Carbon dioxide:Global warning for nephrologists

The large prevalence of respiratory acid-base disordersoverlapping metabolic acidosis in hemodialysis popu-lation should prompt nephrologists to deal with the partial pressure of carbon dioxide （pCO2） complying with the reduced bicarbonate concentration. What the most suitable formula to compute pCO2 is reviewed. Then, the neglected issue of CO2 content in the dialysis fluid is under the spotlight. In fact, a considerable amount of CO2 comes to patients’ bloodstream every hemodialysis treatment and “acidosis by dialysate” may occur if lungs do not properly clear away this burden of CO2. Moreover, vascular access recirculation may be easy diagnosed by detecting CO2 in the arterial line of extracorporeal circuit if CO2-enriched blood from the flter reenters arterial needle.

Respiratory Control by Phox2b-expressing Neurons in a Locus Coeruleus–pre B?tzinger Complex Circuit

The locus coeruleus(LC) has been implicated in the control of breathing.Congenital central hypoventilation syndrome results from mutation of the paired-like homeobox 2 b(Phox2 b) gene that is expressed in LC neurons.The present study was designed to address whether stimulation of Phox2 b-expressing LC(Phox2 b~(LC)) neurons affects breathing and to reveal the putative circuit mechanism.A Cre-dependent viral vector encoding a Gqcoupled human M3 muscarinic receptor(hM3 Dq) was delivered into the LC of Phox2 b-Cre mice.The hM3 Dqtransduced neurons were pharmacologically activated while respiratory function was measured by plethysmography.We demonstrated that selective stimulation of Phox2 b~(LC) neurons significantly increased basal ventilation in conscious mice.Genetic ablation of these neurons markedly impaired hypercapnic ventilatory responses.Moreover,stimulation of Phox2 b~(LC) neurons enhanced the activity of preBotzinger complex neurons.Finally,axons of Phox2 b~(LC) neurons projected to the preBotzinger complex.Collectively,Phox2 b~(LC) neurons contribute to the control of breathing most likely via an LC-preBotzinger complex circuit.

Inwardly rectifying potassium channel 5.1:Structure,function,and possible roles in diseases

Inwardly rectifying potassium(Kir)channels make it easier for K^(+)to enter into a cell and subsequently regulate cellular biological functions.Kir5.1(encoded by KCNJ16)alone can form a homotetramer and can form heterotetramers with Kir4.1(encoded by KCNJ10)or Kir4.2(encoded by KCNJ15).In most cases,homomeric Kir5.1 is non-functional,while hetero-meric Kir5.1 on the cell membrane contributes to the inward flow of K^(+)ions,which can be regulated by intracellular pH and a variety of signaling mechanisms.In the form of a heterotetramer,Kir5.1 regulates Kir4.1/4.2 activity and is involved in the maintenance of nephron function.Actually,homomeric Kir5.1 may also play a very important role in diseases,including in the ventilatory response to hypoxia and hypercapnia,hearing impairment,cardio-vascular disease and cancer.With an increase in the number of studies into the roles of Kir channels,researchers are paying more attention to the pathophysiological functions of Kir5.1.This minireview provides an overview regarding these Kir5.1 roles.