This study was undertaken to determine whether arginine vasopressin, infused or injected in doses within known physiological ranges, can alter pressor responses to injected or endogenously liberated catecholamines. In 8 pentobarbital-anesthetized dogs, 14 pithed rats, and 7 spinal cats, the pressor responses to catecholamine injections were definitely potentiated by administration of nonpressor doses of vasopressin. In eight dogs anesthetized with N2O-O2, readily reproducible pressor responses to bilateral carotid artery occlusion were subsequently potentiated by infusions of vasopressin. Vasopressin also potentiated both isometric and isotonic responses of 37 rat aortic strip preparations to norepinephrine or epinephrine added to the Krebs-bicarbonate bath. Vasopressin, in physiological dose ranges, potentiates pressor responses to catecholamines by a direct rather than a central action. Endogenously liberated vasopressin may play a role in the responsiveness of vascular smooth muscle to endogenously liberated catecholamines in dog, rat, and cat.

The major vessel occlusion method applied to the supine, anesthetized dog with an open chest has proven useful in elucidating the role of the venous system in the complex phenomenon of venous return. This method momentarily isolates a large part of the venous system from the arterial system and from the action of the heart and the respiratory and muscle pumps. Simultaneous occlusion of the thoracic inferior vena cava and the descending aorta (MVO) divides the dog's circulation into a cephalad zone and a caudad zone. Experimentally induced changes in the status of the cephalad circulation during MVO can affect the caudad zone only through neuronal pathways. Therefore, MVO makes it possible to investigate the responses of the venous system to vascular reflex activity as well as direct and indirect actions of drugs. During the "resting" state, blood returns to the heart because of the existence of a venous pressure gradient of 3 to 4 mm. Hg, operant between the reactive venous reservoir and the central venous conduit ("intra-venous" gradient). Augmentation of sympathetic tone produces an increase in venous return, of venous origin, due to an increase in the effective "intra-venous" pressure gradient from 3 to 4 mm. Hg to 5 to 10 mm. Hg. The ability of the venous system to increase venous return independently, has been shown to be a significant factor in the arterial hypertensive response to carotid occlusion. The venous system can serve as a buffer against the effects of sudden, momentary changes in arterial flow by maintaining, reducing, or augmenting venous return.

SUMMARY1. The influence of adenosine cyclic 3',5'-monophosphate (3',5'-AMP) and of drugs believed to increase or decrease its concentration in the tissues has been determined on the response of vascular and uterine smooth muscles to catecholamines. Generally, drugs believed to increase tissue content of 3',5'-AMP potentiated the responses and those believed to decrease it depressed them.2. The cardiovascular responses of dogs (with major vessels occluded in the chest) to carotid occlusion were potentiated by infusions of theophylline and sodium fluoride. Infusion of theophylline also potentiated the response of the occluded abdominal vessels to noradrenaline.3. Intravenous infusions of theophylline and sodium fluoride potentiated pressor responses to catecholamines in the pithed rat. Infusions of iminazole depressed the responses in two animals and was without effect in two others.4. In spinal cats intravenous infusions of theophylline potentiated pressor responses to catecholamines, but sodium fluoride was without effect.5. Contractions of the isolated rat aortic strip to noradrenaline were always potentiated by sodium fluoride and by theophylline, and depressed by iminazole, when they were recorded isometrically. Theophylline always potentiated the contractions, when they were recorded isotonically but sodium fluoride was mostly, and iminazole always, ineffective.6. 3',5'-AMP in concentrations from 041 to 20,g/ml. potentiated the responses of the isolated rat aortic strip to noradrenaline in thirty-eight experiments out of hundred. Concentrations from 10 to 500 ,ug/ml.

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Isolated preparations of mammalian cardiac muscle have been employed to study possible mechanisms responsible for changes in diastolic compliance. Muscles have been studied at rest and during isometric and afterloaded contractions, at fixed initial length and during programmed, cyclic changes in length, and under the influence of paired stimulation, catecholamines, and elevated extracellular calcium concentrations. The results obtained indicate that, although there is a series viscous element in cardiac muscle, which accounts for stress-relaxation, some changes in compliance apparently result from alterations in the extensibility of the contractile element. This conclusion is based primarily on experiments showing shifts in the apex of the length-tension curve produced by action of inotropic agents which alter diastolic compliance and on experiments showing that the rate and extent of relaxation of afterloaded contractions depend on the extent of shortening during contraction. • During the past forty years a variety of considerations have suggested that the diastolic pressure-volume relationship for the mammalian ventricle might vary as a result of some change in the characteristics of the myocardium (1-8). Moreover, it was recognized early that under appropriate conditions variability in the pressure-volume relationship would influence both the performance of the heart as well as any evaluation of performance which employed measurement of enddiastolic pressure as an index of fiber length. A change in the pressure-volume or lengthtension relationship might result either from an alteration in the contractile elements or