Drugs online research references
Diabetes Res. 1984 Nov;1(4):201-7.
Comparison of the hypotensive and metabolic effects of metoprolol therapy with a high fibre, low sodium, low fat diet in hypertensive type 2 diabetic subjects.
Pacy PJ, Dodson PM, Kubicki AJ, Fletcher RF, Taylor KG.
The clinical and biochemical response over a 3 month trial period of 21 hypertensive diabetics who were given metoprolol, 200 mg twice daily, have been compared to an age, sex, blood pressure, known duration of diabetes and diabetic treatment matched group who were treated with a high cereal fibre, low sodium and low fat diet. Both treatment groups had a significant reduction of systolic (p less than 0.001 on the diet; p less than 0.02 on metoprolol) and diastolic blood pressure (p less than 0.001 respectively). On metoprolol the heart rate significantly decreased throughout the study (p less than 0.001). Only the modified diet was accompanied with a reduction of mean glycosylated haemoglobin (p less than 0.01) and weight (p less than 0.001). By the end of the study mean serum triglyceride level was lower in the diet treated group (p less than 0.05) compared to the metoprolol group. In hyperlipidaemic patients only dietary therapy significantly decreased mean serum triglyceride (p less than 0.02) and glycosylated haemoglobin (p less than 0.001). We conclude that although both treatments had a similar hypotensive response only the modified diet beneficially influenced other cardiovascular risk factors. These data suggest that this diet might be considered an alternative to metoprolol in hypertensive diabetic patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6099231&dopt=Abstract
J Cardiovasc Pharmacol. 1999 Sep;34(3):321-6.
Effects of a DA2/alpha2 agonist and a beta1-blocker in combination with an ACE inhibitor on adrenergic activity and left ventricular remodeling in an experimental model of left ventricular dysfunction after coronary artery occlusion.
Masson S, Masseroli M, Fiordaliso F, Calvillo L, D'Aquila S, Bernasconi R, Garrido G, Torri M, Razzetti R, Bongrani S, Latini R.
Department of Cardiovascular Research, Instituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
Renin-angiotensin-aldosterone and sympathetic nervous systems overactivity play a major role in worsening the extent of heart failure. Attenuation of neurohumoral activation with angiotensin-converting enzyme (ACE) inhibitors and beta-blockers has proven beneficial in congestive heart failure. Because ACE inhibition is a recommended treatment for heart failure, this study was designed to test the effects on neurohumoral activation, hemodynamics, and left ventricular (LV) volume of the combination of an ACE inhibitor (delapril) with a DA2-dopaminergic receptor/alpha2-adrenoceptor agonist (CHF-1024) or a beta1-adrenoceptor antagonist (metoprolol) after a moderate to large myocardial infarction (MI) in rats. MI was induced by left coronary artery ligation in 134 rats, and six were not operated on. After 2 months, the animals with ECG evidence of MI were treated for 1 more month with CHF- 1024, 0.33 mg/kg/day or with metoprolol (10 mg/kg/day), delivered through implanted osmotic minipumps, in addition to delapril (6 mg/kg/day) in the drinking water. Daily urinary excretion of norepinephrine (NE) and circulating concentration were measured. Hemodynamic variables were measured, and three-dimensional morphometric analysis was done on the diastole-arrested hearts to quantify infarct size and LV geometry. In conscious animals, delapril alone or with CHF-1024 or metropolol did not modify heart rate or systolic blood pressure. Both combination treatments, however, significantly reduced heart rate in anesthetized animals compared with the group receiving vehicle. Infarct size was not different between treatments, averaging 20-22% of LV volume. The threefold increase of LV chamber volume in infarcted rats was significantly attenuated by delapril alone or with CHF-1024 or metoprolol (-37 to -44%, p<0.05). Treatment with a combination of the ACEi and CHF-1024 tended to normalize the shape of the LV cavity. Urinary NE excretion was unaffected by delapril alone but was reduced by the addition of CHF-1024 or metoprolol. In conclusion, 1 month of treatment with doses of delapril having no hemodynamic effect, reduced LV volume in a model of chronic heart failure. When CHF-1024 or metoprolol was given with delapril, sympathetic activation decreased with no unwanted effects, such as excessive hypotension.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10470987&dopt=Abstract
Neuropharmacology. 1985 Dec;24(12):1187-94.
The pharmacology of the hypothermic response in mice to 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). A model of presynaptic 5-HT1 function.
Goodwin GM, De Souza RJ, Green AR.
In the mouse, injection (subcutaneously) of the putative 5-HT1 agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), produced a dose-related hypothermia (ED50:0.36 mg/kg). A maximum response was elicited by intracerebroventricular (i.c.v.) injection of 8-OH-DPAT (3 micrograms) and almost abolished by lesion of 5-HT-containing terminals in the brain with 5,7-dihydroxytryptamine (5,7-DHT; i.c.v.) or long-term treatment with p-chlorophenylalanine. The response was unaltered by a range of neurotransmitter antagonists: prazosin (alpha1-adrenoceptor), idazoxan (alpha2-adrenoceptor), metoprolol (beta1-adrenoceptor), erythro-DL-1-(7-methylindan-4-yloxy)-3-isopropylamino-but an-2-ol (beta2-adrenoceptor), (-)propranolol or (+/-)pindolol (beta-adrenoceptor), flupenthixol (dopamine) or Ro 15-1788 (benzodiazepine binding site). Classical 5-HT antagonists (methysergide, metergoline, cinanserin and methiothepin) were either without effect or facilitated the response and the 5-HT2 antagonist, ritanserin was also without effect. In contrast, quipazine and haloperidol produced a dose-related antagonism of the response. Since the response was almost abolished by a lesion induced by 5,7-DHT and was antagonised by quipazine, which is known to antagonise presynaptic 5-HT function in vitro, it is suggested that the hypothermic response is due to 8-OH-DPAT acting as an agonist at a presynaptic 5-HT receptor, which also appears to be sensitive to butyrophenones (the antagonism elicited by haloperidol but not by flupenthixol). The hypothermic response of mice to 8-OH-DPAT, therefore, may provide a simple and convenient in vivo model in which to measure the function of the presynaptic 5-HT receptor.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2869435&dopt=Abstract
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