Fluid reabsorption in Henle's loop and urinary excretion of sodium and water in normal rats and rats with chronic hypertension

Abstract

A B S T R A C T The function of the short loops of Henle was investigated by micropuncture technique in normal rats, in rats with spontaneous hypertension, and in the untouched kidney of rats with experimental renal hypertension. All animals received a standard infusion of 1.2 ml of isotonic saline per hr.With increasing arterial blood pressure (range from 90 to 220 mm Hg), a continuous decrease in transit time of Lissamine green through Henle's loop from 32 to 10 sec was observed. Fractional water reabsorption along the loop declined progressively from 26 to 10%, and fractional sodium reabsorption decreased from 40 to 36% of the filtered load. The fluid volume in Henle's loop calculated from transit time and mean flow rate also decreased with increasing blood pressure. There was no change in superficial single nephron filtration rate but there was a slight increase in total glomerular filtration rate (GFR). Sodium and water reabsorption in the proximal tubule remained unchanged.Urine flow rate, sodium excretion, osmolar clearance, and negative free water clearance increased with increasing blood pressure. The osmolal urine to plasma (U/P) ratio declined but did not fall below a value of 1.5. It is concluded that the increase in sodium and water excretion with chronic elevation of arterial blood pressure is caused by a decrease of sodium and water reabsorption along the loop of Henle, presumably as a consequence of increased medullary blood pressure. The following three groups of animals were used: (a) normal rats, (b) rats with a moderate spontaneous hypertension, and (c) rats with experimental hypertension 4-5 wk after clamping one renal artery with a Goldblatt clamp. In the last group, only the untouched kidney, which is exposed to the high blood pressure, was investigated. All animals received an isotonic saline infusion of 1.2 ml/hr. Micropuncture experiments were done on superficial nephrons. Accordingly, only the function of short loops of Henle was studied. METHODSThe experiments were performed on Albino rats of about the same weight (190-210 g). The animals were divided into three groups differing from each other by the level of arterial blood pressure. For the first group male rats-of the FW4, strain (Paderborn) were chosen, having a mean arterial blood pressure between 90 and 110 mm Hg. The second group consisted of female rats of the Wistar strain with a blood pressure from 110 to 160 mm Hg. In the third group female Wistar rats with experimental renal hypertension of 4-5 wk duration (for the method see reference 12, 13) were used, their blood pressure ranging from 160 to 220 mm Hg. In this last group only the untouched kidney exposed to the high arterial blood pressure was investigated. All animals were kept on the same standard rat diet (Altromin, sodium content: 1200 mg/kg) and had free access to water. The animals were anaesthetized by intraperitoneal injection of Inactin Hamburg,(70)(71)(72)(73)(74)(75)(76)(77)(78)(79)(80) mg/kg body weight) and prepared for micropuncture as previously describe...

Effects of Acute Volume Expansion and Altered Hemodynamics on Renal Tubular Function in Chronic Caval Dogs

“…Micropuncture data confirm that reabsorption of sodium and water in the loop of Henle was not maximally depressed until arterial blood pressure had been elevated. These findings are in agreement with recent observations in the rat by Bank, Aynedjian, Bansal, and Goldman (35) and Stumpe, Lowitz, and Ochwadt (36) and in saline-loaded hypertensive patients by Buckalew, Puschett, Kintzel, and Goldberg (37). These investigators have demonstrated that sodium transport by the ascending limb of the loop of Henle may be depressed by either acute or chronic elevations of arterial blood pressure.…”

“…Other workers have suggested the importance of either intrarenal humoral factors (35,36) or that the transmission of increased perfusion pressure to vasa rectae will interfere with the peritubular removal of reabsorbate in a manner similar to that thought to be operative for the proximal tubule (38).…”

Regulation of sodium balance in hypertension.

“…Most studies of regulation of sodium excretion in hypertension have been designed to explore the effect of volume-loading. *" 10 ' *° However, the natriuresis resulting from volume expansion is not the same as that resulting from increases in arterial pressure; in fact, these two stimuli increase sodium excretion by different mechanisms. 11 Hence, modulation of pressure natriuresis in hypertension can only be established by examining the effect on sodium excretion of alterations in arterial pressure per se.…”

Studies of the mechanism of contralateral polyuria after renal artery stenosis.

“…There was an increase in urinary sodium from 95±16 to 116±17 ueq/min (P < 0.01) but no rise in osmolar clearance, 1.46±0.2 before and 1.39±0.2 ml/min after renal artery stenosis. There was no change in renal blood flow; however, a small, but insignificant, decrease in glomerular filtration from 24.9±1.7 to 22.3±1.9 ml/min occurred after induction of renal hypertension. The fall in GFR accounted for the unchanged osmolar clearance in spite of the significant natriuresis.…”

“…Hypertension is known to be associated with an exaggerated natriuresis during volume expansion (23,24), and in rats with Goldblatt or spontaneous hypertension transit time, and fractional water absorption through the loop of Henle is decreased (24). With volume expansion hypertensive animals had a greater increase in urine volume, sodium excretion, osmolar clearance, and TCHZO which was felt to be caused by increased pressure in the medullary circulation decreasing sodium reabsorption in the loop of Henle.…”