Drugs online research references
Can J Physiol Pharmacol. 1984 Jun;62(6):665-72.
Hepatic venoconstrictor effects of isoproterenol and nifedipine in anesthetized cats.
Seaman KL, Greenway CV.
In cats anesthetized with pentobarbital, isoproterenol infused into a peripheral vein causes a reduction in hepatic blood volume measured by plethysmography. As this response is accompanied by increases in portal and hepatic lobar venous pressures, the decrease in hepatic volume cannot be a passive emptying secondary to reduced intrahepatic pressure. We conclude that intravenous isoproterenol causes an active hepatic venoconstriction. Nifedipine produced similar responses. From this and our previous data, we conclude that in anesthetized cats, arteriolar vasodilators which increase cardiac output cause hepatic venoconstriction (hydralazine, adrenaline, dopamine, isoproterenol, and nifedipine), while those which do not increase cardiac output have no effect on the hepatic venous bed (nitroprusside and diazoxide) or cause venodilatation (nitroglycerine). The mechanism of the hepatic venoconstrictor effect of isoproterenol was investigated further. Because previous work has shown that this response does not occur when isoproterenol is infused locally into the hepatic artery or portal vein, the venoconstrictor effect of peripheral intravenous infusions must be indirectly mediated. The response was still present after hepatic denervation, adrenalectomy, nephrectomy, and after indomethacin administration indicating it is not mediated by the hepatic nerves, adrenal catecholamines, the renal renin-angiotensin system, or prostaglandins. The mechanism remains unknown.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6744110&dopt=Abstract
J Cardiovasc Pharmacol. 1993 May;21(5):739-48.
Functional study on the effects of nifedipine, cromakalim, and the absence of extracellular Ca2+ on alpha 1-adrenoceptor-mediated excitation-contraction coupling in isolated rat portal vein: comparison with depolarization-mediated excitation-contraction coupling.
Schwietert R, Wilhelm D, Wilffert B, van Zwieten PA.
Department of Pharmacotherapy, Academic Medical Centre, University of Amsterdam, The Netherlands.
The effects of Ca(2+)-entry blockade by nifedipine, K+ channel opening by cromakalim, and of omitting extracellular Ca2+ on the contractile response elicited by a supramaximum concentration of the "full" and selective alpha 1-adrenoceptor agonist phenylephrine (10(-4) M) were compared with those elicited by a supramaximal concentration of KCl (50 mM) in isolated rat portal vein. The contractile response to phenylephrine appeared to be biphasically composed of an early "transient" phase and a slowly developing "sustained" phase that reached maximum values after 30 s and 5 min after initiation of contraction, respectively. The contractile response to KCl (50 mM) exhibited a triphasic pattern consisting of "spike," "transient", and "sustained" components that peaked after 8 s, 25 s, and 10 min, respectively. Nifedipine was able to eliminate all components of the contractions in response to both phenylephrine and KCl almost completely. Nifedipine was approximately 10 times more potent at suppressing the slowly developing sustained components of the contractions in response to both stimuli than the early transient components. The spontaneous myogenic contractions were inhibited by nifedipine with intermediate potency. Cromakalim, in contrast to nifedipine, selectively eliminated the early transient components of the contractions in response to both phenylephrine and KCl. The sustained components of the contractions in response to both stimuli were relatively resistant to K+ channel opening, although higher concentrations (> 1 microM) of cromakalim were capable of antagonizing the sustained response to phenylephrine accompanied by oscillations in tone. Cromakalim was most potent in counteracting spontaneous myogenic contractions. When phenylephrine and KCl were added with or without external Ca2+ after different periods of equilibration in nominally Ca(2+)-free medium, different washout kinetics for the different components of the contractions in response to both stimuli were observed. The early transient phases of tension development in response to both stimuli were completely lost after approximately 6 min of equilibration in nominally Ca(2+)-free medium, whereas the slowly developing sustained components of the contractions were immediately lost after the change to nominally Ca(2+)-free medium. Externally added Ca2+, when administered together with phenylephrine or KCl after the preparations had been exposed for different times to nominally Ca(2+)-free medium, could not restore the early transient components.(ABSTRACT TRUNCATED AT 400 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7685443&dopt=Abstract
Cardiovasc Res. 1993 Dec;27(12):2205-11.
Characterisation of the effect of oxygen tension on response of fetal rabbit ductus arteriosus to vasodilators.
Smith GC, McGrath JC.
Institute of Physiology, University of Glasgow, United Kingdom.
OBJECTIVE: The aims of the study were (1) to elucidate the effects of raised oxygen tension on the response of the ductus arteriosus to a range of vasodilators; and (2) to establish the effect, if any, of cyclo-oxygenase inhibition on the interaction between oxygen and prostaglandin (PG)E2. METHODS: Rings of ductus arteriosus were isolated from fetal New Zealand White rabbits at 28 d gestation (term = 31) and precontracted with 10 microM noradrenaline in the presence of the cyclo-oxygenase inhibitor indomethacin (1 microM). Cumulative relaxation response curves were obtained from a range of vasodilators and their pEC50 (-log10 of the interpolated molar concentration causing 50% of the maximum response) and maximum relaxant response (MRR) were determined in 15% oxygen (neonatal oxygen tension, 13-14.3 kPa) and 2% oxygen (fetal oxygen tension, 2.5-3.0 kPa). In addition, the effects of (1) omitting indomethacin and (2) its substitution by 1 microM flubriprofen were studied on the interaction between oxygen and PGE2. RESULTS: In 1 microM indomethacin, nifedipine and atrial natriuretic peptide had no effect on ductal tone in either oxygen tension. In 15% oxygen, the rank order of MRR was forskolin > cicaprost > PGE2 >> cromakalim >> sodium nitroprusside approximately adenosine approximately 0. The MRR of all agonists was increased in 2% oxygen except forskolin which caused complete relaxation in 15% oxygen. In 15% oxygen, the rank order of pEC50 was PGE2 >> cicaprost approximately cromakalim approximately forskolin. PGE2 was 70.8 times more potent than cicaprost. The pEC50 of all four agonists was increased in 2% oxygen. The increase in pEC50 could not be explained by a decreased extent of precontraction. The MRR to PGE2 in 15% oxygen and the magnitude of the increase in pEC50 to PGE2 going from 15% to 2% oxygen were the same in 1 microM flubriprofen, 1 microM indomethacin, or in the absence of these drugs. However, in 2% oxygen, the MRR to PGE2 was increased in 1 microM indomethacin or 1 microM flubriprofen compared with control. CONCLUSIONS: (1) Increasing oxygen tension from fetal to neonatal levels desensitises the ductus arteriosus to a range of vasodilators. (2) There is evidence that prostacyclin has a physiological role in the control of the rabbit ductus arteriosus. (3) The effect of oxygen on the potency of PGE2 is independent of cyclo-oxygenase products, whereas its effect on the efficacy of PGE2 is modulated by an endogenous cyclo-oxygenase product.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8313430&dopt=Abstract
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