Effects of single dose and cbronic administration of nitrendipine on arterial pressure. plazma renin activity (PRA). glomerular filtration rate (GFR) in essential hypertension

Bu çalışmada esansiyel hipertansiyonlu olgularda kalsiyum kanal blokerleri Nitrendipin 'in tek doz ve kronik (5 gün) kullanımının sistemik arter basıncı, plazma renin aktivitesi (PRA), aldosteron düzeyi, serum elektrolitleri ve glomerüler filtrasyon hızına (GFR) etkileri araştırıldı. 31 hafif ve orta esansiyel hipertansiyonlu olguda 20 mg tek doz oral Nitrendipin alımından 1 saat sonra sistolik ve diastolik kan basıncında anlamlı düşme gözlendi. Nitrendipin 'in sistolik ve diastolik basınçtaki antihipertansif etkisi takip süresi olan 24 saat boyunca devam etti. Tek doz ve kronik kullanımda PRA, Aldosteron serum elektrolitleri ve GFR de herhangi bir değişiklik saptanmadı. % 88 olguda tedavi periyodu sonunda arteriyel kan basıncı ideal düzeylere düştü. Nitrendipin tedavisi alan 31 olgunun 4'ünde baş ağrısı, 3'ünde klinik taşikardi, l'inde de flushing gözlendi. Sonuç olarak esansiyel hipertansiyonlu olgularda kalsiyum kanal blokeri Nitrendipin 'in 20 mg tek doz kullanımı ile oral alımdan I saat sonra antihipertansif etkinin başladığı, bu etkinin 24 saat devam ettiği, tedavi periyodunda ilacın iyi tolere edebildiği, akut ve kronik kullanım döneminde serum elektrolitleri, PRA. Aldosteron düzeylerinin ve GFR değerinin etkilenmediği kanısına varılmıştır.Effects of single dose and chronic (five days) administration of Nitrendipine (20 mg) on systemic arterial pressure, Plasma Renin Activity, Serum Na+, K+, Cr, üric acid, ürea, creatinine, glukoz, Aldosterone levels and Glomerular Filtration Rate have been investigated. A significant decrease was observed in systolic and diastolic blood pressure I hour after the oral administration of Nitrendipine in 31 patients with mild or moderate essential hypertension. Furtlter more, in on observation period of 24 hours. It was also established that the effects of Nitrendipine on systolic and diastolic blood pressure sustained. In 27 of 31 patients (% 88), a diastolic pressure 90 mmHg was achieved in the long-tenn treatment. No change was observed in plasma renin activity, serum Na+, K+, cı+, üric acid, Aldosteron, ürea, creatinin, glucose levels and GFR after single dose and chronic administration of Nitrendipine

Platelet-T cell aggregates in lung cancer patients: Implications for thrombosis.

Platelet-leukocyte aggregates (PLAs) are associated with increased thrombosis risk. The influence of PLA formation is especially important for cancer patients, since thrombosis accounts for approximately 10% of cancer-associated deaths. Our objective was to characterize and quantify PLAs in whole blood samples from lung cancer patients compared to healthy volunteers with the intent to analyze PLA formation in the context of lung cancer-associated thrombosis. Consenting lung cancer patients (57) and healthy volunteers (56) were enrolled at the Dana Cancer Center at the University of Toledo Health Science Campus. Peripheral blood samples were analyzed by flow cytometry. Patient medical history was reviewed through electronic medical records. Most importantly, we found lung cancer patients to have higher percentages of platelet-T cell aggregates (PTCAs) than healthy volunteers among both CD4+ T lymphocyte and CD8+ T lymphocyte populations. Our findings demonstrate that characterization of PTCAs may have clinical utility in differentiating lung cancer patients from healthy volunteers and stratifying lung cancer patients by history of thrombosis

Targeted disruption of Cd40 in a genetically hypertensive rat model attenuates renal fibrosis and proteinuria, independent of blood pressure

High blood pressure is a common cause of chronic kidney disease. Because CD40, a member of the tumor necrosis factor receptor family, has been linked to the progression of kidney disease in ischemic nephropathy, we studied the role of Cd40 in the development of hypertensive renal disease. The Cd40 gene was mutated in the Dahl S genetically hypertensive rat with renal disease by targeted-gene disruption using zinc-finger nuclease technology. These rats were then given low (0.3%) and high (2%) salt diets and compared. The resultant Cd40 mutants had significantly reduced levels of both urinary protein excretion (41.8 ± 3.1 mg/24 h vs. 103.7 ± 4.3 mg/24 h) and plasma creatinine (0.36 ± 0.05 mg/dl vs. 1.15 ± 0.19 mg/dl), with significantly higher creatinine clearance compared with the control S rats (3.04 ± 0.48 ml/min vs. 0.93 ± 0.15 ml/min), indicating renoprotection was conferred by mutation of the Cd40 locus. Furthermore, the Cd40 mutants had a significant attenuation in renal fibrosis, which persisted on the high salt diet. However, there was no difference in systolic blood pressure between the control and Cd40 mutant rats. Thus, these data serve as the first evidence for a direct link between Cd40 and hypertensive nephropathy. Hence, renal fibrosis is one of the underlying mechanisms by which Cd40 plays a crucial role in the development of hypertensive renal disease