Ion transport in cortical collecting tubule; effect of amiloride

Lc, Stoner; Burg, M. B.; Orloff, Jack

doi:10.1152/ajplegacy.1974.227.2.453

Cited by 243 publications

(110 citation statements)

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“…It is difficult to define exactly the locus of the amiloride sensitive portion of the nephron in the new-born or adult dog. In the rabbit, it lies in the cortical collecting duct where amiloride inhibits 90 %/ of the sodium reabsorption (Stoner et al 1974). …”

Section: Resultsmentioning

confidence: 99%

“…Amiloride is a pyrazine diuretic which inhibits sodium reabsorption in the distal nephron (beyond the loop of Henle), particularly in the late distal and cortical collecting tubule (Baer, Jones, Spitzer & Russo, 1967;Duarte, Chomety & Giebisch, 1971;Guignard & Peters, 1970;Stoner, Burg & Orloff, 1974). Under normal conditions, amiloride inhibits the reabsoTption of approximately 2-3 % of the filtered sodium and at the same time inhibits the secretion of potassium.…”

Section: Introductionmentioning

confidence: 99%

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Effect of amiloride on the renal response to saline expansion in new‐born dogs.

Banks¹,

Kleinman²

1978

The Journal of Physiology

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SUMMARY1. The renal effects of amiloride were studied in twenty-six new-born and nine adult dogs, with and without saline expansion.2. Without saline expansion, amiloride inhibited more sodium reabsorption (normalized to GFR) in puppies than in adults (5.95 vs. 2-18 ,tequiv/ml. GFR, P < 0.01).Amiloride inhibited sodium reabsorption more in saline expanded than in nonexpanded puppies (9.39 vs. 5.95 #sequiv/ml. GFR, P < 0.01) but there was no difference between expanded and non-expanded adults.3. Saline expansion by itself increased fractional sodium excretion (CNa/GFR) more in the adult than in the puppy (0-071 vs. 0-019, P < 0-01). During amiloride inhibition, saline expansion increased CNa/GFR to 0*045 in the puppy (compared to 0X019 in the nonamiloride inhibited puppy) but saline expansion increased CNa/GFR to the same degree in the amiloride as in the non-amiloride inhibited adult. 4. In all puppies amiloride inhibited more sodium reabsorption than potassium secretion and there was poor correlation between the degree of inhibition of sodium reabsorption and potassium secretion for both the puppy (r = 0.14) and the adult (r = 0.05).5. Assuming that amiloride acts by inhibiting sodium reabsorption and potassium secretion in the late distal and cortical collecting tubules, these results support the conclusion that in these regions of the nephron of the new-born dog (a) a greater fraction of the filtered sodium is reabsorbed than in the adult and (b) increased fractional sodium reabsorption is responsible, in part, for the attenuated natriuretic response to saline expansion.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of amiloride on the renal response to saline expansion in new‐born dogs.

Banks¹,

Kleinman²

1978

The Journal of Physiology

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“…In the collecting duct, it was thought until recently that chloride is mostly absorbed passively because of the lumennegative transepithelial potential difference that results from ENaC-dependent electrogenic absorption of Na + . 22,23 As a consequence, most efforts have been made to dissect the mechanisms accounting for renal sodium absorption and its regulation, whereas the pathogenic effects of abnormal renal chloride transport have not been studied as extensively.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Pendrin in Intercalated Cells Produces Chloride-Sensitive Hypertension

Jacques

Picard

Miller

et al. 2013

Journal of the American Society of Nephrology

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Inherited and acquired disorders that enhance the activity of transporters mediating renal tubular Na + reabsorption are well established causes of hypertension. It is unclear, however, whether primary activation of an Na + -independent chloride transporter in the kidney can also play a pathogenic role in this disease. Here, mice overexpressing the chloride transporter pendrin in intercalated cells of the distal nephron (Tg B1-hPDS mice) displayed increased renal absorption of chloride. Compared with normal mice, these transgenic mice exhibited a delayed increase in urinary NaCl and ultimately, developed hypertension when exposed to a high-salt diet. Administering the same sodium intake as NaHCO 3 instead of NaCl did not significantly alter BP, indicating that the hypertension in the transgenic mice was chloride-sensitive. Moreover, excessive chloride absorption by pendrin drove parallel absorption of sodium through the epithelial sodium channel ENaC and the sodium-driven chloride/bicarbonate exchanger (Ndcbe), despite an appropriate downregulation of these sodium transporters in response to the expanded vascular volume and hypertension. In summary, chloride transport in the distal nephron can play a primary role in driving NaCl transport in this part of the kidney, and a primary abnormality in renal chloride transport can provoke arterial hypertension. Thus, we conclude that the chloride/bicarbonate exchanger pendrin plays a major role in controlling net NaCl absorption, thereby influencing BP under conditions of high salt intake.

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“…As pyrazine carboxamides have natriuretic activity on the kidney by an action on the luminal border of the distal nephron (Cragoe, Woltersdorf, Bicking, Kwong & Jones, 1967;Stoner, Burg & Orloff, 1974) (Stoner et al 1974). Frusemide (100 /sM) and N-methylnicotinamide (10 mM) had no effect suggesting that binding activity was not associated with chloride reabsorption in the loop of Henle and was not due to the organic base carrier.…”

Section: Wmaieanddmentioning

confidence: 99%

Communications

1979

The Journal of Physiology

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The total active transport of Cl ions across the frog's gastric mucosa can be considered as:net Cl-flux (serosa to mucosa) = H+ + SCC (short-circuit current), all terms expressed as usmole cm-2 hr-. 25PPROCEEDINGS OF THE The net chloride flux (Hogben, 1955; Durbin & Heinz, 1958) may be divided into two fractions: an acidic one which is equivalent to the acid secreted and an electromotive one which accounts for the gastric electromotive force. The changes in SCC can accordingly be used as a partial index to the activity of the chloride pump.Experiments were designed to investigate the effects of histamine, metiamide (H2 receptor antagonist), cystic fibrosis (CF) and non-CF plasma on the above parameters using the frog's isolated gastric mucosa.The SCC and the resistance of the mucosal preparation is measured by means of an automatic SCC apparatus (de Jesus, 1977).The H ion secretion is measured by pH meter.Results obtained (expressed as mean change (A)+ ±.E. of mean) for histamine (10-4 M) (n = 10) show an initial increase of the SCC by 36-94 + 2.95 1sA cm-2 and a parallel small increase in H+ output by 0-045 + 0-003 ,mole cm-2 hr-'. This initial increase in SCC is followed by a drop to a steady-state level of 23-62 + 2-23 1sA cm-2 and also by a large increase in H+ secretion 2-26 + 0-22 ,mole cm-2 hr-1.These results support the work of Rehm (1961) in that histamine has an effect first on the Cl-pump and then on the H+ secretion.Metiamide (10-4 M) (n = 12) caused a drop in the SCC by 20-16 + 2-32 HA cm-2 and also reduced the acid secretion by 2-21 + 0-14 ,mole cm-2 hr-1, thus suggesting an effect on the Cl-pump as well as on the H+ secretion.Significant differences are shown (P < 0-001) between CF and non-CF plasma results. The CF plasma (n = 8) increased the SCC by 17-25 ± 2-94 ,uA cm-2 and H+ secretion by 2-38 + 0 43 molee cm-2 hr-1. Non-CF plasma caused a slight increase in SCC by 5*17 + 1.1 ,uA cm-2 and had little effect on the H+ secretion, 0*34 + 0 01 jumole cm-2 hr'L (n = 8).The effect of the CF plasma on the Cl-and H+ mechanisms is of interest since in cystic fibrosis there is an abnormal increase of Cl-and Nat in the sweat of patients

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Ion transport in cortical collecting tubule; effect of amiloride

Cited by 243 publications

References 0 publications

Effect of amiloride on the renal response to saline expansion in new‐born dogs.

Effect of amiloride on the renal response to saline expansion in new‐born dogs.

Overexpression of Pendrin in Intercalated Cells Produces Chloride-Sensitive Hypertension

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