Drugs online research references
Medicina (B Aires). 1992;52(3):240-4.
[Cardiovascular effects of ketamine anesthesia in rats treated with enalapril and propranolol]
[Article in Spanish]
Reyes Toso CF, Linares LM, Rodriguez RR.
Departamento de Fisiologia, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
It is well-known that ketamine (Kt) anaesthesia produces a rise in blood pressure and heart rate in man. These cardiostimulatory effects were adscribed to several factors such as: a) increased sympathetic nervous system activity by direct stimulation of central nervous structures, b) increased catecholamine release from the peripheral sympathetic system, c) high plasmatic renin levels. However, the quantitative participation of these mechanisms in the cardiovascular effects of this anaesthetic agent is unknown. While some authors have shown a major rise in serum renin activity in experimental anaesthesia, others have been unable to confirm these results. The present study was undertaken to assess if the cardiostimulatory effects of Kt anaesthesia were due to an activation of renin-angiotensin system or to increased sympathetic activity. In consequence we used rats treated with enalapril (an angiotensin-converting enzyme inhibitor) or propranolol prior to anaesthetic procedures. Thirty male Wistar and six spontaneously hypertensive rats (SHR) weighing 240-300 g were used in all the experiments. The rats were randomly grouped into six groups. I- Non-anaesthetized rats, II- Anaesthetized rats (trained in the experimental procedures), III- Anaesthetized rats (without training), IV- Anaesthetized rats previously treated with enalapril, V- Anaesthetized rats pretreated with propranolol, VI- SHR treated with enalapril. The rats of groups IV and VI received enalapril p.o. for three weeks (25 mg/Kg body wt). The animals of group V were submitted to acute beta-adrenergic blockade. Propranolol dose: 10 mg/Kg body wt, was given i.p. 15 min before Kt anaesthesia. Blood pressure and heart rate were measured with a sphygmomanometer and photoelectric sensors and recorded.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1342690&dopt=Abstract
Am J Physiol. 1992 Nov;263(5 Pt 2):F858-69.
Enalaprilat handling by the kidney: barrier-limited cell entry.
Schwab AJ, de Lannoy IA, Goresky CA, Poon K, Pang KS.
McGill University Medical Clinic, Montreal, Quebec, Canada.
The angiotensin-converting enzyme inhibitor enalaprilat is formed in vivo in liver and kidney by esterolysis of the antihypertensive drug enalapril. To gain insight into the renal elimination of enalaprilat, we carried out multiple-indicator dilution experiments in the isolated perfused rat kidney. Kidneys were perfused single pass with an amino acid-supplemented Krebs-Henseleit buffer containing 20% bovine red blood cells and 4% bovine serum albumin, at a flow rate of 0.11 +/- 0.02 (SD) ml.s-1 x g-1. A bolus of 51Cr-labeled red blood cells (vascular red blood cell indicator), 125I-labeled albumin (vascular plasma indicator), L-[14C]glucose (interstitial space indicator), and [3H]-enalaprilat was injected into the renal artery, and timed samples of venous blood (up to 1 min) and urine (up to 10 min) were collected. The data were analyzed using a variable-transit-time, space-distributed model with modifications accounting for glomerular filtration and the observed 14% protein binding of enalaprilat; the glomerular filtration rate (GFR) estimated from L-glucose clearance was 9.0 +/- 2.9% of total plasma flow. The ratio of renal clearance of unbound enalaprilat to GFR was 1.56 +/- 0.29, indicating both glomerular filtration and net tubular secretion of enalaprilat. Unidirectional influx from plasma to tubular cells exceeded tubular secretion by a factor of 2.2 +/- 0.5. Thus only about one-half of the enalaprilat taken up by the tubular cells was excreted into urine, with the remainder refluxing into the capillary blood stream, indicating bidirectional permeation of enalaprilat across the basolateral tubular membrane.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1332505&dopt=Abstract
Indian J Physiol Pharmacol. 1993 Jul;37(3):217-20.
Effects of enalapril, an ACE-inhibitor, on bronchial responsiveness in asthmatics.
Talwar D, Jindal SK.
Department of Pulmonary Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh.
To assess the effects of enalapril on bronchial responsiveness, we studied ten stable asthmatics and five healthy normal volunteers. Spirometry and methacholine bronchoprovocation dose (PC20) were measured before and after oral administration of 20 mg enalapril. Significant hypotensive effect was observed in all. More than two fold (2.73) increase in bronchial responsiveness was observed in the asthmatics (P < 0.01) without significant change in the expiratory flows. PC20 after enalapril fell by 56.8 +/- 23.0% of baseline value (P < 0.001). No significant change was observed in spirometric parameters and bronchial responsiveness in normal subjects. We conclude that enalapril significantly enhances BR and cannot be used safely in treatment of hypertension in asthmatics.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8276499&dopt=Abstract
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