texture evolved with increase in γ fraction, and had a maximum between 60 and 90% of transformed γ phase.(6) These results were reasonably understood on the basis of a new theory, proposed by the present authors, on the formation mechanism of the transformation texture.

Chemical removal of the endothelium by saponin in the isolated dog femoral artery was investigated by comparing the relaxant responses to endothelium-dependent and -independent vasodilators of saponin-treated rings with the responses of non-treated rings. Saponin treatment was done by incubating rings with Krebs-Henseleit solution containing 0.1, 0.3 or 1 mg/ml of saponin for 45 min at 37 degrees C. In non-treated rings, acetylcholine (10(-8)-3 X 10(-6) M) caused a concentration-dependent relaxation of rings precontracted with prostaglandin F2 alpha (3 X 10(-6) M). The acetylcholine-induced relaxation was reduced in rings pretreated with 0.1 mg/ml of saponin and almost abolished with 0.3 or 1 mg/ml. Prostaglandin F2 alpha-induced contraction was suppressed weakly by treatment with 0.3 mg/ml and markedly with 1 mg/ml saponin. The treatment with 0.3 mg/ml saponin markedly reduced relaxations caused by substance P (10(-9)-3 X 10(-8) M) and by Ca2+-ionophore A23187 (10(-6) M). Relaxant responses of saponin-treated rings to nitroglycerin and to nitroprusside were almost identical with those of non-treated rings. These results showing selective suppression by saponin of the endothelium-dependent relaxation suggest that saponin removes the endothelial cells from the intimal surface of the artery, and this was confirmed by electron microscopy. The endothelium removing method with saponin seems to be useful as a pharmacological tool for vascular investigations.

The effects of nifedipine, classed as a calcium entry blocker, on urinary excretion and renin release were investigated in anesthetized dogs. Nifedipine was infused into one renal artery for three consecutive 10-min periods, at incremental rates of 0.3, 1, and 3 micrograms/min. Intrarenal infusion of nifedipine (3 micrograms/min) produced marked increases in urine flow rate (by 200%) and in urinary sodium (by 210%) and potassium (by 40%) excretion rates of the infused kidney without changes in mean systemic blood pressure, heart rate, glomerular filtration rate, and filtration fraction. Urinary osmolarity was slightly decreased by the drug, but this change was not statistically significant. There were no consistent changes in these parameters for the contralateral noninfused kidney. Renin secretion rate was increased to three times the preinfusion level during infusion of the highest nifedipine dose. The blood flow to the infused kidney was increased, and ipsilateral renal vascular resistance was simultaneously decreased upon nifedipine infusion. These results suggest that a nonhypotensive dose of nifedipine causes an increase in renin secretion and that this drug has a striking effect on the reabsorption of sodium and water by the renal tubules.

The immobility-reducing action of desipramine (DMI) in forced swimming rats was attenuated by intracerebroventricular (i.c.v.) injection of isoproterenol (ISO) and potentiated by i.c.v. atenolol (ATE), a β 1 -adrenoceptor antagonist. The effect of ISO was blocked by ATE. When administered i.c.v. in normal rats, ISO reduced the contents of 3-methoxy-4-hydroxy-phenylethyleneglycol sulfate (MHPG-SO 4 ), a major metabolite of noradrenaline, in the septal area, thalamus and hypothalamus while ATE had no effect in most of the brain regions. However, in forced swimming rats treated with DMI, ISO reduced MHPG-SO 4 in 6 out of 8 brain regions tested and conversely, ATE increased the levels in the amygdala, septal area and hypothalamus. Similar to the behavioral effect, the effect of ISO was antagonized by ATE. These results support the hypothesis that central β 1 -adrenergic mechanisms inhibit the immobility-reducing action of DMI by reducing the activity of noradrenergic neurons in the brain.

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.

For the purpose of investigating the formation mechanism of the texture which is developed by ferrite (α)→austenite (γ)→ferrite (α) transformation, the effects of heating and cooling rates during phase transformation and specimen thickness on the transformation texture have been studied by using an extra low carbon sheet steel with the initial texture of {111}.The results obtained are summarized in the following:(1) A weak {100} and {111} texture was formed in the surface layer of the specimen transformed by rapid heating and rapid cooling.(2) By rapid heating and subsequent slow cooling, a texture with {110} orientations and orientations 20-30 deg shifted away from {100} was obtained in the surface layer.(3) Slow heating and slow cooling produced a distinct {100} texture in the surface layer.(4) There was a marked difference in texture between surface and midsection of thick specimen: In the midsection, the texture similar to that described in (1) was formed, independent of the heating and cooling rates. While, the specimen surface exhibited the texture as mentioned in (1) to (3) on each condition.(5) Those results were consistently explained on the assumptions that the orientation relationship between bcc and fcc follows the Kurdjumov-Sachs relation, and that during a slow progress of α→γ→α transformation the orientation change proceeds preferentially by operation of such variants that generate a larger elastic work in the normal direction of a sheet surface.

The effects of prazosin and yohimbine on sympathetic neurotransmission to the heart were investigated in perfused dog hearts in situ in an attempt to determine whether alpha 1-adrenoceptors are located presynaptically in the cardiac sympathetic nerves. Intra-arterial injections of prazosin (1-30 micrograms) and yohimbine (0.3-10 micrograms) into the right coronary artery during cardiac sympathetic nerve stimulation further increased the tachycardia resulting from the stimulation. Continuous infusions of methoxamine (20-40 micrograms/min) and of clonidine (2-4 micrograms/min) into the right coronary artery during cardiac sympathetic nerve stimulation caused sustained reduction of the tachycardia. Prazosin under methoxamine infusion enhanced the tachycardia to a greater extent than in the absence of methoxamine. Prazosin under clonidine infusion enhanced the tachycardia to the same extent as it did in the absence of clonidine. These results suggest that prazosin antagonizes the effect of methoxamine but does not antagonize that of clonidine. The results obtained with yohimbine were in contrast to the effects of prazosin, showing the antagonism of clonidine by yohimbine. Prazosin and yohimbine both had little effect on the heart rate during either the resting state or the infusion of norepinephrine. These results suggest that the prazosin- and yohimbine-induced enhancement of the tachycardia resulting from cardiac sympathetic nerve stimulation is due to a presynaptic effect. However, the presynaptic effect of prazosin appears to differ from that of yohimbine. The presence of presynaptic alpha 1-adrenoceptors regulating norepinephrine release, as well as of alpha 2-adrenoceptors, is suggested in the cardiac sympathetic nerves of the dog.

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.

SUMMARY 1. The effect of serotonin on cardiac sympathetic transmission was investigated in vagotomized and cardiac decentralized dogs. 2. Administration of serotonin in doses of 10-100 μg/kg i.v., during the resting unstimulated state caused tachycardia and pressor responses which were inhibited by cyproheptadine but not by guanethidine. The tachycardia was reduced by a β-adrenoceptor antagonist, bufetolol. 3. Serotonin in doses of 3-100 μg/kg depressed the elevated heart rate during maintained electrical stimulation of the cardiac sympathetic nerves. 4. Cyproheptadine did not antagonize the serotonin-induced depression of the stimulation-elevated heart rate, while desipramine attenuated but did not abolish it. 5. Serotonin did not have a significant effect on the heart rate elevated by maintained infusion of noradrenaline. 6. The present results suggest that serotonin-induced depression of heart rate during sympathetic nerve stimulation is due to presynaptic inhibition by serotonin of cardiac sympathetic transmission which is not mediated via‘classic’ tryptaminergic receptors.

The present study was designed to investigate the effect of bradykinin on renin release in relation to prostaglandins by use of indomethacin, a cyclooxygenase inhibitor, in pentobarbital-anesthetized rats. A nonhypotensive dose of bradykinin (1 microgram/kg X min), which was infused intrarenally, significantly increased plasma renin activity approximately 1.8-fold as compared to the control period. In indomethacin (5 mg/kg, i.v.)-pretreated rats, bradykinin did not significantly increase plasma renin activity. These results suggest that bradykinin does not directly increase plasma renin activity and that prostaglandins may participate in the bradykinin-induced renin release under these experimental conditions.

The influences of various monoaminergic agents on the immobility-reducing action of desipramine (DMI) in the forced swimming test were examined. 5-Methoxy-N,N-dimethyltryptamine and methysergide, a serotonin agonist and antagonist, respectively, did not affect the duration of immobility. Pimozide, a dopamine antagonist, prolonged the duration of immobility at a dose of 0.5 mg/kg. However, at the doses tested, these drugs had no effect on the action of desipramine. Phenoxybenzamine, an alpha-adrenergic antagonist, prolonged the duration of immobility only with the largest dose (20 mg/kg), but the action of desipramine was completely blocked by this drugs at all doses. Intracerebroventricular injection of a beta-adrenergic agonist, isoproterenol (ISO), and two selective beta 1-adrenergic antagonists, atenolol (ATE) and practolol, dose-dependently diminished and potentiated, respectively, the action of desipramine although these drugs had no effect on the duration of immobility when given alone. A beta 2-adrenergic antagonist derived from oximino-9-fluorene, (IPS 339) did not influence the duration of immobility or affect the action of desipramine. The effect of isoproterenol was almost completely blocked by the pretreatment with atenolol and practolol but not by IPS 339. Subcutaneously-injected isoproterenol did not affect the action of desipramine. Isoproterenol and atenolol had no effect on the concentration of desipramine in brain regions. Phenylephrine, a postsynaptic alpha-adrenergic agonist, reduced the duration of immobility as did desipramine, but this action was not affected by isoproterenol and atenolol.(ABSTRACT TRUNCATED AT 250 WORDS)

The combined activities of cathepsin B and cathepsin L were studied in the forelimb and hind limb muscles of dystrophic mice. The activities of these proteases in the forelimb and hind limb muscles of young and adult dystrophic mice were significantly higher than those in normal mice. However, clinical involvement of dystrophy appeared in the hind limbs but not in the forelimbs. We therefore suggest that the increase in protease activity begins at a very early age and that the clinical involvement is not linked with the increase in cathepsins B and L.

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.