Postoperative improvement of hypertension in primary aldosteronism and Cushing's syndrome.

In 24 cases of primary aldosteronism and 30 cases of Cushing's syndrome, the incidence of preoperative hypertension and postoperative improvement of hypertension was investigated. All the cases of primary aldosteronism showed preoperative hypertension. Postoperative improvement of hypertension was observed in 21 out of those 24 cases. In 14 of these 21 cases, hypertension improved within 1 month postoperatively. In Cushing's syndrome, 23 out of 30 cases showed preoperative hypertension which improved in 20 cases postoperatively. They needed longer periods of time before improvement of hypertension than the cases of primary aldosteronism. The pathological findings in renal biopsy specimens seem to be correlated with postoperative improvement of hypertension in both diseases.     

Mediators involved in decreasing peripheral vascular resistance with carbachol in the rat hind limb perfusion model

We examined the involvement of nitric oxide (NO) and/or endothelium-derived hyperpolarizing factor (EDHF) in decreasing peripheral vascular resistance in the rat hind limb perfusion model and analyzed the identity of EDHF in this model. The potency of carbachol (CCh) to produce relaxation was quantitatively similar to sodium nitroprusside (SNP). CCh-induced relaxation was abolished after endothelial denudation, but resistant to nitroarginine and indomethacin. The relaxation was inhibited by tetraethylammonium, ouabain, charybdotoxin plus apamin, and under depolarization. SNP-induced relaxation was accompanied by increased cGMP production, which was inhibited by ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-l-one). Although CCh produced a similar extent of relaxation to SNP, the cGMP level was 24 times lower than that with SNP. Low KCl produced a definite relaxation, which was inhibited by ouabain, but independent of NO, prostacyclin, and endothelium. 1-EBIO (1-ethyl-2-benzimidazolinone) as an activator of IK(Ca) channel also produced a concentration-dependent relaxation, which was inhibited by charybdotoxin, ouabain, and depolarization, but independent of NO and prostacyclin. Clotrimazole and 17-octadecynoic acid as inhibitors of P(450) monooxygenase inhibited the CCh-induced relaxation. Meanwhile, catalase at a concentration sufficient to inhibit H(2)O(2)-induced relaxation did not exert definite inhibition of the CCh-induced relaxation. These results suggest that CCh produces an endothelium-dependent, EDHF-dependent, and NO-cGMP-independent relaxation and that K(+) and metabolite(s) of P(450) monooxygenase possibly play an important role for this relaxation.     

Strongest correlation of HbA(1c) with 1-month-earlier glucose levels in type 2 diabetes

We examined the correlations of hemoglobin A(1c) (HbA(1c)) with each plasma glucose (PG) level obtained at 0 (the same day), 1 and 2 month(s) prior to HbA(1c) determination. Data were from glycemic profiles of four patients of type 2 diabetes mellitus treated with tablets whose HbA(1c) and pre- and post-breakfast PG levels were monitored each month. There was no significant difference in the correlation coefficients in cases 1 and 2, who presented with linear glycemic time courses. In contrast, HbA(1c) correlated with 1-month-earlier pre-breakfast PG level more strongly than 2-month-earlier post-breakfast PG level in cases 3 and 4, and than same-day post-breakfast PG level in case 3 (P<0.05, ANOVA). The cases 3 and 4 presented with fluctuating glycemic time courses. Samples were separated into upslope's and downslope's sections according to HbA(1c) fluctuation in the latter two cases. Reflecting around the 1-month lag between HbA(1c) and PG, the two sections' regression lines for PG versus HbA(1c) corresponded in the only samples related to 1-month-earlier pre- and post-breakfast PG (t-test). In conclusion, it appears that pre- and post-breakfast PG levels are the most reliable predictors of 1-month-later HbA(1c) in type 2 diabetic outpatients who undergo medical examinations every month.