In the West, as in Asia, patients with cirrhosis of the liver are at substantial risk for hepatocellular carcinoma, with a yearly incidence rate of 3 percent. Our screening program did not appreciably increase the rate of detection of potentially curable tumors.

Abstract-Remodeling of the resistance arteries is a hallmark of arterial hypertension and predicts cardiovascular events, but it was unknown whether it could also predict the blood pressure response to adrenalectomy of patients with an aldosterone-producing adenoma. Therefore, we investigated the outcome of adrenalectomy as a function of vascular remodeling in the context of the preoperative features of aldosterone-producing adenoma patients. At 2 referral centers for hypertension, we prospectively measured the media:lumen ratio of small arteries from fat tissue of 50 consecutive aldosterone-producing adenoma patients treated with adrenalectomy. The blood pressure response to adrenalectomy was assessed by considering the blood pressure values and the number and dosages of antihypertensive medications. Adrenalectomy significantly (PϽ0.001) lowered plasma aldosterone (from 27.3Ϯ4.9 ng/dL to 8.3Ϯ11.2 ng/dL), the aldosterone:renin ratio (from 117Ϯ35 to 11Ϯ2), and blood pressure (from 163Ϯ22/98Ϯ2 mm Hg to 133Ϯ2/ 84Ϯ1 mm Hg), even despite a reduction (from 141Ϯ14 to 100Ϯ15; Pϭ0.02) of the score of antihypertensive treatment.It provided cure of hypertension in 30% of the aldosterone-producing adenoma patients, normotension with less antihypertensive therapy in 52%, and improved blood pressure control in the rest. The media:lumen ratio and the known duration of hypertension significantly predicted the blood pressure response to adrenalectomy at univariate and multivariate analyses. Because a long duration of hypertension and/or the presence of vascular remodeling imply lower chances of blood pressure normalization at long-term follow-up postadrenalectomy, these findings emphasize the importance of an early diagnosis of aldosterone-producing adenoma. Key Words: secondary hypertension Ⅲ aldosterone Ⅲ aldosteronism Ⅲ adrenalectomy Ⅲ outcome Ⅲ vascular remodeling P rimary aldosteronism (PA) is far more common than usually perceived and is attributable to an aldosteroneproducing adenoma (APA) in approximately half of the patients. 1 Thus, it entails the most common endocrine form of secondary arterial hypertension (HT) that is curable by adrenalectomy in many patients. 2 Identification of an APA, or unilateral primary adrenocortical hyperplasia, 3 requires adrenal vein sampling (AVS) that, being minimally risky, should be reserved for patients who are candidates for adrenalectomy and, more importantly, can benefit from it. 4 However, the identification of patients who will benefit more remains a challenging task, because the blood pressure (BP) response to adrenalectomy varies widely across patients. In fact, despite many efforts over the years, only age and lack of family history of HT were suggested to significantly predict the BP response. 5-8 Nevertheless, the large uncertainties in the prediction estimates render them of little, if any, 8 value on an individual basis.The remodeling of resistance arteries is a hallmark of arterial HT and can be implicated in the excess cardiovascular damage associated with HT. Hence, it ...

Large-conductance calcium-activated potassium channels (BK Ca s) are important regulators of arterial tone and represent a mediator of the endogenous vasodilator carbon monoxide (CO). Because an up-regulation of the heme oxygenase (HO)/CO system has been associated with mesenteric vasodilatation of cirrhosis, we analyzed the interactions of BK Ca and of HO/CO in the endothelium-dependent dilatation of mesenteric arteries in ascitic cirrhotic rats. In pressurized mesenteric arteries (diameter, 170 -350 m) of ascitic cirrhotic rats, we evaluated the effect of inhibition of BK Ca , HO, and guanylylcyclase on dilatation induced by acetylcholine and by exogenous CO; and HO-1 and BK Ca subunit protein expression. Inhibition of HO and of BK Ca reduced acetylcholine-induced vasodilatation more in cirrhotic rats than in control rats, whereas inhibition of guanylyl-cyclase had a similar effect in the two groups. CO was more effective in cirrhotic rats than in control rats, and the effect was hindered by BK Ca inhibition. The expression of HO-1 and of BK Ca ␣-subunit was higher in mesenteric arteries of cirrhotic rats compared with that of control animals, whereas the expression of the BK Ca ␤1-subunit was lower. In conclusion, an overexpression of BK Ca ␣-subunits, possibly due to HO up-regulation with increased CO production, participates in the endothelium-dependent alterations and mesenteric arterial vasodilatation of ascitic cirrhotic rats.Mesenteric arterial vasodilation is a key mechanism in the pathophysiology of the hyperdynamic circulatory syndrome of cirrhosis. This syndrome is responsible for serious complications, such as ascites, hepatorenal syndrome, and gastrointestinal hemorrhage. The pathophysiological mechanism that supports the vasodilation of mesenteric arteries in cirrhosis is a decrease in the response of the arteries to vasoconstricting agents (Sieber et al., 1993), caused by an increase in vasodilating substances of endothelial origin, such as nitric oxide (NO), prostacyclin, and, as recently demonstrated, carbon monoxide (CO) (Wiest and Groszmann, 1999;Fernandez et al., 2001;Gonzales-Abraldes et al., 2002).We have recently shown that an increased action of the heme oxygenase (HO)/CO system plays a role in the hyporesponsiveness of small resistance mesenteric arteries to phenylephrine (PE) only in the advanced stage of experimental cirrhosis (Bolognesi et al., 2005). Therefore, the increased activity of the HO/CO system may participate in the evolution of cirrhosis from compensated to decompensated.HO is a microsomal enzyme with two main distinct isoforms: the inducible isoenzyme HO-1 and the constitutive one HO-2 (Zhang et al., 2001;Johnson et al., 2003a). It is the rate-limiting enzyme in the degradation of heme to biliverdin, CO, and free iron (Motterlini et al., 1998). CO, generated by HO in endothelial and smooth muscle layers of arterial vessels, modulates vascular tone by inducing relaxation of vascular smooth muscle cells through stimulation on soluble guanylyl cyclase (sGC) and ope...

The GTE prevented hypertension and target organ damage induced by a high Ang II dose, likely by prevention or scavenging of superoxide anion generation.

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