1. The role of allopurinol in the protection of kidney function following ischaemia—reperfusion injury has been investigated using the novel technique of near-infrared spectroscopy. 2. An in vivo model of rat kidney ischaemia was used, with the expected falls in blood and tissue oxygenation seen and confirmed by near-infrared spectroscopy. 3. Allopurinol infusion increased the rate of reperfusion of oxygenated blood seen in control rats ( P < 0.05). 4. Allopurinol enhanced the rate of tissue oxygenation during early reperfusion ( P < 0.01). 5. This study provides further evidence for the proposed benefits of allopurinol in ischaemia—reperfusion injury. Furthermore, the potential of near-infrared spectroscopy as a technique of value in interventional studies of this nature is confirmed.

1. The binding of angiotensin II to glomerular receptors was studied in spontaneously hypertensive and normotensive Wistar-Kyoto rats in response to 7, 16 and 32% isocaloric, isonatraemic protein diets. 2. Increased dietary protein elevated the systemic angiotensin II levels of both spontaneously hypertensive and Wistar-Kyoto rats [ F 0.05 (2,26)=4.758, P <0.05; n =36], and this was not associated with changes in either systemic blood pressure or cortical renin activity. 3. Furthermore, no significant changes in the affinity or density of angiotensin II receptors were associated with changes of dietary protein intake in either strain. 4. These results indicate a dissociation between the systemic renin-angiotensin system and the tissue renin -angiotensin system in response to protein intake.

1. The induction of selective renal medullary damage by 2-bromoethylamine hydrobromide (BEA) results in polyuria and raised blood pressure. In view of the likely elevation of plasma vasopressin we have investigated the role of vasopressin (AVP) in the elevated blood pressure in this model. 2. Plasma vasopressin levels in BEA pretreated rats were raised significantly (2 ± 0.6 pg/ml vs 0.8 ± 0.1 in normal rat, P < 0.05) but not to pressor levels. 3. In addition, pressor responsiveness was investigated in renal medullary damaged rats. There was a reduced response to vasopressin and noradrenaline but no alteration with angiotensin II. A specific V 1 receptor AVP antagonist [d(CH 2 ) 5 Tyr(Me)AVP] produced no fall in blood pressure but returned the noradrenaline dose-response curve to normal. This suggests an interaction between vasopressin and the sympathetic nervous system in this model. 4. Thus there is no evidence that vasopressin contributes to the rise in blood pressure produced by chemical renal medullectomy and other mechanisms have to be sought.

1. Blood pressure, plasma and aortic renin concentrations were measured in Goldblatt two-kidney one-clip hypertensive rats before and after surgical correction by removing the renal artery clip. 2. Blood pressure fell rapidly in the first hour and then more slowly over 24 h. 3. Plasma renin concentration fell into the normal range by 3 h after unclipping. 4. Aortic renin concentration was markedly raised in hypertensive rats and declined slowly after unclipping, being virtually unchanged at 3 h and reaching normal levels at 24 h. 5. The fall in blood pressure produced by removal of the renal artery clip in Goldblatt two-kidney one-clip hypertensive rats does not depend upon the renin-angiotensin system in plasma and vascular tissue and indicates that a renal vasodepressor system may be involved.

1. Longstanding two-kidney, one-clip hypertension in the rat was rapidly reversed by removal of the constricting clip and the reversal, was complete by 12 h. 2. Blood pressure was lowered by renin-angiotensin inhibition, caused by saralasin or captopril, but not to normotensive levels. Infusion with indomethacin or aprotinin over a 15 h period did not affect the blood pressure. 3. The pattern of fall in blood pressure after removal of the clip was similar when rats were infused with saralasin, captopril, indomethacin or aprotinin. Blood pressure was normal at 24 h and did not differ significantly from that of unclipped rats given an infusion of glucose. 4. The fall in blood pressure produced by unclipping was not altered by inhibition of the renin-angiotensin system and did not appear to be mediated via the prostaglandin or kallikrein systems.

1. Blood pressure was monitored continuously in conscious rats with chronic Goldblatt two-kidney, one-clip hypertension. 2. Hypertension was rapidly reversed by removal of the constricting clip and the reversal was complete by 12 h, although structural vascular changes persisted for much longer. 3. Blood pressure in this model of hypertension was not affected by a 15 h infusion of either indomethacin or aprotinin. 4. The pattern of fall in blood pressure after removal of the clip was similar when animals were infused with either indomethacin or aprotinin. Blood pressure at 24 h was normal and did not differ significantly from that of unclipped rats given a glucose infusion. 5. The fall in blood pressure produced by unclipping therefore did not appear to be mediated via the prostaglandin or kallikrein systems.

1. Within 24 h of surgical reversal of chronic Goldblatt two-kidney, one-clip hypertension in the rat, of >4 months duration, blood pressure had fallen to normal levels. At this time there was no difference between the effects of removal of the clip or the ischaemic kidney but, at 60 days after reversal, the blood pressure of rats which had been nephrectomized was significantly higher than that of normal controls. 2. The fall in blood pressure was associated with a fall in total peripheral resistance to normal by 24 h despite the previous established fact that structural vascular changes take much longer to reverse. There was a corresponding rise in cardiac output, mainly due to an increase in stroke volume. Nephrectomized rats had a significantly higher stroke volume compared with those unclipped 24 h after operation. 3. As blood pressure can become normal in the presence of structural cardiovascular change by a fall in total peripheral resistance it would seem unlikely that resistance vessel hypertrophy is responsible for the maintenance of blood pressure in this model. Another peripherally acting mechanism therefore has to be postulated.

1. Chemical renal medullectomy was produced in rats by injection of 2-bromoethylamine hydrobromide. Plasma creatinine and blood pressure were unchanged although urine volume was increased fourfold. 2. Left renal artery constriction resulted in similar degrees of hypertension in both intact and medullectomized rats. This was associated with a significantly smaller rise in plasma renin concentration in the latter. 3. Blood pressure in conscious intact hypertensive rats became normal within 24 h of unclipping whereas blood pressure of medullectomized rats remained significantly elevated. 4. The presence of an intact renal medulla is essential to the complete reversal of two-kidney, one-clip hypertension in the rat. This may reflect the loss of a medullary vasodepressor system.