RESUMO
The streamline flow in the portal system is a phenomenon by which blood from superior mesenteric vein goes preferentially to the right hepatic lobe, while splenic and inferior mesenteric veins divert preferentially to the left lobe. Such a phenomenon results in different patterns of distribution of several liver diseases. The purpose of this article is to discuss the concepts behind the theory of streamline flow and to perform an imaging-based review of representative cases, demonstrating how it may influence the patterns of liver involvement in different gastrointestinal diseases.
Assuntos
Gastroenteropatias/diagnóstico por imagem , Fígado/irrigação sanguínea , Fígado/diagnóstico por imagem , Veia Porta/fisiologia , Velocidade do Fluxo Sanguíneo , Humanos , Veias Mesentéricas/fisiologia , Fluxo Sanguíneo RegionalRESUMO
To investigate the venoconstrictor effect of angiotensin II (Ang II) in spontaneously hypertensive rats (SHR), we used preparations of mesenteric venular beds and the circular muscle of the portal veins. Vessels were tested with Ang II in the presence or absence of losartan, PD 123319, HOE 140, L-NAME, indomethacin, or celecoxib. In the mesenteric venular bed of SHR, the effect of Ang II (0.1 nmol) was nearly abolished by losartan and enhanced by HOE 140, indomethacin, and celecoxib, while PD123319 and L-NAME had no effect. In portal vein preparations, cumulative-concentration response curves (CCRC) to Ang II (0.1-100 nmol/L) exhibited a lower maximal response (E(max)) in SHR compared to Wistar rats. AT(1) receptor expression was similar in the two strains, while AT(2) receptor levels were lower in SHR portal veins when compared to Wistar. In SHR portal veins, losartan shifted the CCRC to Ang II to the right, while indomethacin and HOE 140 increased the E(max) to Ang II. PD 123319, celecoxib, and L-NAME had no effect. Taken together, our results suggest that Ang II-induced venoconstriction in SHR is mediated by activation of AT(1) receptors and this effect may be counterbalanced by kinin B(2) receptor and COX metabolites. Furthermore, our data indicate that there are different cellular and molecular mechanisms involved in the regulation of venous tonus of normotensive and hypertensive rats. These differences probably reflect distinct factors that influence arterial and venous bed in hypertension.
Assuntos
Angiotensina II/farmacologia , Hipertensão/fisiopatologia , Veias Mesentéricas/efeitos dos fármacos , Veias Mesentéricas/fisiologia , Veia Porta/efeitos dos fármacos , Veia Porta/fisiologia , Vasoconstrição/efeitos dos fármacos , Animais , Masculino , Veias Mesentéricas/anatomia & histologia , Veia Porta/anatomia & histologia , Ratos , Ratos Endogâmicos SHR , Ratos WistarRESUMO
The venoconstrictor effect of Angiotensin II (Ang II) was investigated in the rat mesenteric venules and portal vein. Mesenteric venules were perfused at a constant rate and reactivity to Ang II (0.1 nmol) was evaluated as changes in the perfusion pressure. Rings of portal vein were mounted in organ baths and curves to Ang II (0.1-100 nmol/L) were generated. In venules, Ang II-contraction (10.6+/-1.1 mmHg) was abolished by losartan (0.9+/-0.3 mmHg*), reduced by PD 123,319 (5.8+/-0.9 mmHg*), increased by L-NAME (16.5+/-1.8 mmHg*) and not altered by indomethacin. In portal veins, curves to Ang II (-logEC50: 8.9+/-0.1 mol/L) were shifted to the right by losartan (-log EC50: 7.5+/-0.1 mol/L*) and by PD 123,319 (-logEC50: 8.0+/-0.1 mol/L*). L-NAME increased the maximal response to Ang II (Emax: 0.91+/-0.1g versus 1.62+/-0.3g*) and indomethacin had no effect. In conclusion, Ang II induces venoconstriction by activating AT1 and AT2 receptors. Data obtained with L-NAME provide evidence that the basal nitric oxide release from the endothelium of the venous system can modulate the Ang II-induced venoconstriction.
Assuntos
Angiotensina II/farmacologia , Veias Mesentéricas/fisiologia , Óxido Nítrico/metabolismo , Veia Porta/fisiologia , Receptor Tipo 1 de Angiotensina/metabolismo , Receptor Tipo 2 de Angiotensina/metabolismo , Vasoconstrição/efeitos dos fármacos , Vasoconstritores/farmacologia , Angiotensina II/metabolismo , Animais , Inibidores Enzimáticos/farmacologia , Masculino , NG-Nitroarginina Metil Éster/farmacologia , Técnicas de Cultura de Órgãos , Ratos , Ratos Wistar , Vasoconstrição/fisiologia , Vasoconstritores/metabolismoRESUMO
1. The mechanisms involved in the vasodilator actions of angiotensin II (Ang II) have not yet been completely elucidated. We investigated the potential mechanisms that seem to be involved in the Ang II vasodilator effect using rat isolated mesenteric vascular bed (MVB). 2. Under basal conditions, Ang II does not affect the perfusion pressure of MVB. However, in vessels precontracted with norepinephrine, Ang II induces vasodilation followed by vasoconstriction. Vasoconstrictor, but not the vasodilation of Ang II, is inhibited by AT(1) antagonist (losartan). The vasodilator effect of Ang II was not inhibited by AT(2), angiotensin IV and angiotensin 1-7 receptor antagonists alone (PD 123319, divalinal, A 779, respectively). 3. The vasodilator effect of Ang II is significantly reduced by endothelial removal (deoxycholic acid), but not by indomethacin. Inhibition of NO-synthase by N(G)-nitro-l-arginine methyl ester (l-NAME) and guanylyl cyclase by 1H-[1,2,3] oxadiazolo [4,4-a] quinoxalin-1-one (ODQ) reduces the vasodilator effect of Ang II. This effect is also reduced by tetraethylammonium (TEA) or l-NAME, and a combination of l-NAME plus TEA increases the inhibitory effect of the antagonists alone. However, indomethacin does not change the residual vasodilator effect observed in vessels pretreated with l-NAME plus TEA. 4. In vessels precontracted with norepinephrine and depolarized with KCl 25 mm or treated with Ca(2+)-dependent K(+) channel blockers (charybdotoxin plus apamin), the effect of Ang II was significantly reduced. However, this effect is not affected by ATP and voltage-dependent K(+) channel blockers (glybenclamide and 4-aminopyridine). 5. Inhibition of kininase II with captopril significantly potentiates the vasodilator effect of bradykinin (BK) and Ang II in the rat MVB. The inhibitory effect of the B(2) receptor antagonist HOE 140 on the vasodilator effect of Ang II is further enhanced by PD 123319 and/or A 779. 6. The present findings suggest that BK plays an important role in the endothelium-dependent vasodilator effect of Ang II. Probably, the link between Ang II and BK release is modulated by receptors that bind PD 123319 and A 779.
Assuntos
Angiotensina II/farmacologia , Angiotensina I/fisiologia , Bradicinina/fisiologia , Fatores Relaxantes Dependentes do Endotélio/metabolismo , Fragmentos de Peptídeos/fisiologia , Receptor Tipo 2 de Angiotensina/fisiologia , Vasodilatação/fisiologia , Animais , Técnicas In Vitro , Masculino , Artérias Mesentéricas/efeitos dos fármacos , Artérias Mesentéricas/fisiologia , Veias Mesentéricas/efeitos dos fármacos , Veias Mesentéricas/fisiologia , Ratos , Ratos Wistar , Receptores de Angiotensina/fisiologia , Vasodilatação/efeitos dos fármacosRESUMO
1. The effects of niflumic acid, an inhibitor of calcium-activated chloride currents, were compared with the actions of the calcium channel blocker nifedipine on noradrenaline- and 5-hydroxytryptamine (5-HT)-induced pressor responses of the rat perfused isolated mesenteric vascular bed. 2. Bolus injections of noradrenaline (1 and 10 nmol) increased the perfusion pressure in a dose-dependent manner. Nifedipine (1 microM) inhibited the increase in pressure produced by 1 nmol noradrenaline by 31 +/- 5%. Niflumic acid (10 and 30 microM) also inhibited the noradrenaline-induced increase in perfusion pressure and 30 microM niflumic acid reduced the pressor response to 1 nmol noradrenaline by 34 +/- 6%. 3. The increases in perfusion elicited by 5-HT (0.3 and 3 nmol) were reduced by niflumic acid (10 and 30 microM) in a concentration-dependent manner and 30 microM niflumic acid inhibited responses to 0.3 and 3 nmol 5-HT by, respectively, 49 +/- 8% and 50 +/- 7%. Nifedipine (1 microM) decreased the pressor response to 3 nmol 5-HT by 44 +/- 9%. 4. In the presence of a combination of 30 microM niflumic acid and 1 microM nifedipine the inhibition of the pressor effects of noradrenaline (10 nmol) and 5-HT (3 nmol) was not significantly greater than with niflumic acid (30 microM) alone. Thus the effects of niflumic acid and nifedipine were not additive. 5. In Ca-free conditions the transient contractions induced by 5-HT (3 nmol) were not reduced by 30 microM niflumic acid, suggesting that this agent does not inhibit calcium release from the intracellular store or the binding of 5-HT to its receptor. 6. Niflumic acid 30 microM did not inhibit the pressor responses induced by KCl (20 and 60 mumol) which were markedly reduced by 1 microM nifedipine. In addition, 1 microM levcromakalim decreased pressor responses produced by 20 mumol KCl. These data suggest that niflumic acid does not block directly calcium channels or activate potassium channels. 7. It is concluded that niflumic acid selectively reduces a component of noradrenaline- and 5-HT-induced pressor responses by inhibiting a mechanism which leads to the opening of voltage-gated calcium channels. Our data suggest that the Ca(2+)-activated chloride conductance may play a pivotal role in the activation of voltage-gated calcium channels in agonist-induced constriction of resistance blood vessels.