Role of nitric oxide in hyporeactivity to noradrenaline of isolated aortic rings in portal hypertensive rats

Michielsen, P.; Boeckxstaens, Guy E.; Sys, Stanislas U.; Herman, Arnold G.; Pelckmans, Paul

doi:10.1016/0014-2999(94)00691-y

“…In rat aorta, there are reports that nitric oxide synthase inhibitors failed to restore responses to normal in portal hypertensive animals [26] or that nitric oxide synthase inhibitors restored responses to normal in portal hypertensive [27] and cirrhotic animals [28]. Removal of the endothelium failed to restore responses in portal hypertensive [29] and cirrhotic animals [28], but was found in another study to restore responses in aorta from cirrhotic animals [30].…”

Section: Strain Days Agonistmentioning

confidence: 83%

Portal hypertension increases vasoconstrictor responsiveness of rat aorta

Connolly

¹

,

Cawley

²

,

McCormick

³

et al. 1999

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We have examined the effects of pre-hepatic portal hypertension on the responsiveness of aorta from Wistar and Sprague-Dawley rats. Rats were made portal hypertensive by creating a calibrated portal vein stenosis, or sham operated. In rat aorta, there was no significant difference between portal hypertensive and sham-operated animals in the contractile potency of KCl, noradrenaline or phenylephrine. In aortas from Wistar rats, the maximum response to KCl (0.71+/-0.12 g) and noradrenaline (1.00+/-0.17 g) but not phenylephrine (0.86+/-0.10 g) in portal hypertensive animals was significantly increased compared with that in sham-operated animals (0.45+/-0.04 g, 0.57+/-0.07 g, 0.71+/-0.05 g respectively). In aortas from Sprague-Dawley rats, the maximum response to KCl (1. 21+/-0.21 g) and phenylephrine (1.54+/-0.30 g) but not noradrenaline (0.93+/-0.09 g) in portal hypertensive animals was significantly increased compared with that in sham-operated animals (0.59+/-0.09 g, 0.76+/-0.11 g, 1.04+/-0.10 g respectively). There was no difference between portal hypertensive and sham-operated Wistar rats in the affinity or maximum number of binding sites for [3H]prazosin to alpha1-adrenoceptors in cardiac ventricular membranes. It is concluded that portal hypertension tends to produce an increase rather than a decrease in the contractile response to vasoconstrictors in aorta from both Wistar and Sprague-Dawley rats. This suggests that the diminished responsiveness to vasoconstrictors reported in portal hypertensive rats in vivo is not due to a diminished responsiveness at the level of the vascular smooth muscle.

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“…Different studies give evidence that either NOS (36,37) or iNOS (6,38) or even both enzymes (39) are responsible for excessive NO release. The crucial question arises: Which factor(s) stimulates NOS enzymes already at an early stage of cirrhosis?…”

Section: Discussionmentioning

confidence: 99%

“…There is evidence that nitric oxide plays a major role in vascular hyporeactivity (6,(8)(9)(10) and the hyperdynamic circulatory state (11)(12)(13)(14), since these effects can be at least partly abolished by inhibitors of nitric oxide synthesis.…”

mentioning

confidence: 99%

Time Course-dependent Evolution of Nitric Oxide-mediated Arterial Hyporeactivity to Phenylephrine in Rats with Ligated Bile Duct

Kimpel

¹

,

Folz²,

Hanisch³

1998

Scandinavian Journal of Gastroenterology

9

0

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“…In rat aorta, there are reports that nitric oxide synthase inhibitors failed to restore responses to normal in portal hypertensive animals [26] or that nitric oxide synthase inhibitors restored responses to normal in portal hypertensive [27] and cirrhotic animals [28]. Removal of the endothelium failed to restore responses in portal hypertensive [29] and cirrhotic animals [28], but was found in another study to restore responses in aorta from cirrhotic animals [30].…”

Section: Strain Days Agonistmentioning

confidence: 96%

Portal hypertension increases vasoconstrictor responsiveness of rat aorta

CONNOLLY¹,

CAWLEY²,

MCCORMICK³

et al. 1999

View full text Add to dashboard Cite

We have examined the effects of pre-hepatic portal hypertension on the responsiveness of aorta from Wistar and Sprague-Dawley rats. Rats were made portal hypertensive by creating a calibrated portal vein stenosis, or sham operated. In rat aorta, there was no significant difference between portal hypertensive and sham-operated animals in the contractile potency of KCl, noradrenaline or phenylephrine. In aortas from Wistar rats, the maximum response to KCl (0.71+/-0.12 g) and noradrenaline (1.00+/-0.17 g) but not phenylephrine (0.86+/-0.10 g) in portal hypertensive animals was significantly increased compared with that in sham-operated animals (0.45+/-0.04 g, 0.57+/-0.07 g, 0.71+/-0.05 g respectively). In aortas from Sprague-Dawley rats, the maximum response to KCl (1. 21+/-0.21 g) and phenylephrine (1.54+/-0.30 g) but not noradrenaline (0.93+/-0.09 g) in portal hypertensive animals was significantly increased compared with that in sham-operated animals (0.59+/-0.09 g, 0.76+/-0.11 g, 1.04+/-0.10 g respectively). There was no difference between portal hypertensive and sham-operated Wistar rats in the affinity or maximum number of binding sites for [3H]prazosin to alpha1-adrenoceptors in cardiac ventricular membranes. It is concluded that portal hypertension tends to produce an increase rather than a decrease in the contractile response to vasoconstrictors in aorta from both Wistar and Sprague-Dawley rats. This suggests that the diminished responsiveness to vasoconstrictors reported in portal hypertensive rats in vivo is not due to a diminished responsiveness at the level of the vascular smooth muscle.

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Role of nitric oxide in hyporeactivity to noradrenaline of isolated aortic rings in portal hypertensive rats

Cited by 33 publications

References 42 publications

Portal hypertension increases vasoconstrictor responsiveness of rat aorta

Portal hypertension increases vasoconstrictor responsiveness of rat aorta

Time Course-dependent Evolution of Nitric Oxide-mediated Arterial Hyporeactivity to Phenylephrine in Rats with Ligated Bile Duct

Portal hypertension increases vasoconstrictor responsiveness of rat aorta

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