Drugs online research references
Acta Physiol Scand. 1977 Jun;100(2):165-71.
Effects of prostaglandins on the isolated human bladder and urethra.
Andersson KE, Ek A, Persson CG.
The effects of prostaglandins F2 alpha (PGF2 alpha), E1 (PGE1) and E2 (PGE2) on the human lower urinary tract were studied in vitro in preparations obtained from patients undergoing total cystourethrectomy because of bladder malignancy. Tissue specimens were taken from different parts of the urethra, the urethrovesical junction, and the bladder. From these specimens, smooth muscle preparations were dissected and mounted in organ baths, that were filled with Krebs solution (37 degrees C) and bubbled with carbogen. Isometric tension was recorded. Preparations from the bladder and all parts of the urethra were contracted by PGF2 alpha. This effect was not affected by tetrodotoxin, phenoxybenzamine, or atropine; isoprenaline relaxed the PGF2 alpha induced contractions. PGE1 and PGE1 both contracted strips from the bladder. However, urethral preparations contracted by PGF2 alpha or noradrenaline were relaxed by these agents. This relaxing effect was at least as pronounced as that produced by isoprenaline; it was not affected by propranolol.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=888707&dopt=Abstract
ucl.ac.uk
1. Isolated guinea-pig atria were used to study the neuromodulatory effect of diadenosine polyphosphates (APnA) on cardiac capsaicin-sensitive sensory-motor neurotransmission. 2. In the presence of atropine, guanethidine and propranolol, electrical field stimulation (EFS) of the atrial preparations evoked a positive inotropic response which is known to be mediated by release of calcitonin gene-related peptide (CGRP) from sensory-motor nerves. P1,P2-diadenosine pyrophosphate (AP2A), P1,P3-diadenosine triphosphate (AP3A), P1,P4-diadenosine tetraphosphate (AP4A), P1,P5-diadenosine pentaphosphate (AP5A) and P1,P6-diadenosine hexaphosphate (AP6A) inhibited in a concentration-dependent way (0.1-30 microM) cardiac responses to EFS. The inhibitory effect of APnA was mimicked by adenosine. 3. All the APnA tested had a direct negative inotropic effect, by reducing in a concentration-dependent manner the basal contractile tension. The inotropism of APnA was comparable to that of adenosine. 4. Both inhibition of cardiac responses to EFS and negative inotropism of AP2A, AP3A and AP4A were sensitive to the antagonism by the A1 adenosine receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 0.1-1 nM). The extent of antagonism of DPCPX for the APnA tested was comparable to that for adenosine. 5. Despite the direct negative inotropism, AP4A tested at the highest concentration used did not affect the cardiac responses to the neurotransmitter CGRP, applied exogenously. 6. These results have demonstrated that in isolated guinea-pig atria APnA inhibited sensory-motor neurotransmission, without affecting cardiac responses to exogenous CGRP. The effect of APnA was sensitive to antagonism by DPCPX, which suggests it operates via the activation of prejunctional A1 adenosine receptors. A postjunctional negative inotropism was also shown, mediated by myocardial A1 adenosine receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8887761&dopt=Abstract
Prostaglandins. 1996 Sep;52(3):221-35.
Prostacyclin and thromboxane production of rat and cat arterial tissue is altered independently by several vasoactive substances.
Szekacs B, Nadasy GL, Vajo Z, Juhasz I, Feher J, Monos E.
2nd Clinics of Internal Medicine, Semmelweis University of Medicine, Budapest, Hungary.
The modulation of the production of prostacyclin and thromboxane from cat and cat aortic tissue slices by different vasoactive agents has been studied in order to reveal whether the release of these main two vasoactive prostanoids goes in parallel or may be controlled independently. Norepinephrine, isoproterenol, phentolamine, propranolol, angiotensin II, vasopressin, bradykinin, thrombin, verapamil, gallopamil, dopamine or methionin enkephalin were added to the incubation medium and 6-keto-PGF1 alpha (the stable metabolite of prostacyclin) and TxB2 (the stable metabolite of thromboxane) were determined in the supernatant by radioimmunoassay. The ratio of the release of prostacyclin and thromboxane was computed. Norepinephrine increased both prostacyclin and thromboxane release. Isoproterenol increased the ratio of prostacyclin and thromboxane released in cat aortic tissue slices. Phentolamine and propranolol had no effects. Angiotensin II induced a slight but statistically insignificant increase in the ratio of the two prostanoids released. Vasopressin increased thromboxane release only. Bradykinin stimulated the prostacyclin while thrombin stimulated the thromboxane release. Verapamil decreased both prostacyclin and thromboxane production. Gallopamil decreased prostacyclin release and increased thromboxane release from vessel wall slices in a certain concentration range causing a characteristic dose dependent minimum in the ratio of prostacyclin and thromboxane release. Dopamine separately increased prostacyclin release while enkephalin had no significant effect. The data obtained show that in vascular tissue some unidentified yet cytophysiological mechanisms might exist which specifically control the activities of the prostacyclin synthase and thromboxane synthase enzymes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8908622&dopt=Abstract
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