BACKGROUND: It is unclear whether impaired pulmonary function serves as a risk factor for decreased renal function. This study investigated the association between the forced vital capacity (FVC) and chronic kidney disease (CKD) in middle-aged and elderly men.METHODS: We investigated the association between FVC and CKD in 412 Korean men aged ≥50 years, without diabetes, who have not received treatment for chronic lung disease. CKD was defined based on evidence of renal tissue damage or reduced renal function indicated by estimated glomerular filtration rate < 60 mL/min/1.73 m² or proteinuria level ≥1+. We assessed the association between FVC and CKD using multivariate logistic regression analysis after adjusting for confounders.RESULTS: The overall prevalence of CKD was 29.2% in the study population. Multivariate logistic regression analysis showed that the odds ratio with a 95% confidence interval for CKD was 0.96 (0.92–0.99) with a 1% increment in FVC after adjusting for age, body mass index, smoking status, alcohol intake, regular exercise, systolic and diastolic blood pressures, fasting plasma glucose, triglyceride, and high-density lipoprotein-cholesterol levels, as well as antihypertensive and antidyslipidemic medications.CONCLUSION: We observed that FVC was independently and inversely associated with CKD. This finding suggests that careful monitoring of renal function is necessary to evaluate possible kidney dysfunction in patients with decreased FVC.
Aged ; Blood Glucose ; Body Mass Index ; Fasting ; Glomerular Filtration Rate ; Humans ; Kidney ; Logistic Models ; Lung Diseases ; Male ; Odds Ratio ; Prevalence ; Proteinuria ; Renal Insufficiency, Chronic ; Respiratory Function Tests ; Risk Factors ; Smoke ; Smoking ; Triglycerides ; Vital Capacity

We investigated the inhibitory effect of escitalopram, a selective serotonin reuptake inhibitor (SSRI), on voltage-dependent K⁺ (Kv) channels in freshly separated from rabbit coronary arterial smooth muscle cells. The application of escitalopram rapidly inhibited vascular Kv channels. Kv currents were progressively inhibited by an increase in the concentrations of escitalopram, suggesting that escitalopram inhibited vascular Kv currents in a concentration-dependent manner. The IC₅₀ value and Hill coefficient for escitalopram-induced inhibition of Kv channels were 9.54±1.33 µM and 0.75±0.10, respectively. Addition of escitalopram did not alter the steady-state activation and inactivation curves, suggesting that the voltage sensors of the channels were not affected. Pretreatment with inhibitors of Kv1.5 and/or Kv2.1 did not affect the inhibitory action of escitalopram on vascular Kv channels. From these results, we concluded that escitalopram decreased the vascular Kv current in a concentration-dependent manner, independent of serotonin reuptake inhibition.
Citalopram* ; Coronary Vessels ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Serotonin*

We demonstrated the effect of nortriptyline, a tricyclic antidepressant drug and serotonin reuptake inhibitor, on voltage-dependent K⁺ (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells using a whole-cell patch clamp technique. Nortriptyline inhibited Kv currents in a concentration-dependent manner, with an apparent IC₅₀ value of 2.86±0.52 µM and a Hill coefficient of 0.77±0.1. Although application of nortriptyline did not change the activation curve, nortriptyline shifted the inactivation current toward a more negative potential. Application of train pulses (1 or 2 Hz) did not change the nortriptyline-induced Kv channel inhibition, suggesting that the effects of nortiprtyline were not use-dependent. Preincubation with the Kv1.5 and Kv2.1/2.2 inhibitors, DPO-1 and guangxitoxin did not affect nortriptyline inhibition of Kv channels. From these results, we concluded that nortriptyline inhibited Kv channels in a concentration-dependent and state-independent manner independently of serotonin reuptake.
Coronary Vessels ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Nortriptyline* ; Serotonin