Drugs online research references
J Pharmacol Exp Ther. 1994 Jan;268(1):97-103.
Coronary vascular effects of cocaine in rats.
Mueller PJ, Knuepfer MM.
Department of Pharmacological and Physiological Science, St. Louis University School of Medicine, Missouri.
It has been suggested that ischemia secondary to coronary vasoconstriction is responsible for adverse cardiovascular effects of cocaine. However, the reported coronary vascular effects of cocaine vary considerably. We sought to determine the effects of cocaine on the coronary vasculature in anesthetized and conscious rats. Rats anesthetized with chloralose were instrumented for estimation of ascending aortic and coronary blood flows using pulsed Doppler velocitometry. Cocaine administration resulted in bradycardia and a biphasic mean arterial pressure response. Cocaine elicited highly variable increases in coronary vascular resistance and decreases in cardiac output. Decreases in coronary blood flow and rate-pressure product were directly correlated. Prazosin significantly attenuated the cardiac output but not the coronary vascular responses to cocaine. Propranolol, on the other hand, significantly shortened the duration of both responses. Conscious rats, instrumented for coronary blood flow determination, also exhibited cocaine-induced increases in coronary vascular resistance, yet the changes in coronary blood flow were not correlated with the rate-pressure product. These results provide the first evidence that cocaine produces equivalent increases in coronary vascular resistance in conscious and anesthetized rats. However, because the relationship between coronary blood flow and rate-pressure is different between the two preparations, as are other cardiovascular responses, we suggest that anesthesia alters the mechanism(s) by which cocaine affects the rat coronary vasculature.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8301600&dopt=Abstract
Eur J Pharmacol. 1993 Nov 15;247(3):267-72.
Effects of local anesthetics and related drugs on endogenous glibenclamide-sensitive K+ channels in Xenopus oocytes.
Yoneda I, Sakuta H, Okamoto K, Watanabe Y.
Department of Pharmacology, National Defense Medical College, Saitama, Japan.
Effects of local anesthetics and structurally related drugs on the glibenclamide-sensitive K+ currents evoked by Y-26763 (a K+ channel opener) were investigated in native Xenopus oocytes. The K+ current induced by Y-26763 (100 microM) was reversibly suppressed by all six local anesthetics tested in a concentration-dependent manner with the rank order of potencies (IC50 in microM): bupivacaine (67) > dibucaine (136) > tetracaine (845) > lidocaine (1710) = mepivacaine (1945) > procaine (3112). (+)-Propranolol and mexiletine also suppressed Y-26763-induced K+ currents with IC50 values of 115 microM and 789 microM, respectively. These results suggest that a suppressive action on glibenclamide-sensitive K+ channels is the common property of local anesthetics.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8307100&dopt=Abstract
Am J Physiol. 1998 Nov;275(5 Pt 2):R1674-82.
Apparent thermogenic effect of injected glucagon is not due to a direct effect on brown fat cells.
Dicker A, Zhao J, Cannon B, Nedergaard J.
The Wenner-Gren Institute, The Arrhenius Laboratories F3, Stockholm University, S-106 91 Stockholm, Sweden.
To examine the significance of brown adipose tissue for the thermogenic response to glucagon, we injected glucagon intraperitoneally into rats (that have glucagon-sensitive brown fat cells) and into hamsters (that have glucagon-insensitive brown fat cells). Although a thermogenic response to glucagon injection was apparently observed in rats, this response was not augmented by cold acclimation and was not dose dependent. Similar observations were made in hamsters. The thermogenic response could be fully blocked by prior injection of the beta-adrenergic blocker propranolol. Thus no direct thermogenic response to injected glucagon could be demonstrated, and the thermogenic response observed was fully due to vehicle injection. However, glucagon injection was able to unmask mitochondrial [3H]GDP binding. As expected, isolated brown fat cells from rats and mice responded thermogenically to glucagon but brown fat cells from hamsters were unresponsive. The EC50 of the rat brown fat cells was high (5 nM); these cells also responded to secretin, with an EC50 of 22 nM. It was concluded that, in contrast to earlier observations, no thermogenic response to injected glucagon could be observed; this may be related to differences in glucagon preparations. Brown fat cells from certain species are, however, glucagon sensitive. It is uncertain whether glucagon is the endogenous agonist for these receptors, but the presence of the glucagon-responsive receptor indicates alternative means to norepinephrine for stimulation of brown adipose tissue thermogenesis and, probably, of recruitment.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9791090&dopt=Abstract
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