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Arteries Isolated (artery + isolated)
Selected AbstractsRole of Vascular Heme Oxygenase in Reduced Myogenic Reactivity Following Chronic HypoxiaMICROCIRCULATION, Issue 2 2006JAY S. NAIK ABSTRACT Objective: Exposure to chronic hypoxia (CH) results in a persistent endothelium-dependent vascular smooth muscle hyperpolarization that diminishes vasoconstrictor reactivity. Experiments were performed to test the hypothesis that products of both cytochrome P450 epoxygenase (CYP) and heme oxygenase (HO) are required for the persistent diminished myogenic reactivity following CH. Methods: The authors examined myogenic responses of mesenteric arteries isolated from control and CH (48 h; PB = 380 mmHg) rats in the presence of a HO inhibitor (zinc protoporphyrin IX; ZnPPIX) or combined HO and CYP epoxygenase inhibition (sulfaphenazole). Arteries were isolated and cannulated and the vascular smooth muscle was loaded with the Ca2 + indicator Fura-2. Results: Control vessels maintained their internal diameter in response to step increases in intraluminal pressure, whereas arteries from CH animals passively distended. ZnPPIX augmented myogenic reactivity and [Ca2 +] in arteries from CH animals. Combined administration of sulfaphenazole and ZnPPIX did not have an additional effect compared to ZnPPIX alone. Myogenic reactivity in control vessels was not altered by ZnPPIX or ZnPPIX + sulfaphenazole. Conclusions: HO appears to play a role in regulating myogenic reactivity following CH. Furthermore, these data suggest that products of HO and CYP are both required for the observed attenuation in vasoreactivity following CH. [source] Heterogeneity of the neuropeptide Y (NPY) contractile and relaxing receptors in horse penile small arteriesBRITISH JOURNAL OF PHARMACOLOGY, Issue 8 2004Dolores Prieto The distribution of neuropeptide Y (NPY)-immunorective nerves and the receptors involved in the effects of NPY upon electrical field stimulation (EFS)- and noradrenaline (NA)-elicited contractions were investigated in horse penile small arteries. NPY-immunoreactive nerves were widely distributed in the erectile tissues with a particularly high density around penile intracavernous small arteries. In small arteries isolated from the proximal part of the corpora cavernosa, NPY (30 nM) produced a variable modest enhancement of the contractions elicited by both EFS and NA. At the same concentration, the NPY Y1 receptor agonist, [Leu31, Pro34]NPY, markedly potentiated responses to EFS and NA, whereas the NPY Y2 receptor agonist, NPY(13,36), enhanced exogenous NA-induced contractions. In arteries precontracted with NA, NPY, peptide YY (PYY), [Leu31, Pro34]NPY and the NPY Y2 receptor agonists, N - acetyl[Leu28,31]NPY (24,36) and NPY(13,36), elicited concentration-dependent contractile responses. Human pancreatic polypeptide (hPP) evoked a biphasic response consisting of a relaxation followed by contraction. NPY(3,36), the compound 1229U91 (Ile-Glu-Pro-Dapa-Tyr-Arg-Leu-Arg-Tyr-NH2, cyclic(2,4,)diamide) and eventually NPY(13,36) relaxed penile small arteries. The selective NPY Y1 receptor antagonist BIBP3226 ((R)- N2 -(diphenacetyl)- N -[(4-hydroxyphenyl)methyl]D -arginineamide) (0.3 ,M) shifted to the right the concentration,response curves to both NPY and [Leu31, Pro34]NPY and inhibited the contractions induced by the highest concentrations of hPP but not the relaxations observed at lower doses. In the presence of the selective NPY Y2 receptor antagonist BIIE0246 ((S)- N2-[[1-[2-[4-[(R,S)-5,11-dihydro-6(6h)-oxodibenz[b,e]azepin-11-y1]-1-piperazinyl]-2-oxoethyl]cyclo-pentyl- N -[2-[1,2-dihydro,3,5 (4H)-dioxo-1,2-diphenyl-3H -1,2, 4-triazol-4-yl]ethyl]-argininamide) (0.3 ,M), the Y2 receptor agonists NPY(13,36) and N - acetyl[Leu28,31]NPY (24,36) evoked potent slow relaxations in NA-precontracted arteries, under conditions of nitric oxide (NO) synthase blockade. Mechanical removal of the endothelium markedly enhanced contractions of NPY on NA-precontracted arteries, whereas blockade of the neuronal voltage-dependent Ca2+ channels did not alter NPY responses. These results demonstrate that NPY can elicit dual contractile/relaxing responses in penile small arteries through a heterogeneous population of postjunctional NPY receptors. Potentiation of the contractions evoked by NA involve both NPY Y1 and NPY Y2 receptors. An NO-independent relaxation probably mediated by an atypical endothelial NPY receptor is also shown and unmasked in the presence of selective antagonists of the NPY contractile receptors. British Journal of Pharmacology (2004) 143, 976,986. doi:10.1038/sj.bjp.0706005 [source] PARTICIPATION OF VASOPRESSIN IN THE DEVELOPMENT OF CEREBRAL VASOSPASM IN A RAT MODEL OF SUBARACHNOID HAEMORRHAGECLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2004Cristina C Trandafir SUMMARY 1.,Previous studies have suggested the involvement of arginine vasopressin (AVP) and inflammation in the development of cerebral vasospasm after subarachnoid haemorrhage (SAH). The aim of the present study was to clarify the role of AVP in the arterial narrowing following cerebral haemorrhage by examining the effect of SR 49059 (a V1 receptor antagonist) on the diameter of rat basilar artery exposed to SAH. The effect of the 5-lipoxygenase inhibitor ZM 230487 on AVP-induced contraction of rat basilar arteries was also investigated. 2.,After 1 h and 2 days from SAH induction, brains were removed and pictures of the basilar arteries were taken. The external diameter of the basilar artery was measured in the presence and absence of SR 49059 (1 mg/kg, i.v.). For in vitro experiments, the basilar arteries isolated from control and SAH rats (at 1 h and at 2 days from SAH induction) were cut into spiral preparations and the AVP (0.3 nmol/L)-induced contraction in the presence of ZM 230487 was investigated. Each group analysed (i.e. control, SAH 1 h and SAH 2 days) consisted of eight rats. 3.,The diameter of rat basilar arteries decreased by 43 and 25% at 1 h and 2 days from SAH induction, respectively, compared with control. The administration of SR 49059 significantly reduced cerebral vasospasm. After SAH induction, the diameter of the basilar artery in SR 49059-treated groups decreased by only 22% (at 1 h) and by 3% (at 2 days) compared with the control group (P < 0.01). In basilar arterial strips, ZM 230487 attenuated the vasopressin-induced contraction in both control and SAH groups. However, SAH groups showed a significant resistance of the AVP-induced contraction in the presence of ZM 230487 compared with control (P < 0.05). 4.,The results suggest that the cerebral vasospasm in SAH rats is due, at least in part, to endogenous AVP and may involve an increase in the activity of 5-lipoxygenase. SR 49059 may represent a potential therapeutic strategy for the treatment of cerebral vasospasm. [source] Heat stress increases endothelium-dependent relaxations and prevents reperfusion-induced endothelial dysfunctionCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2002Vincent Richard Summary 1.,Heat stress has been widely used to stimulate the expression of stress proteins and is associated with various cardiovascular changes, including anti-ischaemic effects. However, the effect of heat stress on endothelial function is less clear. 2.,Heat stress was induced in anaesthetized rats by increasing body temperature to 42°C for 15 min. Twenty-four hours later, segments of rat aorta and mesenteric and coronary arteries were mounted in organ chambers. 3.,Heat stress markedly increased relaxation to acetylcholine (ACh) in all three blood vessels studied, without affecting the response to the nitric oxide (NO) donor sydnonimine-1. 4.,Heat stress also increased aortic relaxation to histamine and the calcium ionophore A23187. 5.,In the aorta, an inhibitor of NO synthesis abolished the response to ACh in both control and heat stressed-rings, whereas a cyclo-oxygenase inhibitor had no effect. 6.,Heat stress also prevented completely the impaired response to ACh in coronary arteries isolated from rats subjected to myocardial ischaemia and reperfusion. 7.,Thus, heat stress increases the stimulated release of NO the rat aorta and mesenteric and coronary arteries and prevents reperfusion-induced injury at the level of the coronary endothelium. [source] | ||||||||||