SUMMARY1. Anaesthetized Brattleboro rats with hereditary diabetes insipidus were infused with vasopressin at three different doses (1P3, 13 or 130 mu./hr) in order to study the effect ofthe hormone on renal blood flow and its distribution. Radioactive microspheres were used to determine intrarenal blood flow. 2. The plasma vasopressin level during infusion of the lowest dose was calculated to be within the physiological range. At this dose vasopressin was antidiuretic but was without effect on arterial blood pressure or solute excretion, whereas the two higher doses were both pressor and natriuretic.3. All doses of vasopressin increased renal vascular resistance and decreased renal blood flow. The vasoconstrictor effect of the lowest dose was confined to the outer cortex, whereas the two higher doses affected the entire cortex.4. In separate experiments, [1-(,-mercapto-fl,fl-cyclopentamethylenepropionicacid), 2(0-methyl) tyrosine] arginine vasopressin, an antagonist of the vascular action of vasopressin, was administered to anaesthetized Long Evans or Brattleboro rats. In the Long Evans rats the antagonist caused a decrease in renal vascular resistance and a consequent increase in renal blood flow, this effect being restricted to the outer cortex. In Brattleboro rats the antagonist had no effect on renal vascular resistance or renal blood flow.5. It is concluded that physiological levels of vasopressin influence the distribution of renal blood flow by causing vasoconstriction in the outer region of the renal cortex. Higher levels of the hormone increase vascular resistance throughout the cortex.

The effect of an acute arterial haemorrhage of 15 ml/kg body weight on renal and intrarenal blood flow (measured using radioactive microspheres) was determined in anaesthetized rats. In order to assess the role of vasopressin in mediating the observed changes, the response to haemorrhage of animals lacking the ability to synthesize vasopressin (Brattleboro rats) was compared with that of the parent strain (Long Evans rats). In addition, a group of Long Evans rats was treated with an antagonist of the vascular action of vasopressin before being bled. Thirty minutes after haemorrhage the mean arterial blood pressure of untreated Long Evans rats was significantly higher than that of Brattleboro or vasopressin antagonist‐treated Long Evans rats. Following haemorrhage, total renal vascular resistance increased markedly in untreated Long Evans rats. In these animals there were substantial increases in calculated vascular resistance in both inner and outer halves of the renal cortex. In Brattleboro rats there was only a small increase in renal vascular resistance, confined to the outer cortex, whilst in vasopressin antagonist‐treated Long Evans rats there was no significant change in the vascular resistance of either cortical region. It is concluded that much of the increase in renal vascular resistance which follows haemorrhage is due to vasopressin. This vasoconstrictor effect of the hormone, which contributes to its pressor action after haemorrhage, occurs in both the inner and outer regions of the renal cortex.