Biomedical subjects

P A Naess

Publications and source records attributed to P A Naess.

At least 19 recordsLinked to original sources

PubMed1998

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.

Animals↗

PubMed1998

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.

Analysis of Variance↗

PubMed1997

[Lipoblastoma. A rare, benign tumor in children].

Lipoblastoma is a rare, benign tumour of embryonal fat seen almost exclusively in infancy and early childhood. It occurs mostly in the extremities, but it is also seen in other parts of the body. The tumour may grow rapidly, and the fact that lipoblastomas show immature fat cells could lead to the wrong diagnosis of liposarcoma. Complete surgical excision appears to be the treatment of choice. A correct, preoperative diagnosis is possible in most cases. Two cases of lipoblastoma of the upper limb and one case in the scapular region are reported.

Arm↗

PubMed1997

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.

Absorption↗

PubMed1996

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.

Animals↗

PubMed1996

Equal changes in L-type calcium channel density after 60 min of ischaemia in normal and ischaemically preconditioned porcine myocardium.

Long-lasting myocardial ischaemia reduces the density of sarcolemmal L-type calcium channels (LCC). Ischaemic preconditioning protects the myocardium against development of infarction. The aim of this study was to investigate if ischaemia-induced loss in LCC is affected by ischaemic preconditioning. Specific (+) - [3H]isradipine binding to LCC was compared in membranes and homogenates from control and ischaemic regions of non-preconditioned and ischaemically preconditioned hearts [two 10 min left anterior descending coronary artery (LAD) occlusions, each followed by 30 min reperfusion]. Biopsies were sampled after 60 min mid LAD occlusion from ischaemic and control (supplied by circumflex artery) regions. Sixty min ischaemia reduced binding density of specific (+) - [3H]isradipine in membranes by 23 +/- 11% (n = 7, P < 0.05) in the non-preconditioned group and by 20 +/- 8% (n = 6, P < 0.05) in the preconditioned group. Binding density in homogenates was reduced by 36 +/- 5% (n = 5. P < 0.05) in the non-preconditioned group and by 21 +/- 5% (n = 5. P < 0.05) in the preconditioned group. The reductions in the two groups and reductions in membranes and homogenates were not statistically different. The dissociation constant of binding was similar in the groups. In conclusion, 60 min of ischaemia reduced the binding density of (+)-[3H]isradipine in membranes and homogenates by 20-36%. The reduction in density of binding sites was not caused by redistribution of sarcolemmal LCC to an intracellular compartment. Ischaemic preconditioning did not affect the decline in binding density as hypothesized.

Animals↗

PubMed1996

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.

Angiotensin I↗

PubMed1995

Nitric oxide regulates coronary blood flow at various coronary arterial pressures in intact porcine hearts.

Nitric oxide (NO) is known to regulate basal coronary blood flow (CBF). The objective of the present study was to examine the importance of NO in CBF regulation at various coronary arterial pressures (CAPs) in vivo. Experiments were performed in 11 open-chest pentobarbitone sodium anesthetized pigs. CAP was reduced in steps by a hydraulic occluder on the mid left anterior descending coronary artery (LAD) before and after a 5-min intracoronary infusion of the inhibitor of NO synthesis, NG-nitro-L-arginine (NOARG, 30 mumol min-1). CAP was recorded and NOARG infused through a catheter inserted into the LAD just distal to the occluder. CBF was measured by Doppler flowmetry on the LAD. NOARG significantly reduced CBF by 11 +/- 4, 20 +/- 5, 10 +/- 3, 15 +/- 4, 19 +/- 2, 25 +/- 4 and 25 +/- 5 mL min-1 100 g-1 (mean +/- SE) at CAPs of 30 (n = 6), 40 (n = 9), 50 (n = 9), 60 (n = 9), 70 (n = 9), 80 (n = 8) and 90 (n = 6) mmHg, respectively. These decrements were not statistically different, but the percentage reductions in CBF after infusion of NOARG were significantly greatest at the lowest CAPs. The slight haemodynamic alterations induced by NOARG could not explain the reductions in CBF. Thus, the reductions in CBF after infusion of NOARG were caused by inhibition of a continuous NO release from the coronary endothelium. Coronary NO contributes significantly to CBF at all CAPs between 30 and 90 mmHg. The pronounced reduction in CBF during NO inhibition at the lower CAPs indicates an important vasodilating role of intact endothelium in a region supplied by a stenosed coronary artery.

Animals↗

PubMed1995

Increased in vivo expression and production of endothelin-1 by porcine cardiomyocytes subjected to ischemia.

Circulating levels of the endothelium-derived vasoconstrictor peptide endothelin-1 (ET-1) are increased in association with myocardial ischemia and infarction. The present study investigates whether ET-1 is synthesized and produced locally in the ischemic heart. Sixteen pigs were divided into three groups. In the first group, the left anterior descending coronary artery was occluded for 90 minutes, followed by 150 minutes of reperfusion (group A, n = 8). Two additional groups were subjected to 90 minutes (group B, n = 4) or 240 minutes (group C, n = 4) of ischemia without reperfusion. Biopsies from the nonischemic and ischemic myocardium were rapidly obtained from the beating heart and subsequently examined by Northern blot, in situ hybridization, and immunohistochemistry. Arterial plasma ET-1 was measured before ischemia and at the end of the experiments. Northern blot revealed a twofold increase in ET-1 mRNA in the ischemic myocardium compared with the nonischemic myocardium. In situ hybridization showed a considerable increase in ET-1 mRNA over the ischemic cardiomyocytes. Substantial ET-1-like immunoreactivity (ET-1-ir) was detected in cardiomyocytes in the ischemic region. In contrast, little or no ET-1-ir or mRNA was detected in nonischemic cardiomyocytes. Both in the ischemic and nonischemic regions, little ET-1-ir was detected in vascular endothelial cells or vascular smooth muscle cells. There was no difference in the intensity and distribution of ET-1 mRNA expression or ET-1-ir among experimental groups A, B, and C. Arterial plasma ET-1 was increased only in group A, the reperfused group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

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.

Animals↗

PubMed1994

Effects of regional inhibition of nitric oxide synthesis in intact porcine hearts.

The importance of nitric oxide (NO) in coronary blood flow (CBF) regulation was examined in anesthetized pigs. NO synthesis was inhibited by intracoronary infusion of NG-monomethyl-L-arginine (L-NMMA) or NG-nitro-L-arginine (L-NNA). L-NMMA (30 mumol/min) reduced CBF (Doppler flowmetry) by 16.3% (13.1-20.2%; P < 0.001) and L-NNA (30 mumol/min) by 16.1% (13.9-18.9%; P < 0.001). During NO blockade, myocardial oxygen consumption was unaltered as an increase in oxygen extraction occurred due to a reduced partial pressure of oxygen and oxygen saturation in blood from the anterior interventricular vein. L-Arginine completely reestablished CBF after giving L-NMMA, but not after giving L-NNA. L-NNA reduced the coronary flow response to ADP by 66-83%, whereas the selected dose of L-NMMA did not affect it. The flow response to adenosine was not affected by either L-NMMA or L-NNA. L-NNA reduced reactive hyperemia after occluding the left anterior descending coronary artery for 10 and 30 s but not for 120 s. Our data show that NO produced in the coronary endothelium plays an important role in CBF regulation in vivo, accounting for approximately 16% of CBF and a major part of the flow response to ADP. NO also contributes to reactive hyperemia after brief, but not longer, ischemic periods.

Adenosine↗

PubMed1994

Cardiac contractile function following repetitive brief ischemia: effects of nucleoside transport inhibition.

The effects of nucleoside transport inhibition on cardiac contractile function were examined in anesthetized pigs subjected to five 6-min left anterior descending coronary artery (LAD) occlusions, separated by 20-min reperfusion, and followed by 150-min reperfusion. In group 1 (n = 8), saline was infused. In group 2 (n = 9), endogenous myocardial accumulation of adenosine was increased by intracoronary infusion of the specific nucleoside transport inhibitor R-75 231. Left ventricular segment lengths were recorded by ultrasonic crystals in the inner one-third of the myocardium. Percent systolic segment length shortening (SS) (normalized to percent of preischemic value) was significantly better maintained in the R-75 231 group compared with the saline group after each occlusion. SS in the saline group reached a nadir of 30% (22-40) at 30-min reperfusion after the last occlusion compared with 66% (54-73) in the R-75 231 group. In the R-75 231 group, but not in the saline group, maximal postischemic decline in SS and decline at 20-min reperfusion were significantly reduced following the last occlusion. We conclude that R-75 231, which inhibits nucleoside transport, attenuates contractile dysfunction following repetitive brief ischemia and results in a preconditioning-like effect against stunning in the pig. On the basis of the well-documented biochemical effects of R-75 231, increased accumulation of endogenous adenosine most likely explains these findings.

Animals↗

PubMed1993

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.

Animals↗

PubMed1993

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.

Animals↗

PubMed1993

Endothelin is released from the porcine coronary circulation after short-term ischemia.

Endothelin (ET) is increased in plasma after myocardial infarction. Whether brief periods of myocardial ischemia not leading to myocardial infarction also increase plasma ET is not known. The purpose of the present study was to examine cardiac ET balance in association with a 10-min LAD occlusion followed by reperfusion. Venous blood was selectively sampled from the transiently ischemic myocardium using a shunt between the anterior interventricular vein and the right atrium in eight pentobarbital-anesthetized pigs. Flow in the shunt was measured with a Doppler flow probe. Arterial blood was drawn from the aortic arch. Plasma ET was measured using an ET [1-21]-specific 125I assay system. This assay system has no cross-reactivity with big ET. A net cardiac ET uptake of 0.7 (0.3-1.4) fmol min-1 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 g-1 after 1.5 min of reperfusion. Cardiac venous ET 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 ET 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). ET is released from the porcine heart for several minutes during reperfusion after a brief coronary artery occlusion.

Animals↗

PubMed1993

Plasma potassium concentration as a determinant of proximal tubular NaCl and NaHCO3 reabsorption in dog kidneys.

To examine whether an acute increase in plasma potassium concentration ([K]p) may inhibit proximal tubular transport, clearance studies were performed in seven anaesthetized, volume expanded dogs treated with amiloride (1 mg kg-1 body wt) to block tubular potassium secretion, and with bumetanide (30 micrograms kg-1 body wt) to inhibit NaCl reabsorption in Henle's loop. As [K]p was raised in steps from 2.6 +/- 0.2 to 7.9 +/- 0.2 mM, bicarbonate, chloride, and sodium reabsorption decreased by 232 +/- 56, 520 +/- 59 and 958 +/- 112 mumol min-1, respectively, at constant glomerular filtration rate (GFR). On average, the molar ratio between the inhibitory effects on bicarbonate and chloride reabsorption were 1:2.2-2.4. Reabsorption was calculated at GFR 100 ml min-1: (reabsorption 100/GFR (mmol min-1). It was inversely correlated to ln [K]p with r = -0.82 for bicarbonate and with r = -0.89 for chloride. Fractional potassium reabsorption remained constant at 0.31 +/- 0.03. Administration of acetazolamide (100 mg kg-1 body wt) in eight dogs at [K]p 8 mM reduced fractional reabsorption of bicarbonate, chloride and sodium as much as in previous studies on normokalaemic dogs. We conclude that acute elevation of [K]p inhibits NaHCO3 transport and passive proximal tubular NaCl reabsorption. This inhibition is not related to changes in potassium secretion and carbonic anhydrase activity, but may be secondary to depolarization of the basolateral membrane.

Absorption↗

PubMed1993

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)

Adrenergic beta-Antagonists↗

PubMed1993

Effect on renin release of inhibiting renal nitric oxide synthesis in anaesthetized dogs.

Nitric oxide plays an important role in the regulation of basal renal blood flow. This study was performed to examine whether selective inhibition of renal nitric oxide synthesis affects renin release in vivo. Accordingly, in six barbiturate-anaesthetized dogs renin release was examined before and after intrarenal infusion of the selective inhibitor of nitric oxide synthesis, NG-nitro-L-arginine (NOARG). NOARG was infused into the renal artery to yield a renal arterial blood concentration of 0.4 mumol ml-1. NOARG did not change systemic arterial blood pressure and glomerular filtration rate, but reduced basal renal blood flow by 26 +/- 2%. Urine flow, sodium and potassium excretion were reduced after inhibition of renal nitric oxide synthesis. Basal renin release (3 +/- 2 micrograms AI min-1) was not altered by NOARG infusion (1 +/- 1 micrograms AI min-1). To stimulate renin release the renal artery was constricted to a renal perfusion pressure of 50 mmHg. At this perfusion pressure infusion of NOARG reduced renin release significantly from 48 +/- 11 micrograms AI min-1 to 14 +/- 4 micrograms AI min-1. In conclusion, inhibition of renal nitric oxide synthesis reduces basal renal blood flow and reduces renin release stimulated by renal arterial constriction. These findings indicate that renal nitric oxide modulates both renal blood flow and renin release in vivo.

Animals↗