Renal blood flow and its distribution following haemorrhage in the rat: the role of vasopressin.

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.