Central cholinergic mechanism for control of urine volume and electrolyte excretion.

1. Studies were conducted on urine volume and electrolyte excretion chiefly of Na and K in anaesthetized hydrated dogs. 2. Central injection of acetylcholine caused a dose dependent antidiuretic response but without any change in excretion of urinary Sodium (UNa) and Potassium (UK). 3. After central atropinization, antidiuretic response to acetylcholine was partially blocked without any effect on electrolyte excretion. 4. Intracerebroventricularly (I.C.V.) administered acetylcholine after vagotomy and spinalectomy, each done separately and together also elicited an antidiuretic response. There was no effect on electrolyte excretion. 5. It is thus suggested that acetylcholine may be acting on central cholinergic receptors concerned with A.D.H. release.

Effect of centrally administered glucagon on urine output in dogs.

The effect of minimal doses of glucagon, administered by intracerebroventricular (ICV) and intracisternal(IC) routes, on urine output in mongrel dogs have been studied. The dose of 2.0 mug of glucagon was found to be the minimal dose for diuresis on peripheral administration. This dose when centrally administered, produced an oliguric effect in animals. This effect was not observed in vagosympathectomised-spinal cord transectomised or adrenalectomised animals. It is suggested that the probable efferents might be the sympathetic fibres as they are present in vagi nerves as well in the spinal cord (26). The observations made in an attempt to find out the organ responsible for the oliguric effect, showed that some substance released from the adrenal cortex has an influence on the kidney's excretory function.

Central component of the cario-accelerator action of angiotensin II in dogs.

Injection of angiotensin II into a lateral cerebral ventricle (I.C.V.) or into a peripheral vein of anaesthetized dog elicited a rise in blood pressure and transient bradycardia followed by sustained tachycardia. Spinal transection at C2 and bilateral vagotomy abolished the central cardiovascular effect of I.C.V. angiotensin. However, in spinal transected dogs the usual pressor response to intravenous angiotensin was observed. Since the transient bradycardia was absent in bilaterally vagotomized dogs or in dogs with their blood pressure stabilized by means of a mechanical buffer devise it must be reflex in origin. The tachycardia was more marked in vagotomized dogs. Prior administration of a beta adrenergic receptor blocking agent propranolol, blocked the tachycardia, but the pressor response was unaffected. The cardiovascular responses to centrally administered angiotensin were practically abolished by prior treatment of dogs with reserpine or by extirpation of both adrenal glands. Thus it may be concluded that ICV angiotensin induces a centrogenic release of catecholamines from the adrenal medulla which is responsible for the cardiovascular responses.