Non-operative management and immune function after splenic injury.

BACKGROUND: There is still considerable controversy about the importance and method of preserving splenic function after trauma. Recognition of the immune function of the spleen and the risk of overwhelming postsplenectomy infection led to the development of spleen-preserving surgery and non-operative management. More recently angiographic embolization has been used to try to reduce failure of conservative management and preserve splenic function. METHODS: A literature review was performed of the changing treatment of splenic injury over the last century, focusing on whether and how to maintain splenic immune function. RESULTS: Non-operative management continues to be reported as a successful approach in haemodynamically stable patients without other indications for laparotomy, achieving high success rates in both children and adults. Except for haemodynamic instability, reported predictors of failure of conservative treatment should not be seen as absolute contraindications to this approach. Angiographic embolization is generally reported to increase success rates of non-operative management, currently approaching 95 per cent. However, the optimal use of angioembolization is still debated. Splenic immunocompetence after angioembolization remains questionable, although existing studies seem to indicate preserved splenic function. CONCLUSION: Non-operative management has become the treatment of choice to preserve splenic immune function. Current knowledge suggests that immunization is unnecessary after angiographic embolization for splenic injury. Identifying a diagnostic test of splenic function will be important for future studies. Most importantly, in efforts to preserve splenic function, care must be taken not to jeopardize patients at risk of bleeding who require early surgery and splenectomy.

Viscoelastic haemostatic assay augmented protocols for major trauma haemorrhage (ITACTIC): a randomized, controlled trial.

PURPOSE: Contemporary trauma resuscitation prioritizes control of bleeding and uses major haemorrhage protocols (MHPs) to prevent and treat coagulopathy. We aimed to determine whether augmenting MHPs with Viscoelastic Haemostatic Assays (VHA) would improve outcomes compared to Conventional Coagulation Tests (CCTs). METHODS: This was a multi-centre, randomized controlled trial comparing outcomes in trauma patients who received empiric MHPs, augmented by either VHA or CCT-guided interventions. Primary outcome was the proportion of subjects who, at 24 h after injury, were alive and free of massive transfusion (10 or more red cell transfusions). Secondary outcomes included 28-day mortality. Pre-specified subgroups included patients with severe traumatic brain injury (TBI). RESULTS: Of 396 patients in the intention to treat analysis, 201 were allocated to VHA and 195 to CCT-guided therapy. At 24 h, there was no difference in the proportion of patients who were alive and free of massive transfusion (VHA: 67%, CCT: 64%, OR 1.15, 95% CI 0.76-1.73). 28-day mortality was not different overall (VHA: 25%, CCT: 28%, OR 0.84, 95% CI 0.54-1.31), nor were there differences in other secondary outcomes or serious adverse events. In pre-specified subgroups, there were no differences in primary outcomes. In the pre-specified subgroup of 74 patients with TBI, 64% were alive and free of massive transfusion at 24 h compared to 46% in the CCT arm (OR 2.12, 95% CI 0.84-5.34). CONCLUSION: There was no difference in overall outcomes between VHA- and CCT-augmented-major haemorrhage protocols.

Importance of nitric oxide in canine femoral circulation: comparison of two NO inhibitors.

OBJECTIVE: The aim was to assess the importance of endothelium derived nitric oxide (NO) in the regulation of vascular tone in the limbs. Changes in the canine femoral circulation were investigated after inhibition of NO synthesis. METHODS: The effects of two NO inhibitors, NG-monomethyl-L-arginine (LNMMA) and NG-nitro-L-arginine (NOARG), were compared on basal femoral blood flow and on endothelium dependent (acetylcholine) and endothelium independent (glyceryl trinitrate) vasodilatation in 15 pentobarbitone anaesthetised mongrel dogs. An electromagnetic flow probe was placed on the femoral artery to measure femoral blood flow. One catheter was advanced into the femoral artery proximal to the flow probe for blood pressure recording and another catheter distal to the flow probe for drug infusions. RESULTS: LNMMA (0.28 mumol.ml-1) reduced basal femoral blood flow by 44(SEM 3)%, NOARG (0.07 mumol.ml-1) by 21(4)%, and NOARG (0.56 mumol.ml-1) by 29(3)%. The flow responses to acetylcholine were reduced after LNMMA by 27(8)%, unaltered after NOARG (0.07 mumol.ml-1), and reduced after NOARG (0.56 mumol.ml-1) by 60(7)%. The flow response to glyceryl trinitrate was unaltered. L-arginine re-established femoral blood flow after infusion of LNMMA and NOARG (0.07 mumol.ml-1), but L-arginine did not re-establish femoral blood flow after NOARG (0.56 mumol.ml-1), even when infused in a 60-fold molar excess. CONCLUSIONS: There is a continuous basal release of NO in the canine femoral circulation. The results obtained by infusing LNMMA suggest that more than 40% of basal femoral blood flow is mediated by endothelium derived NO. Whereas LNMMA was more potent than NOARG in reducing basal NO release, NOARG (0.56 mumol.ml-1) reduced acetylcholine induced vasodilatation by as much as 60%.

Release of endothelin from the porcine heart after short term coronary artery occlusion.

OBJECTIVE: Endothelin is increased in plasma following myocardial infarction. Whether brief periods of myocardial ischaemia not leading to myocardial infarction increase plasma endothelin is not known. Thus, the present study was designed to examine cardiac endothelin balance in association with a 10 min coronary artery occlusion followed by reperfusion. METHODS: Venous blood was selectively sampled from the transiently ischaemic myocardium using a shunt between the anterior interventricular vein and the right atrium in eight pentobarbitone anaesthetised pigs. Flow in the shunt was measured with a Doppler flow probe. Arterial blood was drawn from the aortic arch. Plasma endothelin was measured using an Endothelin 1-21 specific [125I] assay system. This assay system has no cross reactivity with big endothlin. RESULTS: A net cardiac endothelin uptake of 0.7(0.3-1.4) fmol.min-1 x g-1 (median, 95% confidence interval) in the control period shifted to a net release during the first 10 min of reperfusion. The release reached a maximum of 2.8(0.4-6.0) fmol.min-1 x g-1 after 1.5 min of reperfusion. Cardiac venous endothelin concentration increased from 3.4(2.5-4.8) to 4.4(3.6-6.9) and 4.4(3.6-6.6) fmol.ml-1 at 1.5 and 5 min of reperfusion, respectively (p < 0.001 for both). Arterial endothelin concentration decreased from 4.8(3.9-6.1) to 2.7(2.4-4.3) fmol.ml-1 at 10 min of reperfusion (p < 0.001). CONCLUSION: Endothelin is released from the heart for several minutes during reperfusion following a brief coronary artery occlusion.

Alterations in plasma endothelin during passage through the left heart chambers before and after brief myocardial ischaemia.

OBJECTIVE: Although the lung can both produce and extract endothelin, its role in regulating plasma endothelin is not settled. Whether the endocardium is able to affect plasma endothelin is also unknown. The first aim of this study was to examine if endothelin concentration in plasma changes when passing through the pulmonary circulation or the left heart chambers. A marked decrease in endothelin concentration has been shown to occur in the aortic arch during early reperfusion following a 10 min mid left anterior descending coronary artery occlusion. A second aim was therefore to investigate whether this decrease was due to removal of endothelin in the pulmonary circulation or through the left heart chambers. METHODS: In seven open chest, pentobarbitone anaesthetised pigs blood was obtained from the pulmonary artery, the left atrium, and the aortic arch at control conditions and at 10 and 20 min reperfusion following a 10 min coronary occlusion. Endothelin measurements were performed using an endothelin 1-21 specific [125I] assay system (RPA 555). RESULTS: At control conditions there was no difference in endothelin concentration in blood obtained from the pulmonary artery [3.9 (2.7-5.2) fmol.ml-1, median (95% confidence interval)] and the left atrium [3.8 (2.8-5.8) fmol.ml-1], whereas there was a significantly higher endothelin concentration in the aortic arch [4.9 (3.8-7.2) fmol.ml-1]. At 10 min reperfusion following the 10 min coronary occlusion there was still no difference in endothelin concentration between the pulmonary artery [4.3 (2.8-6.0) fmol.ml-1] and the left atrium [4.1 (2.7-5.7) fmol.ml-1]. However, in contrast to the increase observed before myocardial ischaemia, the endothelin concentration was significantly reduced in the aortic arch [2.8 (2.4-4.4) fmol.ml-1] compared to the left atrium. At 20 min reperfusion, all endothelin concentrations had returned to preischaemic values. CONCLUSIONS: These findings suggest a role for the left heart chambers in regulating the endothelin concentration in blood entering the aorta.

Simultaneous active compression-decompression and abdominal binding increase carotid blood flow additively during cardiopulmonary resuscitation (CPR) in pigs.

The effects of adding active compression-decompression and abdominal binding separately or combined to standard compression CPR was tested in a randomized cross-over design during ventricular fibrillation in eight pigs. The flow and pressure effects of the two techniques appeared to be additive with no interference between the two. Carotid blood flow increased 22% with active compression-decompression, 34% with abdominal binding and 59% with the combination compared to flow with standard compression. Peak antegrade carotid flow occurred in early systole with retrograde flow in early diastole and close to zero in late diastole with no profound alterations induced by active decompression or abdominal binding. Abdominal binding increased the intrathoracic pressure during the compression phase as estimated from the esophageal pressure, while active decompression caused a negative esophageal pressure during the decompression phase. Neither active decompression nor abdominal binding caused any changes in the coronary perfusion pressure, nor in the left ventricular transmural pressure except for a rise in mid-diastolic pressure with active decompression.

Improved haemodynamics with increased compression-decompression rates during ACD-CPR in pigs.

The haemodynamic effects of variations in the compression-decompression frequency, 60, 90 and 120 min(-1) during ACD-CPR, were tested in a randomized cross-over design during ventricular fibrillation (VF) in 12 anaesthetized pigs (17-22 kg) using an automatic hydraulic chest compression-decompression device. There were significant increases with increasing frequency for mean (+/- S.D.) carotid blood flow (17 +/- 5, 25 +/- 9 and 36 +/- 12 ml min(-1), transit time flow probe), cerebral blood flow (17 +/- 7, 30 +/- 17 and 40 +/- 13 ml min(-1) 100 g(-1), radionuclide microspheres) and mean aortic pressure (34 +/- 8, 37 +/- 10 and 43 +/- 7 mmHg), respectively. Myocardial blood flow (radionuclide microspheres) and diastolic coronary perfusion pressure, CPP, increased significantly from 60 to 90 min(-1) with no further significant increase to 120 min(-1) (28 +/- 13, 46 +/- 23 and 49 +/- 19 ml min(-1) 100 g(-1) and 25 +/- 8, 31 +/- 11 and 32 +/- 9 mmHg, respectively). Renal and hepatic blood flow also increased with increasing rate. No significant differences in the expired CO2 levels were observed. In conclusion increasing the compression-decompression frequency from 60 to 90 and 120 min(-1) improved the haemodynamics during ACD-CPR in a pig model with VF.

Effect of different compression--decompression cycles on haemodynamics during ACD-CPR in pigs.

The haemodynamic effects of variations in the relative duration of the compression and active decompression (4 cm/2 cm) during active compression-decompression cardiopulmonary resuscitation (ACD-CPR), 30/70, 50/50 and 70/30, were tested in a randomized cross-over design during ventricular fibrillation in seven anaesthetized pigs (17-23 kg) using an automatic hydraulic chest compression-decompression device. Duty cycles of 50/50 and 70/30 gave significantly higher values than 30/70 for mean carotid blood flow (32 and 36 vs. 21 ml min-1, transit time flow probe, cerebral blood flow (30 and 34 vs. 19, radionuclide microspheres), mean aortic pressure (35 and 41 vs. 29 mmHg) and mean right atrial pressure (24 and 33 vs. 16 mmHg). A higher mean aortic, mean right atrial and mean left ventricular pressure for 70/30 were the only significant differences between 50/50 and 70/30. There were no differences in myocardial blood flow (radionuclide microspheres) or coronary perfusion pressure (CPP, aortic-right atrial pressure) between the three different duty cycles. CPP was positive in both the early and late compression period and during the whole decompression period. The expired CO2 was significantly higher with 70/30 than 30/70 during the compression phase of ACD-CPR. Beyond that no significant differences in the expired CO2 levels were observed. In conclusion a reduction of the compression period to 30% during ACD-CPR reduced the cerebral circulation, the mean aortic and right atrial pressures with no effect on the myocardial blood flow of varying the compression-decompression cycle.

Effects of various degrees of compression and active decompression on haemodynamics, end-tidal CO2, and ventilation during cardiopulmonary resuscitation of pigs.

UNLABELLED: The effects of various degrees of compression and active decompression during cardiopulmonary resuscitation were tested in a randomized cross-over-design during ventricular fibrillation in eight pigs using an automatic hydraulic chest compression device. Compared with 4/0 (compression/decompression in cm), mean carotid arterial blood flow rose by 60% with 5/0, by 90% with 4/2 and 4/3, and 105% with 5/2. Two cm active decompression increased mean brain and myocardial blood flow by 53% and 37%, respectively, as compared with 4/0. Increasing standard compression from 4 to 5 cm caused no further increase in brain or heart tissue blood flow whether or not combined with active decompression. Tissue blood flow remained unchanged or decreased when active decompression (4/3) caused that 50% of the pigs were lifted from the table due to the force required. Myocardial blood flow was reduced with 5/0 vs. 4/0 despite no reduction in end decompression coronary perfusion pressure ((aortic-right atrial pressure) (CPP), (7 +/- 8 mmHg with 4/0, 14 +/- 11 mmHg with 5/0)(NS)). End decompression CPP increased by 186% with 4/2 vs. 4/0, by 200% with 4/3, and by 300% with 5/2. Endo-tracheal partial pressure of CO2 was significantly increased during the compression phase of active decompression CPR compared with standard CPR. Active decompression CPR generated an significantly increased ventilation compared with standard CPR. CONCLUSION: Carotid and tissue blood flow, ventilation, and CPP increase with 2 cm of active decompression. An attempt to further increase the level of active decompression or increasing the compression depth from 4 to 5 cm did not improve organ blood flow.

Observational study of child restraining practice on Norwegian high-speed roads: restraint misuse poses a major threat to child passenger safety.

OBJECTIVE: Restraint misuse and other occupant safety errors are the major cause of fatal and, severe injuries among child passengers in motor vehicle collisions. The main objectives of the present, study were to provide estimates of restraining practice among children younger than 16 years, traveling on Norwegian high-speed roads, and to uncover the high-risk groups associated with, restraint misuse and other safety errors. METHODS: A cross-sectional observational study was performed in conjunction with regular traffic, control posts on high-speed roads. The seating and restraining of child occupants younger than 16, years were observed, the interior environment of the vehicles was examined, and a structured, interview of the driver was conducted according to a specific protocol. RESULTS: In total, 1260 child occupants aged 0-15 years were included in the study. Misuse of restraints, was observed in 38% of cases, with this being severe or critical in 24%. The presence of restraint, misuse varied significantly with age (p<0.001), with the frequency being highest among child, occupants in the age group 4-7 years. The most common error in this group was improperly routed, seat belts. The highest frequency of severe and critical errors was observed among child occupants in, the age group 0-3 years. The most common errors were loose or improperly routed harness straps and, incorrect installations of the child restraint system. Moreover, 24% of the children were seated in, vehicles with heavy, unsecured objects in the passenger compartment and/or the trunk that were, likely to move into the compartment upon impact and cause injury. No totally unrestrained children, were observed. CONCLUSIONS: This study provides a detailed description of the characteristics of restraint misuse and, the occupant's exposure to unsecured objects. Future education and awareness campaigns should, focus on children aged <8 years. The main challenges are to ensure correct routing and tightness of, harness straps and seat belts, correct installation of child restraints, and avoidance of premature, graduation from child restraints to seat belts only. Information campaigns should also advocate the use, of chest clips and address the potential risks of hard, heavy objects in the passenger compartment and, the importance of the placement and strapping of heavy objects in the trunk.

[Incarcerated obturator hernia]. / Inkarserert obturatorhernie.

Incarcerated obturator hernia is rare. One case is described which demonstrates many of the clinical features of the condition. Most affected are elderly women with chronic diseases, and the dominating symptoms are the same as for obstruction of the small bowel. The Howship-Romberg sign is said to be pathognomonic but is present in less than half of the cases. A correct preoperative diagnosis is rare. Resection of the small bowel is often necessary. The high mortality rate is due to the high age and often poor health of the patients, combined with late diagnosis.

[Luxatio erecta. An uncommon shoulder luxation]. / Luxatio erecta. En uvanlig skulderluksasjon.

Luxatio erecta (erect dislocation) is an uncommon form of dislocation of the shoulder. One typical case is described. It is important to recognize an erect dislocation of the shoulder, since the method of reduction differs from that used for the more common forms of dislocation. Immediate reduction is important in order to reduce risk of serious neurological damage.

[Hemorrhagic compression of the median nerve after streptokinase treatment]. / Hemoragisk kompresjon av nervus medianus etter streptokinasebehandling.

Hemorrhagic events in patients undergoing fibrinolytic therapy for acute myocardial infarction are well known. We report a case of acute compression of the median nerve caused by a hematoma in the carpal tunnel following infusion of streptokinase in a 71 year-old man with acute myocardial infarction. Operative decompression was carried out. The postoperative course was uneventful, with complete recovery from symptoms of median nerve entrapment.

[Aortic aneurysm misinterpreted as pulmonary tumor]. / Aortaaneurisme misoppfattet som lungetumor.

Two cases have been reported of patients with an atherosclerotic saccular aneurysm of the descending aorta which simulated a left-sided lung neoplasm. Despite advanced diagnostic procedures, the diagnosis was not made before thoracotomy. The authors discuss some of the diagnostic problems related to thoracic saccular aneurysms.

Inhibitory effect of endothelin on renin release in dog kidneys.

To investigate the effect of endothelin on renin release, experiments were performed in barbiturate-anaesthetized dogs with denervated kidneys. Intrarenal infusion of endothelin (1 ng min-1 kg-1 body wt) reduced renal blood flow (RBF) from 145 +/- 10 ml min-1 to 98 +/- 9 ml min-1 without altering renin release (1 +/- 1 microgram angiotensin I (AI) min-1). Renin release was then increased either by renal arterial constriction or ureteral occlusion. When renal arterial pressure was reduced to 50 mmHg, renin release averaged 79 +/- 20 micrograms AI min-1 in six dogs and fell significantly to 24 +/- 6 micrograms AI min-1 during endothelin infusion. During ureteral occlusion the inhibitory effect of endothelin on renin release either during inhibition of beta-adrenergic activity with propranolol or after inhibiting prostaglandin synthesis by indomethacin during intrarenal infusion of isoproterenol was examined. After propranolol administration ureteral occlusion increased renin release from 5 +/- 2 micrograms AI min-1 to 38 +/- 12 micrograms AI min-1 in six dogs. Subsequent intrarenal endothelin infusion (1 ng min-1 kg-1 body wt) during maintained ureteral occlusion reduced renin release to 10 +/- 3 micrograms AI min-1. In six other dogs prostaglandin synthesis was inhibited by indomethacin. Subsequent infusion of isoproterenol (0.2 microgram min-1 kg-1 body wt) to stimulate beta-adrenoceptor activity increased renin release from 13 +/- 4 micrograms AI min-1 to 68 +/- 8 micrograms AI min-1 during ureteral occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Dissociation between water and lithium transport during acute changes in plasma potassium concentration in dog kidney.

Lithium clearance is often used as a marker for proximal tubular water transport. Proximal tubular transport may be modulated by changing plasma potassium concentration. The aim of the present study was to examine the effect of acute changes in plasma potassium concentration on proximal tubular fluid and lithium transport. Clearance studies were performed in seven anaesthetised, volume-expanded dogs treated with amiloride (1 mg kg-1 body weight) to block distal tubular potassium secretion, and with bumetanide (30 micrograms kg-1 body weight) to inhibit sodium reabsorption in Henle's loop. When plasma potassium concentration was raised from 2.6 +/- 0.2 to 7.9 +/- 0.2 mmol l-1, water reabsorption decreased from 23.9 +/- 2.9 to 19.8 +/- 2.2 ml min-1, whereas lithium reabsorption increased from 10.5 +/- 2.3 to 18.1 +/- 2.3 mumol min-1, at constant glomerular filtration rate. We conclude that acute elevation of plasma potassium concentration inhibits proximal tubular fluid reabsorption, but stimulates renal lithium reabsorption. Thus, lithium reabsorption cannot be used as a marker for proximal tubular transport during acute changes in plasma potassium concentration.

Inhibition of granulocyte-derived proteases reduces the increase in plasma endothelin associated with myocardial ischemia in the pig.

Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemia-induced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of granulocyte-derived proteases could reduce the increase in plasma ET observed in association with myocardial ischemia. We infused Eglin C, a selective inhibitor of the granulocyte-derived proteases elastase, cathepsin G, and chymotrypsin, in pigs subjected to 90 min left anterior descending coronary artery occlusion followed by 210 min reperfusion (n = 7). Arterial plasma ET increased in an untreated control group (n = 7) from 5.0 +/- 0.6 (mean +/- SEM) fmol . ml-1 before myocardial ischemia to 6.1 +/- 0.6 fmol . ml. at 90 min ischemia and reached a maximum of 6.8 +/- 0.9 fmol . ml-1 at 90 min reperfusion. The increase in plasma ET associated with myocardial ischemia was almost completely abolished in the Eglin C treated group (p = 0.005). Plasma ET in the Eglin C treated animals was 4.7 +/- 0.4, 4.7 +/- 0.4, and 4.6 +/- 0.4 fmol . ml-1 before myocardial ischemia, at 90 min ischemia, and at 90 min reperfusion, respectively. Our study suggests a role for granulocyte-derived proteases in the increase in plasma ET associated with myocardial ischemia. We have shown that the increase in plasma ET associated with myocardial ischemia was reduced by inhibition of granulocyte-derived proteases using the selective protease inhibitor Eglin C.

Lack of inhibitory effect of atrial natriuretic factor on renin release induced by renal hypotension.

To examine the effect of atrial natriuretic factor (ANF) on renin release induced by renal hypotension, experiments were performed in seven barbiturateanaesthetized dogs with denervated kidneys. Renin release induced by renal arterial constriction to 55 mmHg was measured before and during intrarenal infusion of ANF (200 ng min-1 kg-1 body weight). Before ANF infusion, renal arterial constriction increased renin release from 0.2 +/- 0.1 to 21.8 +/- 3.3 micrograms angiotensin I min-1 (p < 0.05). During ANF infusion renal arterial constriction increased renin release as much as before from 0.8 +/- 0.6 to 23.7 +/- 4.6 micrograms angiotensin I min-1 (p < 0.05). Although ANF increased glomerular filtration rate from 33.9 +/- 4.2 to 43.4 +/- 5.6 ml min-1 (p < 0.05) and sodium excretion from 72 +/- 22 to 567 +/- 112 mumol min-1 (p < 0.05) at normal renal perfusion pressure, ANF was without effect on glomerular filtration rate and sodium excretion during renal arterial constriction. The present study shows that ANF is not an inhibitor of renin release induced by renal arterial constriction in anaesthetized dogs with denervated kidneys. Our findings indicate that ANF does not influence renin release induced by the haemodynamic mechanism.

Atrial natriuretic factor reduces renin release by opposing alpha-adrenoceptor activity.

To examine how atrial natriuretic factor (ANF) inhibits renin release during renal sympathetic nerve stimulation, experiments were performed in barbiturate-anesthetized dogs. In five dogs, intravenous ANF infusion (50 ng.min-1.kg body wt-1) reduced renin release induced by renal nerve stimulation (1 Hz) from 16.8 +/- 8.4 to 3.5 +/- 2.1 micrograms angiotensin I (ANG I)/min. In two groups, renin release was raised by ureteral occlusion, which enhances the effects of beta-adrenoceptor stimulation and increased prostaglandin synthesis. During ureteral occlusion, intrarenal infusion of isoproterenol (0.2 micrograms.min-1.kg body wt-1) increased renin release in eight dogs to 82.6 +/- 10.9 micrograms ANG I/min, which was not significantly reduced by ANF infusion (81.1 +/- 10.1 micrograms ANG I/min). Similarly, intrarenal infusion of arachidonic acid (80 micrograms.min-1.kg body wt-1) during ureteral occlusion increased renin release in five dogs to 22.2 +/- 3.0 micrograms ANG I/min, which was not significantly reduced by ANF infusion (22.5 +/- 3.5 micrograms ANG I/min). Finally, in six dogs examined at free urine flow, intrarenal infusion of phenylephrine, an alpha-adrenergic agonist, raised renin release from 0.5 +/- 0.3 to 20.1 +/- 6.8 micrograms ANG I/min, which was reduced to 10.6 +/- 3.9 micrograms ANG I/min by intravenous ANF infusion (100 ng.min-1.kg body wt-1). These results indicate that ANF does not counteract stimulation of renin release by beta-adrenoceptors and prostaglandins but reduces nerve-stimulated renin release by opposing alpha-adrenoceptor activity.