Vascular and renal effects of leukotriene C4 in conscious rats

1985 ◽  
Vol 249 (5) ◽  
pp. F739-F744 ◽  
Author(s):  
J. Filep ◽  
B. Rigter ◽  
J. C. Frolich
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Statistical Significance ◽  
Renal Hemodynamics ◽  
Leukotriene C4 ◽  
Electrolyte Excretion ◽  
Renal Effects ◽  
Intravenous Injections ◽  
Induced Changes ◽  
Dose Dependent Increase

To investigate the possible renal effects of leukotriene C4 (LTC4) renal function was monitored in conscious unrestrained rats. Intravenous injections of 2, 4, and 8 micrograms/kg LTC4 markedly and dose-dependently elevated urine flow (by 64, 91, and 133%, respectively) with a concomitant increase in urinary sodium (61, 81, and 118%) and potassium (39, 50, and 76%) excretion. All changes were statistically significant. There was a tendency for glomerular filtration rate to increase, but this change reached statistical significance only after the highest dose of LTC4. Moreover, 8 micrograms/kg LTC4 reduced p-aminohippurate clearance by 33%. A dose-dependent increase in mean arterial pressure (15 mmHg at 2 micrograms/kg, 20 mmHg at 4 micrograms/kg, and 30 mmHg at 8 micrograms/kg) was observed following LTC4 administration. While the administration of FPL 55712, a putative antagonist of leukotrienes, had no effect on mean arterial pressure and kidney function, it significantly attenuated the vasopressor effect of LTC4 and practically completely abolished LTC4-induced changes in both renal hemodynamics and water and electrolyte excretion. These results raise the possibility that leukotrienes might be involved in the regulation of renal hemodynamics and could modify urinary electrolyte excretion under conditions in which leukotriene formation is enhanced.

Acute central effects of L-glutamate in pentobarbital-anesthetized dogs

1987 ◽  
Vol 252 (3) ◽  
pp. R594-R598
Author(s):  
J. E. Chelly ◽  
M. F. Doursout ◽  
J. P. Buckley
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Dose Effect ◽  
Central Effects ◽  
Intravenous Injections ◽  
Induced Hypertension ◽  
Anesthetized Dogs ◽  
The Right ◽  
Dose Dependent Increase ◽  
Dose Dependent

Microinjections of L-glutamate (10(-10) to 2 X 10(-8) mol/kg) into the nucleus of tractus solitarii produced a dose-dependent increase in mean arterial pressure and a decrease in heart rate. L-Glutamate-induced hypertension was prevented by spinal transection and pretreatment with atropine (1 mg/kg iv) reversed the bradycardia. L-Glutamate also produced a dose-dependent increase in mean arterial pressure when injected intravenously and into the cisterna magna, but the dose-effect curves were shifted to the right. Finally, pretreatment with hexamethonium (30 mg/kg iv) abolished the hypertension resulting from intravenous injections of L-glutamate. These data demonstrate that the nucleus of tractus solitarii may play a determinant role in the central pressor effects of L-glutamate. In addition, we demonstrated that this hypertension was due to a central sympathetic stimulation and that the autonomic nervous system also mediated the pressor effects of intravenous L-glutamate.

Effects of hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume

1987 ◽  
Vol 252 (1) ◽  
pp. F91-F98
Author(s):  
R. D. Manning
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Urinary Sodium Excretion ◽  
Renal Hemodynamics ◽  
Fluid Volume ◽  
Urinary Sodium ◽  
Plasma Aldosterone Concentration

The effects of long-term hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume were studied in eight conscious dogs over a 34-day period. Plasma protein concentration (PPC) was decreased by daily plasmapheresis, and the effects of decreasing and increasing sodium intake were measured. By the 12th day of plasmapheresis, during which sodium intake was 30 meq/day, PPC had decreased to 2.5 g/dl from a control value of 7.2 g/dl, mean arterial pressure had decreased to 78% of control, glomerular filtration rate (GFR) was 75.2% of control, and urinary sodium excretion was decreased. By day 18 of plasmapheresis, estimated renal plasma flow (ERPF) was decreased to 60% of control due to the decreased arterial pressure and an increase in renal vascular resistance. Also, plasma renin activity and plasma aldosterone concentration were both increased, and the relationship between mean arterial pressure and urinary sodium excretion was distinctly shifted to the left along the arterial pressure axis. In contradistinction to acute experiments, chronic hypoproteinemia results in decreases in GFR, ERPF, and urinary sodium excretion and has marked effects on both fluid volume and arterial pressure regulation.

scholarly journals Comparative study of labetalol and nifedipine in management of hypertensive disorders in pregnancy

2016 ◽  
Vol 6 (1) ◽  
pp. 194
Author(s):  
U. S. Hangarga ◽  
Rita D. ◽  
K. Harshitha
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Heart Diseases ◽  
Statistical Significance ◽  
Fetal Outcome ◽  
Research Centre ◽  
Renal Diseases ◽  
College Hospital ◽  
Hematological Disorders ◽  
Hypertensive Disorders

Background: Hypertensive disorders complicate 5 to 10 percent of all pregnancies, and together they are one member of the deadly triad, of haemorrhage and infection.Methods: The Present study was conducted at Navodaya Medical College, Hospital and Research Centre, Raichur from January 2014 to December 2015. The efficacy of labetalol verses nifedipine in management of hypertensive disorders of pregnancy was studied. The study consisted of 100 antenatal patients irrespective of parity and gestational age from 20-40weeks patients, with severe PIH with imminent eclampsia. Heart diseases, Hematological disorders, Liver diseases renal diseases and Bronchial asthma were excluded from the study.Results: In the study, fall in mean arterial pressure of >20mm Hg was noted 6hrs after initiation of treatment in nifedipine group which is statistically significant; no statistical significance was observed in both groups at 12hrs. A fall of mean arterial pressure to normal was noted at 48hrs and 72 hrs in labetalol, which is statistically highly significant.Conclusions: The present study indicates labetalol to be a better anti-hypertensive in terms of control of hypertension, mode of vaginal delivery and fetal outcome.

scholarly journals Acute Cardiovascular Effects of Epidural Spinal Cord Stimulation

2007 ◽  
Vol 5;10 (9;5) ◽  
pp. 677-685
Author(s):  
David M. Schultz
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Spinal Cord Stimulation ◽  
Statistical Significance ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Arterial Blood

Background: Several animal studies support the contention that thoracic spinal cord stimulation (SCS) might decrease arterial blood pressure. Objective: To determine if electrical stimulation of the dorsal spinal cord in humans will lower mean arterial pressure (MAP) and heart rate (HR). Design: Case Series Methods: Ten normotensive subjects that were clinically indicated for SCS testing were studied. Two of the 10 patients who underwent testing were excluded from the analysis because they did not respond to the Cold Pressor Test (CPT). Systolic blood pressure, diastolic blood pressure, and heart rate were measured continuously at the wrist (using the Vasotrac device). SCS was administered with quadripolar leads implanted into the epidural space under fluoroscopic guidance. SCS was randomly performed either in the T1-T2 or T5-T6 region of the spinal cord during normal conditions as well as during transient stress induced by CPT. The CPT was conducted by immersing the non-dominant hand in ice-cold water for 2 minutes. Results: There were moderate decreases in MAP and HR during SCS at the T5-T6 region compared to baseline that did not reach statistical significance. However, SCS at the T1-T2 region tended to increase MAP and HR compared to baseline but the change did not reach statistical significance. Arterial blood pressure was transiently elevated by 9.4 ± 3.8 mmHg using CPT during the control period with SCS turned off and also during SCS at either the T1-T2 region or T5-T6 region of the spinal cord (by 9.2 ± 5 mmHg and 10.7 ± 8.4 mmHg, respectively). During SCS at T5-T6, the CPT significantly increased MAP by 5.9±7.1 mmHg compared to control CPT (SCS off). Conclusion: This study demonstrated that SCS at either the T1-T2 or T5-T6 region did not significantly alter MAP or HR compared to baseline (no SCS). However, during transcient stress (elevated sympathetic tone) induced by CPT, there was a significant increase in MAP and moderate decrease in HR during SCS at T5-T6 region, which is not consistent with previous data in the literature. Acute SCS did not result in adverse cardiovascular responses and proved to be safe. Key words: Spinal cord stimulation, mean arterial pressure, heart rate, cold pressor test

Structural prerequisites for the hypotensive action of parathyroid hormone

1984 ◽  
Vol 246 (5) ◽  
pp. F551-F556 ◽  
Author(s):  
D. H. Ellison ◽  
D. A. McCarron
Keyword(s):  
Parathyroid Hormone ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Amino Acid Residues ◽  
Hypotensive Action ◽  
Intravenous Injections ◽  
Wistar Kyoto ◽  
Acute Changes ◽  
Urinary Phosphorus Excretion ◽  
Dose Dependent

We assessed the vascular, phosphaturic, and calcemic responses to several synthetic parathyroid hormone (PTH) analogues. Bovine (b) PTH (1-34), human (h) PTH (1-34), hPTH (53-84), [ Nle8 , Nle18 , Tyr34 ]bPTH (1-34), and [ Nle8 , Nle18 , Tyr34 ]bPTH (3-34) were administered in doses between 1 and 500 micrograms/kg as bolus intravenous injections to male Wistar-Kyoto rats aged 18-26 wk. Antagonism of the action of PTH was assessed in rats pretreated with 10 or 100 micrograms/kg [ Nle8 , Nle18 , Tyr34 ]bPTH (3-34) followed by 10 micrograms/kg of bPTH (1-34), or with 10 micrograms/kg hPTH (53-84) followed by 10 micrograms/kg hPTH (1-34). Bovine PTH (1-34), hPTH (1-34), and [ Nle8 , Nle18 , Tyr34 ]bPTH (1-34) produced virtually identical log dose-dependent hypotension, with 100 micrograms/kg of each analogue producing a 56% reduction in mean arterial pressure. Neither hPTH (53-84) nor [ Nle8 , Nle18 , Tyr34 ]bPTH (3-34) demonstrated any effect on mean arterial pressure at doses up to 500 micrograms/kg. Pretreatment with the inactive analogues failed to antagonize the vasodilating response to either bPTH (1-34) or hPTH (1-34). The vasoactive analogues significantly increased urinary phosphorus excretion while the inactive analogues did not modify it. hPTH (1-34) produced a modest decrease in serum Ca2+ at 1 min after injection. The results document that the vasodilating effect of PTH is a specific action of the peptide. Deletion of the first two amino acid residues abolishes both the phosphaturic and hypotensive effects of the peptide. Acute changes in serum Ca2+ do not appear to be a prerequisite for the vasodilatory response. Inactive analogues of PTH do not antagonize the vascular actions of the peptide.

Sensitization of baroreceptor reflex by central endothelin in conscious rats

1991 ◽  
Vol 260 (4) ◽  
pp. H1106-H1112 ◽  
Author(s):  
S. Itoh ◽  
M. van den Buuse
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Femoral Artery ◽  
Curve Fitting ◽  
Baroreflex Sensitivity ◽  
Cardiovascular Regulation ◽  
Baroreceptor Reflex ◽  
Sigmoidal Curve ◽  
Induced Changes

Effect of centrally administered endothelins (ETs) on cardiovascular regulation was investigated in conscious normotensive rats. ET-1, ET-2, or ET-3 was injected through a cannula into the cisterna magna, and mean arterial pressure (MAP) and heart rate (HR) were measured through a cannula in the femoral artery. Baroreceptor HR reflex was measured by monitoring the changes in HR in response to changes in MAP induced by slow intravenous injection of phenylephrine or nitroprusside. MAP and HR responses were then analyzed in individual animals by sigmoidal curve fitting. Intracisternal (ic) administration of ET-1 did not change resting MAP or HR at doses of 2.5 or 25 pmol/kg. The higher dose of ET-1 induced a significant increase of baroreflex sensitivity without a change of HR range. Sympathetic and vagal components of the baroreflex were examined by testing reflex responses after pretreatment with methylatropine (0.5 mg/kg iv) and atenolol (1.0 mg/kg iv), respectively. An increased baroreflex sensitivity was observed after ET-1 treatment in the atenolol-treated rats but not in the methylatropine-treated rats, suggesting that the peptide selectively affected the vagal component of the reflex. Intravenous 25 pmol/kg ET-1 did not cause an increase in baroreflex sensitivity. Neither ET-2 nor ET-3 (25 pmol/kg ic) induced changes in resting MAP or HR, but both significantly increased baroreflex sensitivity without changes in HR range. Order of potency of the ETs on baroreflex gain was ET-3 greater than or equal to ET-1 greater than ET-2. In conclusion, ETs at doses that do not change resting values for MAP or HR, may induce significant centrally mediated sensitization of the baroreceptor HR reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Sildenafil citrate on retrobulbar and retinal circulation of rabbits

2014 ◽  
Vol 44 (8) ◽  
pp. 1431-1436 ◽  
Author(s):  
Andréia Vitor Couto do Amaral ◽  
Germana Alegro da Silva ◽  
Ana Paula Araújo Costa ◽  
Cássia Maria Molinaro Coelho ◽  
Roberta Renzo ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Fluorescein Angiography ◽  
Perfusion Pressure ◽  
Statistical Significance ◽  
Sildenafil Citrate ◽  
Retinal Circulation ◽  
Ocular Perfusion ◽  
Significant Difference ◽  
White Breed

The effects of sildenafil on retrobulbar and retinal circulation were studied in 18 adult male, albino, homozygous rabbits, of the New Zealand White breed, randomly divided into 3 groups of 6 animals, for drug treatment at a dose of 3.5mg kg-1 every 24 hours, for 7, 15 and 30 days. Nine animals used for control were treated with saline solution at 0.9%. It was evaluated intraocular pressure (IOP), mean arterial pressure (MAP), ocular perfusion pressure (PPO), B-mode ultrasonography and fluorescein angiography before and at the end of treatments. A slight decrease in results of IOP, MAP and PPO after treatment with sildenafil was evident, however, there was no statistical significance. It was observed significant increased diameter of the ophthalmic artery after 7 and 30 days of treatment and decreased mean arterial pressure after 7, 15 and 30 days of treatment, with no statistical difference. On fluorescein angiography, it was observed that the arterial, arteriovenous and venous stages initiated more rapidly in animals after treatment, with significant difference on the arteriovenous stage at the 7th and 15th days. It was possible to admit that the sildenafil citrate improves blood circulation in the retina of rabbits, by increasing the speed of blood flow and decreasing the perfusion pressure.

Atrial natriuretic peptide and glomerular hyperfiltration during onset of spontaneous diabetes mellitus

1994 ◽  
Vol 266 (2) ◽  
pp. R572-R577
Author(s):  
M. I. Okwueze ◽  
T. J. Opgenorth ◽  
T. W. von Geldern ◽  
R. C. Vari
Keyword(s):  
Diabetes Mellitus ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Spontaneous Diabetes ◽  
Renal Hemodynamics ◽  
Glomerular Hyperfiltration ◽  
Atrial Natriuretic

The mechanisms responsible for the elevation of glomerular filtration rate (GFR) in early stages of insulin-dependent diabetes mellitus (IDDM) are undefined. The objectives of this study were to define the temporal pattern of onset of glomerular hyperfiltration in the spontaneously diabetes-prone (BB/DP) rat and to evaluate the possible role of atrial natriuretic peptide (ANP) as the primary mediator of the observed alterations in renal hemodynamics. GFR was significantly higher (1.38 +/- 0.07 ml.min-1 x g-1; n = 5) in moderately hyperglycemic BB/DP rats (blood glucose > 270 mg/dl) 14 days after the onset of IDDM compared with age-matched diabetes-resistant rats (BB/DR), which averaged 1.03 +/- 0.07 ml.min-1 x g-1 (n = 7). Circulating ANP levels in moderately hyperglycemic BB/DP rats 1, 7, and 14 days after onset of IDDM were within the normal range, averaging 100 +/- 21, 57 +/- 12, and 65 +/- 6 pg/ml, respectively, and were not significantly different (P > 0.05) from ANP levels in age-matched normoglycemic BB/DR rats. To further test the role of ANP in glomerular hyperfiltration, an ANP receptor antagonist was infused into anesthetized BB/DP rats (n = 10) 14 days after onset of IDDM, after baseline measurements of mean arterial pressure, renal hemodynamics, and renal fluid and electrolyte excretions. ANP receptor antagonism caused a significant reduction in mean arterial pressure from 120 +/- 3 to 103 +/- 2 mmHg; however, there were no significant effects of ANP receptor blockade on GFR.(ABSTRACT TRUNCATED AT 250 WORDS)

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