Vasoactive factors in the mechanism of renal sodium handling in cirrhotics: The effect of acute plasma expansion

Villa, Giorgio La; Pinzani, Massimo; Mannelli, Massimo; Buzzelli, G; Paladini, Stefanía; Pampana, Alessandro; Smorlesi, C; Pedretti, Giorgio; Geñtilini, Paolo

doi:10.1016/s0031-6989(84)80041-7

Cited by 2 publications

(4 citation statements)

References 36 publications

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“…Studies of cultured rat mesangial cells suggested that angiotensin II may activate PDE1 by increasing intracellular Ca 2+ and may contribute to increased hydrolysis of ANP‐stimulated cGMP pool in situ (Haneda et al 1991). These findings reinforce our present data, since it is established that the plasma level of angiotensin II is increased in liver cirrhosis (Schroeder et al 1970; Laffi et al 1984). Consequently, it is possible that PDE5 plays a prominent role at earlier stages of the disease, whereas at later stages PDE1 could become upregulated and contribute to regulation of renal function modifying the effects of ANP, in a manner similar to the association demonstrated for PDE1A1 expression and the development of nitrate tolerance (Kim et al 2001).…”

Section: Discussionsupporting

confidence: 93%

“…The reason DMPPO corrects the response to NG as well even when PDE5 is not upregulated is likely because of a cilostamide like effect of cGMP that accumulates as a result of PDE5 inhibition, causing inhibition of PDE3. As previous studies have shown an increase in the plasma level of prostacyclin which in turn raises cAMP in vascular tissue and can worsen the vasodilation and the hypotension related to the hyperdynamic circulation syndrome of liver cirrhosis (Laffi et al 1984;Blendis & Wong 2001), an increase in PDE3 activity could represent a compensatory mechanism to reduce cAMP accumulation and attenuate the vasodilatation. Interestingly, a significant decrease of PDE2 activity was also observed in aorta, related to endothelial cells underlining smooth muscle cells and controlling NO production, which could participate in an increase in NO production and ⁄ or in vasodilatation previously reported in cirrhotic rats (Atucha et al 2005).…”

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 97%

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PDEs1‐5 activity and expression in tissues of cirrhotic rats reveal a role for aortic PDE3 in NO desensitization

Tahseldar-Roumieh

Keravis

Maarouf

et al. 2009

Int J Experimental Path

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Liver cirrhosis is associated with increased nitric oxide (NO) production in the vasculature. We have previously demonstrated that aorta from rats with liver cirrhosis have a reduced relaxant response to NO donors that is corrected by DMPPO, a PDE5-specific inhibitor. Vasodilator responses to DMPPO itself were also reduced in rings from cirrhotic rats. These results supported previous suggestions that upregulation of PDE5 in liver cirrhosis might contribute to renal sodium retention, and consequently modulate vascular reactivity in the context of increased NO production (Tahseldar-Roumieh et al. in Am. J. Physiol. Heart Circ. Physiol. 290, H481-H488, 2006). Here, we investigated the possible alteration in activity and expression of cyclic nucleotide phosphodiesterase PDE1-PDE5 in kidney and vascular tissues in rats 4 weeks after bile duct ligation. The kidney of rats with cirrhosis had increased activity of PDE1 and PDE4 but not PDE5, and increased expression of PDE1A. Unexpectedly and interestingly, there was no change in cirrhotic aorta PDE5, but an increase in PDE3 and PDE4 activity associated with increased expression of PDE3A and PDE3B. Cilostamide, a specific PDE3 inhibitor, corrected the decreased response to an NO donor in isolated aorta from cirrhotic rats, suggesting that the difference in response to NO donors was due to differences in PDE3-induced hydrolysis of cGMP or to cGMP-induced inhibition of PDE3, rather than to differences in PDE5 contribution. In conclusion, these changes in PDE isozymes could greatly contribute to NO desensitization and to the regulation of vascular and renal function in liver cirrhosis.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 97%

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PDEs1‐5 activity and expression in tissues of cirrhotic rats reveal a role for aortic PDE3 in NO desensitization

Tahseldar-Roumieh

Keravis

Maarouf

et al. 2009

Int J Experimental Path

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“…Previous studies using a variety of nonspecific enzy matic assays have found that urinary kallikrein excretion was either decreased, unchanged or increased in patients with liver disease [27][28][29][30][31][32][33][34][35]. Comparison of our data with these studies is difficult.…”

Section: Discussionmentioning

confidence: 59%

The Kallikrein-Kininogen-Kinin System in Patients with Liver Disease and Ascites

Solomon

Azar

Trebbin

et al. 1988

Nephron

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The urinary excretion of kininogen, kallikrein (total and active), and kinins were measured in 7 men with severe liver disease and ascites. The results were compared with a group of normal controls matched for sodium excretion. Significant reductions in kinin excretion were noted in the patients with liver disease which could not be accounted for by differences in age, plasma renin, aldosterone excretion or sodium excretion. Both active kallikrein and kininogen excretion were reduced suggesting that deficiencies of enzyme and substrate contributed to the kinin deficiency. The importance of kininogen in the physiologic regulation of kinin excretion in this clinical state is discussed.

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Vasoactive factors in the mechanism of renal sodium handling in cirrhotics: The effect of acute plasma expansion

Cited by 2 publications

References 36 publications

PDEs1‐5 activity and expression in tissues of cirrhotic rats reveal a role for aortic PDE3 in NO desensitization

PDEs1‐5 activity and expression in tissues of cirrhotic rats reveal a role for aortic PDE3 in NO desensitization

The Kallikrein-Kininogen-Kinin System in Patients with Liver Disease and Ascites

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