Drugs online research references
J Physiol Pharmacol. 1993 Jun;44(2):171-7.
Kinins and thrombolysis.
Swies J, Chlopicki S, Gryglewski RJ.
Department of Pharmacology, University School of Medicine, Krakow, Poland.
In cats with extracorporeal circulation arterial blood pressure and thrombolysis were assayed. In this model apart from their hypotensive properties kallikrein (3-10 units/kg, i.v.) and captopril (> 200 micrograms/kg, i.v.) dissipated blood clots which were preformed on superfused collagen strips. Captopril at a lower dose of 50 micrograms/kg i.v. potentiated the thrombolytic effect of kallikrein while aprotinin (100,000 unit/kg, i.v.) abolished it. Thrombolysis by kallikrein was mediated by an unstable principle which was decomposed by blood during 15 min of incubation at 37 degrees C. Generation of this principle was inhibited by pretreatment of animals with aspirin (50 mg/kg, i.v.). The above analysis points to prostacyclin which owing to its platelet-suppressant and fibrinolytic properties induces thrombolysis when released by kinins.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8358053&dopt=Abstract
J Pharmacol Exp Ther. 1993 Mar;264(3):1285-92.
Interaction between thromboxane A2 and angiotensin II in postischemic renal vasoconstriction in dogs.
Abels BC, Branch RA, Sabra R.
Department of Surgery, Vanderbilt University School of Medicine, Nashville, Tennessee.
The kidney responds to periods of ischemia with vasoconstriction and a decrease in glomerular filtration rate (GFR) on reperfusion. The mediators of this response have not been fully identified. In this study, we examined the contribution of angiotensin II (AII), thromboxane A2 (TXA2) and the interaction between them to this response. Anesthetized dogs were subjected to 30 min of clamping of both renal arteries. Renal hemodynamics and function were followed from 60 min before and for 105 min after clamping. Dogs were divided into salt-depleted (AII-stimulated) and captopril-treated (AII-inhibited) groups. Each group included dogs that received either the TXA2 synthase inhibitor CGS 13080 or its vehicle (controls) starting 30 min before renal artery clamping and lasting to the end of the experiment. In captopril-treated control dogs, 30 min of ischemia induced a 25% fall in renal blood flow (RBF). GFR initially fell by 75%, but recovered to 64% of base-line value 60 to 90 min after release of the clamp. In captopril-treated dogs, CGS 13080 prevented the fall in RBF, but the GFR response was similar to vehicle-treated dogs. In control dogs, both GFR and RBF responses were enhanced in salt-depleted compared with captopril-treated dogs; the decrease in RBF (44%) was greater, and the recovery in GFR, which fell by 89%, less. In salt-depleted, CGS 13080-treated dogs, the 30% fall in RBF was less than its control, but greater than dogs treated with captopril and CGS 13080. The change in GFR was similar to the other groups.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8450463&dopt=Abstract
Prostaglandins Leukot Med. 1986 Jan;21(1):29-35.
Selective inhibition of thromboxane synthesis partially protected while inhibition of angiotensin II formation did not protect rats against acute renal failure induced with glycerol.
Papanicolaou N, Hatziantoniou C, Bariety J.
Acute renal failure (ARF) was induced in 35 week-old conscious female Wistar rats, by intramuscular (IM) injection of glycerol. Intraperitoneal (IP) injection of imidazole, an inhibitor of thromboxane (TXA2) synthesis, partially protected the animals against ARF. This protection was accompanied by a significant decrease in renal TXB2 (the stable chemical metabolite of TXA2) and a significant increase in renal 6-keto-PGF1 alpha (the stable chemical metabolite of PGI2) synthesis. Intraperitoneal injection of captopril (SQ 14225) an angiotensin-converting-enzyme inhibitor, did not protect the animals against ARF. This lack of protection was accompanied by a significant increase in renal TXB2 and a significant decrease in renal 6-keto-PGF1 alpha synthesis. The results suggest that: (a) the renin-angiotensin (R-A) system does not play a role, or has only a secondary one in the development of ARF; (b) thromboxane A2 (the most potent vasoconstrictor and platelet aggregator agent known) is the preponderant agent responsible for the development of this pathological syndrome.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3513208&dopt=Abstract
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