Drugs online research references
Pharmacol Biochem Behav. 1989 Aug;33(4):923-6.
Behavioral performance effects of nifedipine in normotensive baboons: single dosing.
Turkkan JS, Hienz RD.
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
The effects of single oral doses of the calcium channel blocker nifedipine were assessed on performance of a simultaneous color match-to-sample task in three normotensive baboons. Both accuracy of color matching, and speed and latency of response were measured 30 min after administration of 0.10, 0.34, 0.57, and 1.7 mg/kg and vehicle, with each dose tested on three occasions in randomized order. Systolic and diastolic blood pressures also were measured after testing sessions. Maximal decreases in systolic blood pressures (mean of three subjects = -4.56 mmHg) were obtained after ingestion of the 0.57 mg/kg dose. Nifedipine produced dose-related changes in choice reaction times with a trend toward increased reaction times of approximately 5% obtained at 0.34 and 1.7 mg/kg. A reversal of effect was noted at 0.57 mg/kg such that smaller changes in reaction times were obtained, suggesting a lack of correlation between blood pressure and behavioral performance changes. These results indicate that nifedipine administered in single doses to patients with hypertensive crisis is unlikely to produce large impairments in these aspects of sensory and motor functioning.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2616612&dopt=Abstract
Br J Pharmacol. 1988 Oct;95(2):393-8.
The negative inotropic effect of nicorandil is independent of cyclic GMP changes: a comparison with pinacidil and cromakalim in canine atrial muscle.
Yanagisawa T, Hashimoto H, Taira N.
Department of Pharmacology, Tohoku University School of Medicine, Sendai, Japan.
1. The negative inotropic effects of nicorandil, a nitrate with K-channel opening properties, have been compared with those of pinacidil, cromakalim and nifedipine, in canine right atrial muscle. 2. Cromakalim, pinacidil and nicorandil all produced a negative inotropic effect. However, even at their maximally effective concentrations, the force of contraction remained at about 10% of control levels, whereas contraction was abolished by nifedipine. 3. The pD2 values for the negative inotropic effects of cromakalim, pinacidil and nicorandil were 5.93, 5.37, and 4.35, respectively. 4. The negative inotropic effects of cromakalim (3 x 10(-5)M), pinacidil (3 x 10(-5) M and 3 x 10(-4) M) and nicorandil (3 x 10(-5) M) were not accompanied by changes in cyclic AMP and cyclic GMP levels, whereas that of 3 x 10(-4) M nicorandil was accompanied by an increase in cyclic GMP but not cyclic AMP concentrations. 5. The negative inotropic effect produced by 3 x 10(-4) M nicorandil was greatly reduced by 10(-2) M tetraethylammonium, whereas the increase in cyclic GMP produced by this concentration of nicorandil was not significantly changed. Sodium nitroprusside (10(-3) M) produced a large increase in cyclic GMP concentrations but had no significant negative inotropic effect. 6. It is concluded that the negative inotropic effects of nicorandil like those of cromakalim and pinacidil do not result from an increase in cyclic GMP concentrations. Instead these effects may be due to their action as K-channel openers.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2852521&dopt=Abstract
J Clin Endocrinol Metab. 1988 Apr;66(4):678-83.
The renal vasodilating effect of dopamine is mediated by calcium flux and prostacyclin release in man.
Manoogian C, Nadler J, Ehrlich L, Horton R.
Department of Medicine, Los Angeles County-University of Southern California School of Medicine 90033.
A low dose of dopamine (DA; 1 microgram/kg.min for 3 h) was infused into 10 normal subjects to determine whether vasodilator prostaglandins might be involved in the vascular action of this vasoactive hormone. Although this DA dose did not alter blood pressure, pulse, or cardiac index, it significantly increased renal blood flow (RBF), as estimated by para-amino-hippurate clearance [1.40 +/- 0.10 (+/- SE) to 1.93 +/- 0.18 L/min.1.73 m2; P less than 0.02]. This increase was due to DA receptor action since it was blocked by metoclopramide, a DA antagonist, and was not altered by prazosin, an alpha-adrenergic antagonist. DA simultaneously increased the urinary excretion rate of 6-keto-PGF1 alpha, a stable metabolite of prostacyclin [PGI2; 79 +/- 16 to 154 +/- 32 ng/g creatinine (2 +/- 0.40 to 3.88 +/- 0.78 pmol/mumol creatinine); P less than 0.02], but there was no change in PGE2 excretion. This dose of DA increased urinary Na+ and K+ excretion and slightly increased creatinine clearance from 0.12 +/- 0.01 to 0.16 +/- 0.02 L/min.1.73 m2 (P less than 0.05). Metoclopramide also blocked the increase in PGI2 excretion, indicating that this increase was due to DA. The relationship between RBF and PGI2 was supported by studies in which either indomethacin or ibuprofen, both cyclooxygenase inhibitors, blocked the increase in both RBF and PGI2 excretion rate. Since some DA actions may be mediated through calcium flux, we also administered nifedipine, a calcium channel-blocking drug, and found that the DA effect on RBF and PGI2 was significantly reduced. These studies suggest that the DA effect on RBF is mediated by calcium flux, which probably activates renal vascular phospholipase, leading to release of arachidonic acid and synthesis of PGI2, a potent vasodilator.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3279061&dopt=Abstract
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