Role of non-nitric oxide non-prostaglandin endothelium-derived relaxing factor(s) in bradykinin vasodilation

The most conspicuous effect of bradykinin following its administration into the systemic circulation is a transient hypotension due to vasodilation. In the present study most of the available evidence regarding the mechanisms involved in bradykinin-induced arterial vasodilation is reviewed. It has become firmly established that in most species vasodilation in response to bradykinin is mediated by the release of endothelial relaxing factors following the activation of B2-receptors. Although in some cases the action of bradykinin is entirely mediated by the endothelial release of nitric oxide (NO) and/or prostacyclin (PGI2), a large amount of evidence has been accumulated during the last 10 years indicating that a non-NO/PGI2 factor accounts for bradykinin-induced vasodilation in a wide variety of perfused vascular beds and isolated small arteries from several species including humans. Since the effect of the non-NO/PGI2 endothelium-derived relaxing factor is practically abolished by disrupting the K+ electrochemical gradient together with the fact that bradykinin causes endothelium-dependent hyperpolarization of vascular smooth muscle cells, the action of such factor has been attributed to the opening of K+ channels in these cells. The pharmacological characteristics of these channels are not uniform among the different blood vessels in which they have been examined. Although there is some evidence indicating a role for KCa or KV channels, our findings in the mesenteric bed together with other reports indicate that the K+ channels involved do not correspond exactly to any of those already described. In addition, the chemical identity of such hyperpolarizing factor is still a matter of controversy. The postulated main contenders are epoxyeicosatrienoic acids or endocannabinoid agonists for the CB1-receptors. Based on the available reports and on data from our laboratory in the rat mesenteric bed, we conclude that the NO/PGI2-independent endothelium-dependent vasodilation induced by BK is unlikely to involve a cytochrome P450 arachidonic acid metabolite or an endocannabinoid agonist.

Role of endothelium in angiotensin II formation by the rat aorta and mesenteric arterial bed

We investigated the angiotensin II (Ang II)-generating system by analyzing the vasoconstrictor effect of Ang II, angiotensin I (Ang I), and tetradecapeptide (TDP) renin substrate in the abscence and presence of inhibitors of the renin-angiotensin system in isolated rat aortic rings and mesenteric arterial beds with and without functional endothelium. Ang II, Ang I, and TDP elicited a dose-dependent vasoconstrictor effect in both vascular preparations that was completely blocked by the Ang II receptor antagonist saralasin (50 nM). The angiotensin converting enzyme (ACE) inhibitor captopril (36 muM) completely inhibited the vasoconstrictor effect elicited by Ang I and TDP in aortic rings without affecting that of Ang II. In contrast, captopril (36 muM) significantly reduced (80-90 percent) the response to bolus injection of Ang I, without affecting those to Ang II and TDP in mesenteric arteries. Mechanical removal of the endothelium greatly potentiated (70-95 percent) the vasoconstrictor response to Ang II, Ang I, and TDP in aortic rings while these responses were unaffected by the removal of the endothelium of mesenteric arteries with sodium deoxycholate infusion. In addition, endothelium disruption did not change the pattern of response elicited by these peptides in the presence of captopril. These findings indicate that the endothelium may not be essential for Ang II formation in rat mesenteric arteries and aorta, but it may modulate the response to Ang II. Although Ang II formation from Ang I is essentially dependent on ACE in both vessels, our results suggest the existence of an alternative pathway in the mesenteric arterial bed that may play an important role in Ang II generation from TDP in resistence but not in large vessels during ACE inhibition.

Determinaçäo da digestibilidade aparente em equídeos através do óxido crômico, da lignina e da coleta total das fezes / Apparent digestibility using total fecal collection, chromic oxide and lignin as markers in equids

Foram comparados os coeficientes de digestibilidade da proteína bruta (PB), matéria seca (MS), hemicelulose (HCEL), fibra em detergente neutro (FDN), fibra em detergente ácido (FDA), energia bruta (EB) e celulose (CEL), obtidos pela coleta total das fezes (CT) e pelo uso dos marcadores óxido crômico (OC) e lignina (LIG). Foram utilizados 24 animais, nove equinos, seis asininos e nove muares, em delineamento experimental inteiramente ao acaso, com nove tratamentos em esquema fatorial 3 x 3 (três espécies e três marcadores), com três repetiçöes para equinos e muares e duas para jumentos. O experimento teve duraçäo de 28 dias. A dieta era composta de feno de "Coast cross" picado (PB=7,8 por cento) e concentrado (PB=12,7 por cento) à base de milho desintegrado com sabugo, milho gräo, farelo de trigo, farelo de soja, calcário e fosfato bicálcio. A relaçäo volumoso/concentrado foi de 1:1, fornecida no equivalente a 2 por cento do peso vivo em MS/dia, de acordo com o seguinte esquema de arraçoamento: A=7h e 13h (volumoso), 9h e 15h (concentrado);B=7h e 15h (volumoso), 11h e 19h (concentrado); C=7h (concentrado total e 1/3 do volumoso), 15h (2/3 do volumoso). Näo foram encontradas diferenças significativas entre os coeficientes de digestibilidade da HCEL (67,12 e 63,55) e CEL (51,06 e 46,58) obtidos pelos indicadores CT, LIG, mas diferentes pelo indicador OC (58,34 e 38,41). Os coeficientes de digestiblidade da PB (71,01, 67,78 e 63,12), da MS (64,15, 59,03 e 52,99), da FDN (51,20, 46,53 e 38,61), da EB (64,60, 60,77 e 54,94) e da FDA (33,23, 66,03 E 18,84) obtidos respectivamente pela CT, LIG e OC diferiram entre si