Drugs online research references
Acta Physiol Scand. 1994 Jul;151(3):403-11.
Natriuresis in conscious dogs caused by increased carotid [Na+] during angiotensin II and aldosterone blockade.
Emmeluth C, Drummer C, Gerzer R, Bie P.
Department of Medical Physiology, University of Copenhagen, Denmark.
The renal response to a selective increase in the Na+ concentration of the blood perfusing the central nervous system was investigated in conscious dogs treated with the converting enzyme inhibitor enalaprilat and the aldosterone antagonist canrenoate. In split-infusion experiments the plasma [Na+] of carotid blood was increased (approx. 6 mM) by bilateral infusion of hypertonic NaC1. Concomitantly distilled water was infused into the v. cava making the sum of the infusions isotonic. In control experiments isotonic saline was infused at identical rates into all three catheters. Na+ excretion increased markedly in both series, 103 +/- 14 to 678 +/- 84 mumol min-1 during split-infusion and 90 +2- 14 to 496 +/- 74 mumol min-1 during the isotonic volume expansion. Peak rate of excretion, peak fractional sodium excretion, and cumulative sodium excretion were all significantly higher (P < 0.05) during split-infusion than during control experiments. Plasma vasopressin increased only during split-infusion (0.68 +/- 0.11 to 2.4 +/- 0.8 pg ml-1) while the increases in plasma atrial natriuretic peptide were similar in the two series. Urinary excretion of urodilatin (ANP95-126) increased significantly more during split-infusion (46 +/- 11 to 152 +/- 28 fmol min-1) than during the isotonic volume expansion (45 +/- 14 to 84 +/- 16 fmol min-1) (P < 0.05). It is concluded that the natriuretic mechanisms activated by a selective increase in the Na+ concentration of carotid blood and associated with increased excretion of urodilatin cannot be eliminated by blockade of the renin-angiotensin-aldosterone system.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7976412&dopt=Abstract
Aust N Z J Med. 1995 Dec;25(6):698-702.
The effects of increasing doses of enalapril on insulin sensitivity in normotensive non-insulin dependent diabetic subjects.
Walker RJ, Lewis-Barned NJ, Edwards EA, Robertson MC.
Department of Medicine, University of Orago Medical School, Dunedin, New Zealand.
BACKGROUND: There are conflicting reports about the effects of ACE inhibitors (ACEI) on insulin sensitivity and glycaemic control. Most studies have used a standard high dose of an ACEI but there have been no studies reported to establish whether any changes in glycaemic control or insulin sensitivity associated with ACEI are dose-related. AIM: To examine the effect of increasing doses of enalapril on insulin sensitivity in normotensive non-insulin dependent diabetic subjects. METHODS: The effects of increasing doses of enalapril on insulin sensitivity in ten normotensive non-insulin dependent diabetic subjects were measured, using the hyperinsulinaemic isoglycaemic clamp technique. Following a baseline study, enalapril was commenced at 5 mg daily and increased to 10 mg daily then 20 mg daily at 14 day intervals. Repeat studies were undertaken after 14 days at each dosage. RESULTS: There was a significant dose-related reduction of systolic blood pressure with enalapril. In contrast enalapril at 5-20 mg daily produced no significant changes in insulin mediated glucose uptake (M-value) or insulin sensitivity index (ISI). CONCLUSIONS: These findings indicate that in this insulin resistant population of normotensive non-insulin dependent diabetics, angiotensin converting enzyme inhibition with enalapril has no significant effect on insulin mediated glucose uptake.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8770334&dopt=Abstract
Clin Exp Pharmacol Physiol. 1986 Jul;13(7):525-34.
Baroreflex sensitivity alteration following transient hemispheric ischaemia in rats: protective effect of alphamethyldopa and guanfacine.
Saad MA, Elghozi JL, Meyer P.
The reflex tachycardia to arterial vasodilation was analysed in anaesthetized and ventilated Long Evans rats. Nicardipine was given by slow intravenous injection. The decrease in blood pressure was accompanied by a sympathetically mediated reflex tachycardia. The slope of the mean blood pressure-pulse period relationship was considered as an index of baroreflex sensitivity. Two injections of nicardipine were given during a single experiment. For studying the suprapontine control of the baroreflex arc, rats were subjected to transient (10 min) bilateral hemispheric ischaemia. These rats exhibited a blood pressure drop following recirculation and baroreflex sensitivity was impaired. Pretreatment with alpha-methyldopa, guanfacine and enalapril lowered mean blood pressure to a similar extent. In those rats pretreated with alpha-methyldopa and guanfacine transient hemispheric ischaemia did not alter baroreflex sensitivity while enalapril pretreated rats exhibited an impaired baroreflex. The protective effect of alpha-methyldopa and guanfacine against the cardiovascular consequence of hemispheric ischaemia may depend on reduced monoamine turnover resulting from central alpha-adrenoceptor stimulation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3024888&dopt=Abstract
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