Renal failure is a medical condition in which the kidneys are not working properly. There are two types of kidney failure： 1） acute kidney failure, which is sudden and often reversible with adequate treatment; and 2...Renal failure is a medical condition in which the kidneys are not working properly. There are two types of kidney failure： 1） acute kidney failure, which is sudden and often reversible with adequate treatment; and 2） chronic renal failure, which develops slowly and often is not reversible. The last stage of chronic renal failure is fatal without dialysis or kidney transplant. The treatment for chronic renal failure is focusing on slowing the progression of kidney damage. Several reports have described a promising approach to slow the loss of renal function through inhibition of the basolateral membrane, Ca^2＋-activated K^＋ （KCa3.1） channel with a selective and nontoxic blocker TRAM-34. This review summarizes pathophysiological studies that describe the role of KCa3.1 in kidney diseases.展开更多
Background Recent studies have showed that perivascular adipose tissue （PVAT） may secrete the adventitial-derived relaxing factor （ADRF） to affect vascular function.However,the functional change of ADRF in hyperte...Background Recent studies have showed that perivascular adipose tissue （PVAT） may secrete the adventitial-derived relaxing factor （ADRF） to affect vascular function.However,the functional change of ADRF in hypertensive status is seldom studied;and the mechanisms of ADRF remain unclear.Our study examined the ADRF secreted by perivascular adipose tissue of control rats with normal blood pressure （Wistar Kyoto rats,WKY） and discussed the mechanisms of ADRF;We observed the functional change in ADRF of perivascular adipose tissue in spontaneously hypertensive rats （SHRs）.Method The two adjacent thoracic aorta rings of SHR and WKY rats were divided into naked vessel subgroup and PVAT subgroup.The differences of vascular contractility between the two subgroups induced by 10-6 mmol/L phenylephrine were compared.The effect of PVAT culture medium of WKY on the vascular tension of Fat （-） vessels was observed by liquid transfer measure.The mechanism of ADRF was determined by tool drugs.Results In WKY group,vascular contractility of Fat （＋） subgroup was lower than that of the Fat （-） subgroup （P 0.05）;while in SHR group,there was no difference between the two subgroups （P 0.05）.Transferring the incubation solution of WKY Fat （＋） subgroup to the matched Fat （-） subgroup induced rapid vasodilation.When incubating blood vessels in calcium free PSS solution,there was no significant difference of phenylephrine-induced vasoconstriction between Fat （-） and Fat （＋） subgroup.Both glibenclamide,the blocker of ATP-sensitive potassium （KATP） channel and Tetraethy-lammonium chloride （TEA）,the inhibitor of calcium-dependent potassium （KCa） channel,effectively inhibited vasodilation function of ADRF.Conclusions Perivascular adipose tissue in WKY releases ADRF which can cause vasodilation,while this function was inhibited in SHR.ADRF acts through the activation of KCa and KATP channels and calcium ion is involved.展开更多
文摘Renal failure is a medical condition in which the kidneys are not working properly. There are two types of kidney failure： 1） acute kidney failure, which is sudden and often reversible with adequate treatment; and 2） chronic renal failure, which develops slowly and often is not reversible. The last stage of chronic renal failure is fatal without dialysis or kidney transplant. The treatment for chronic renal failure is focusing on slowing the progression of kidney damage. Several reports have described a promising approach to slow the loss of renal function through inhibition of the basolateral membrane, Ca^2＋-activated K^＋ （KCa3.1） channel with a selective and nontoxic blocker TRAM-34. This review summarizes pathophysiological studies that describe the role of KCa3.1 in kidney diseases.
文摘Background Recent studies have showed that perivascular adipose tissue （PVAT） may secrete the adventitial-derived relaxing factor （ADRF） to affect vascular function.However,the functional change of ADRF in hypertensive status is seldom studied;and the mechanisms of ADRF remain unclear.Our study examined the ADRF secreted by perivascular adipose tissue of control rats with normal blood pressure （Wistar Kyoto rats,WKY） and discussed the mechanisms of ADRF;We observed the functional change in ADRF of perivascular adipose tissue in spontaneously hypertensive rats （SHRs）.Method The two adjacent thoracic aorta rings of SHR and WKY rats were divided into naked vessel subgroup and PVAT subgroup.The differences of vascular contractility between the two subgroups induced by 10-6 mmol/L phenylephrine were compared.The effect of PVAT culture medium of WKY on the vascular tension of Fat （-） vessels was observed by liquid transfer measure.The mechanism of ADRF was determined by tool drugs.Results In WKY group,vascular contractility of Fat （＋） subgroup was lower than that of the Fat （-） subgroup （P 0.05）;while in SHR group,there was no difference between the two subgroups （P 0.05）.Transferring the incubation solution of WKY Fat （＋） subgroup to the matched Fat （-） subgroup induced rapid vasodilation.When incubating blood vessels in calcium free PSS solution,there was no significant difference of phenylephrine-induced vasoconstriction between Fat （-） and Fat （＋） subgroup.Both glibenclamide,the blocker of ATP-sensitive potassium （KATP） channel and Tetraethy-lammonium chloride （TEA）,the inhibitor of calcium-dependent potassium （KCa） channel,effectively inhibited vasodilation function of ADRF.Conclusions Perivascular adipose tissue in WKY releases ADRF which can cause vasodilation,while this function was inhibited in SHR.ADRF acts through the activation of KCa and KATP channels and calcium ion is involved.
