D. G. Shirley

The role of vasopressin in blood pressure regulation immediately following acute haemorrhage in the rat

1. The possible pressor effect of vasopressin immediately after acute haemorrhage has been studied using anaesthetized Brattleboro rats with diabetes insipidus and rats of the Long Evans parent strain.

TRANSEPITHELIAL ELECTROCHEMICAL GRADIENTS IN THE PROXIMAL CONVOLUTED TUBULE DURING POTASSIUM DEPLETION IN THE RAT

1 In order to examine the electrochemical gradient for potassium reabsorption across the S2 segment of the proximal convoluted tubule, transepithelial potential differences and transepithelial potassium concentrations were measured in anaesthetized potassium‐replete and potassium‐depleted rats. 2 Potassium‐depleted rats were markedly hypokalaemic (plasma potassium, 1.4 ± 0.1 vs. 4.1 ± 0.1 mmol l−1 in potassium‐replete rats) and had a significantly reduced muscle potassium content. In confirmation of previous reports, glomerular filtration rate was slightly reduced, while fractional reabsorption in the proximal convoluted tubule was enhanced. 3 In potassium‐replete animals, the transepithelial potential difference (PD) at the late proximal convoluted tubule was +2.1 ± 0.3 mV (lumen positive) and the tubular fluid to plasma ultrafiltrate concentration ratio for potassium (TFK/UFK) at the same site was 1.03 ± 0.01. In potassium‐depleted rats, there was a striking reversal of the transepithelial PD (to −4.0 ± 0.4 mV), while the TFK/UFK was increased to 1.19 ± 0.03. 4 The data from both potassium‐replete and potassium‐depleted animals are consistent with accumulating evidence that potassium reabsorption in the proximal convoluted tubule is passive in nature and depends partly on diffusion down an electrochemical gradient.

Contribution of Na+‐H+ exchange to sodium reabsorption in the loop of Henle: a microperfusion study in rats

1 The contribution of apical Na+‐H+ exchange to sodium reabsorption in the thick ascending limb of the loop of Henle (TALH) in vivo was examined in anaesthetized rats by perfusing loops of Henle of superficial nephrons with solutions containing the Na+‐H+ exchange inhibitor, ethyl isopropyl amiloride (EIPA). 2 Using a standard perfusate, no statistically significant effect of EIPA on net sodium reabsorption (JNa) was detected. However, when sodium reabsorption in the pars recta of the proximal tubule was minimized by using a low‐sodium perfusate, EIPA reduced JNa from 828 ± 41 to 726 ± 37 pmol min−1 (P < 0.05), indicating that apical Na+‐H+ exchange can make a small contribution to net sodium reabsorption in the TALH in vivo. This contribution appears to be dependent on the bicarbonate load, since an increase in the latter led to an enhancement of EIPA‐sensitive sodium transport. 3 Addition of the Na+‐K+‐2Cl− cotransport inhibitor, bumetanide, to the low‐sodium perfusate reduced baseline JNa to 86 ± 27 pmol min−1. In this setting, EIPA reduced JNa further, to −24 ± 18 pmol min−1 (P < 0.05), an effect similar to that seen in the absence of bumetanide. This finding argues against previous suggestions (based on in vitro evidence) that inhibition of the Na+‐K+‐2Cl− cotransporter leads to an increase in apical Na+‐H+ exchange in the TALH.