The role of endothelium in the decreased contraction to phenylephrine in aorta of pregnant Wistar rats has been studied. Contractions in response to phenylephrine were significantly decreased in aortic rings from pregnant rats compared to those from non-pregnant rats. Pretreatment of the rings with indomethacin did not significantly alter the pattern of responses. When endothelium was removed from the rings, contractions of rings from non-pregnant rats were similar to those from pregnant rats. Acetylcholine-induced relaxations of rings from pregnant and non-pregnant rats precontracted with phenylephrine were not significantly different. The results suggest that in the rat aorta and under in vitro conditions, pregnancy-induced attenuation of contraction to phenylephrine is, at least partly, endothelium dependent and that the release of the endothelium factor responsible for this alteration in response may be indomethacin insensitive.
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http://dx.doi.org/10.1113/expphysiol.1993.sp003694 | DOI Listing |
Br J Pharmacol
January 2025
Department of Pharmacology, University of Oxford, Oxford, UK.
Background And Purpose: TMEM16A chloride channels constitute a depolarising mechanism in arterial smooth muscle cells (SMCs) and contractile cerebral pericytes. TMEM16A pharmacology is incompletely defined. We elucidated the mode of action and selectivity of a recently identified positive allosteric modulator of TMEM16A (PAM_16A) and of a range of TMEM16A inhibitors.
View Article and Find Full Text PDFIntroduction: The pathogenic role of nitric oxide (NO) signaling during development of thoracic aortic aneurysm (TAA) in Marfan syndrome (MFS) is currently unclear. We characterized vasomotor function and its relationship to the activity of the NO-generating enzymes in mice with early onset progressively severe MFS.
Methods: Wire myography, immunoblotting, measurements of aortic NO and superoxide levels were used to compare vasomotor function, contractile-protein levels, and the activity of endothelial and inducible NO synthase (eNOS and iNOS, respectively) in ascending thoracic aortas of Fbn1mgR/mgR mice relative to wild type (WT) littermates.
J Ethnopharmacol
January 2025
State Key Laboratory of Southwestern Chinese Medicine Resources, School of Medical Technology, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China. Electronic address:
Ethnopharmacological Relevance: The rhizomes of Curcuma phaeocaulis Val. are a Rhizoma curcumae source in Chinese pharmacopoeia, and this traditional Chinese medicine has been extensively used in China to promote blood circulation and remove blood stasis. However, little is known regarding the vasodilatory effects and underlying mechanisms.
View Article and Find Full Text PDFGen Physiol Biophys
January 2025
Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Comenius University, Bratislava, Slovakia.
The study aimed to evaluate the basic pharmacological effects of modified phenyl carbamic acid derivates with a basic part made of N-phenylpiperazine (compounds 6a, 6b, 6c, 6d) in Wistar rats. The compounds were evaluated for their ability to decrease the phenylephrine-induced contraction of the aortic strips of rats after repeated administration of the compounds and their ability to inhibit the positive chronotropic effect of isoproterenol on spontaneously beating rat atria. The ability to inhibit the vasoconstriction effect of phenylephrine was confirmed in all compounds in the range from 10.
View Article and Find Full Text PDFToxicol Appl Pharmacol
January 2025
Institute of Medical Sciences, Department of Physiology, Kangwon National University School of Medicine, Chuncheon 24341, South Korea. Electronic address:
This study explored the vasodilatory mechanisms of the sodium-glucose cotransporter-2 inhibitor remogliflozin using femoral arteries of rabbits. Remogliflozin dilated femoral arterial rings pre-contracted with phenylephrine in a concentration-dependent manner. Pretreatment with the Ca-sensitive K channel inhibitor (paxilline), the ATP-sensitive K channel inhibitor (glibenclamide), or the inwardly rectifying K channel inhibitor (Ba) did not alter the vasodilatory effect.
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