Drugs online research references
J Cardiovasc Pharmacol. 1987;10 Suppl 6:S97-102.
Media hypertrophy in hypertensive coronary resistance vessels.
Klepzig M, Eisenlohr H, Steindl J, Schmiebusch H, Strauer BE.
Department of Medicine, University of Dusseldorf, F.R.G.
Coronary reserve is reduced in human hypertensive hypertrophy and in the model of spontaneously hypertensive rats (SHRs). In isolated coronary resistance vessels, the role of structural and functional changes was evaluated. Furthermore, the effect of long-term antihypertensive therapy was also studied. At the age of 20 weeks, SHR and Wistar-Kyoto (WKY) rats were examined. Distal segments of the left anterior descending coronary artery were dissected and mounted on a myograph developed by Mulvany and Halpern. After recording of radius-wall tension curves, the vessels were set up to a wall tension equal to two-thirds of the systolic blood pressure. In SHRs, the vessel diameters were reduced. After equilibration with Ringer's solution, vessel dilatation was decreased in calcium-free solution (10 +/- 3 vs. 34 +/- 7%, p less than 0.05), but contraction increased after 123 mM of potassium stimulation (78 +/- 19 vs. 33 +/- 9%). There was no difference in calcium sensitivity during methoxamine or potassium activation. In the coronary resistance vessels of SHRs, electron microscopy revealed media hypertrophy (15.6 +/- 2.9 vs. 9.5 +/- 2.1 microns, p less than 0.05) and media hyperplasia (4.5 +/- 3 vs. 3.7 +/- 6 muscle layers, p less than 0.05). Media hypertrophy and a decrease in the vasodilatating capacity of resistance vessels contribute to the reduction of coronary reserve in hypertensive hypertrophy. The minimal coronary vascular resistance, a parameter of the vasodilatating capacity, was significantly increased in SHRs. Antihypertensive therapy with metoprolol and hydralazine or nifedipine resulted in an improvement of coronary reserve.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2485036&dopt=Abstract
J Cardiovasc Pharmacol. 1981 Jan-Feb;3(1):179-85.
Adrenaline-induced hypertension in rats.
Majewski H, Tung LH, Rand MJ.
Rats were given a slow-release depot implantation containing adrenaline (0.33 mumole/kg). Adrenaline was released from the implant, giving a plasma level of 1.0 nmole/liter the day after implantation. Adrenaline-treated rats had elevated blood pressures compared to control rats from 1 day to 8 weeks after treatment. However, 8 weeks after treatment no adrenaline from the implant was found in the plasma, suggesting that at this time factors other than the adrenaline were responsible for maintaining the rise in blood pressure. In rats given metoprolol tartrate (5 mg/kg/day, p.o.), adrenaline treatment did not increase the blood pressure.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6160347&dopt=Abstract
Clin Sci (Lond). 1981 Dec;61 Suppl 7:191s-193s.
Adrenaline-induced hypertension in rats.
Tung LH, Rand MJ, Majewski H.
1. Rats implanted with osmotic minipumps delivering adrenaline intraperitoneally at the rate of 2.9 nmol/h had significantly higher systolic and diastolic pressures from days 2 to 6 after implantation than sham-operated controls rats. 2. Concomitant treatment with metoprolol tartrate (2.5 mg/kg, intraperitoneally, twice daily) prevented the elevation in blood pressure induced by adrenaline from osmotic minipumps. Such metoprolol treatment did not affect the blood pressure of controls rats. 3. Noradrenaline administered intraperitoneally from osmotic minipumps at the rate of 2.9 nmol/h had no significant effect on blood pressure over a 6-day period of observation. 4. Tachyphylaxis developed to the acute pressor responses to intermittent intravenous infusions of adrenaline in doses of 0.78 microgram (4.24 nmol) every 10 min, but after 14 days of such treatment systolic and diastolic blood pressures were significantly greater than in controls rats. 5. It is suggested that the increase in blood pressure produced by chronic treatment with adrenaline is due to the uptake and accumulation of adrenaline in noradrenergic nerve terminals, from which it is subsequently released as a cotransmitter that mediates a positive feedback loop on transmission by acting on prejunctional beta-adrenoceptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7318322&dopt=Abstract
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