The Distribution of Glutaminase Isoenzymes in the Various Structures of the Nephron in Normal, Acidotic, and Alkalotic Rat Kidney

If high sodium intake is involved in the pathogenesis of essential hypertension, the effects of changing the sodium intake should be demonstrable in the susceptible part of the normotensive population. Therefore, we have investigated the effects of moderate salt restriction in 52 young normotensive subjects with and without a family history of hypertension; 22 (42%) responded to moderate salt restriction (200 to 50 mmol/day) over 2 weeks, with a significant fall in blood pressure shown by continuous automatic blood pressure recordings. Accordingly, these subjects were classified as salt-sensitive, and the remainder as salt-resistant. Compared to salt-resistant subjects, salt-sensitive subjects showed a 2.5-fold higher incidence of a positive family history of hypertension (p less than 0.01), and a significantly higher blood pressure and lower salivary sodium concentration during the usual high sodium diet. Although there were no differences in Na,K-ATPase activity and in Na-K cotransport of erythrocytes, the pressor response to infused norepinephrine in salt-sensitive subjects was double that of salt-resistant subjects independent of the diet and this was linked to indirect evidence for enhanced proximal tubular sodium reabsorption. On the usual high sodium diet, 40% of the normal population may be salt-sensitive and prone to develop hypertension. Hypersensitivity to catecholamines (genetically determined?) may be the cause of salt sensitivity. A low sodium concentration in saliva deserves further study as a simple screening test to identify salt-sensitive subjects.

Salt sensitivity in humans is linked to enhanced sympathetic responsiveness and to enhanced proximal tubular reabsorption.

/pdf/studies-on-digitalis-i-direct-effects-on-peripheral-vascular-3jzuvkzjx5.pdf

Studies on digitalis. i. direct effects on peripheral vascular resistance

Ammonia production was measured directly in 10 segments of the rat nephron to determine the relative importance of the segments as sites of renal ammonia production. Tubules were microdissected from normal rats and rats drinking 0.28 M NH4Cl or 0.28 M NaHCO3 for 3-8 d. The segments were incubated in vitro with and without 2 mM glutamine. Ammonia concentrations in the incubation fluid were measured by microfluorometry to determine ammonia production rates. All segments produced ammonia from glutamine. In normal rats, production with glutamine was highest (greater than 5 pmol/min per mm) in the proximal convoluted (S-1), proximal straight (S-3), and distal convoluted tubules, and lowest (less than or equal to 2) in cortical and medullary collecting ducts and thin descending limbs. Metabolic acidosis increased production by 60% in the S-1 segment of the proximal convoluted tubule and by 150% in the S-2 segment of the proximal straight tubule without significant effect in any other segment. Bicarbonate loading decreased production by S-1 but had no effect on S-2 or S-3. Thus, acid-base changes altered production only in specific segments of the proximal tubule. We infer that the bulk of ammonia production occurs in the proximal tubules and that production by collecting ducts can account for only a few percent of renal ammonia production and excretion in the rat.

/pdf/ammonia-production-by-individual-segments-of-the-rat-nephron-4phveb6raj.pdf

Ammonia production by individual segments of the rat nephron.

We have previously shown that ouabaln-sensitive Rb uptake, a measure of Na-K pump activity, is decreased in the blood vessels of dogs with one-kidney, one wrapped hypertension and rats with onekidney, DOCA, saline hypertension. We here extend the study to rats with one-kidney, one clip and reduced renal mass-saline hypertension. We also assayed supernates of boiled plasma from three of these models for ouabain-sensitive Rb uptake suppressing activity. Finally, we examined the influence of the anteroventral third ventricle (AV3V) lesion in the rat on vascular pump and plasma supernate activities. We found that ouabain-sensitive Rb uptake is suppressed in the tail arteries of rats with one-kidney, one clip and reduced renal mass hypertension and that plasma supernates from these rats and from dogs with one-kidney, one wrapped hypertension suppress Rb uptake when applied to tail arteries from normal rats. We also found that, in the volume-expanded state, rats with AV3V lesions had higher vascular ouabain-sensitive Rb uptake than rats with sham lesions and evidence for decreased inhibitory activity of the plasma. These findings suggest that reduced vascular Na-K pump activity is common to several models of experimental hypertension and that this defect results from a heat-stable ouabain-like agent in plasma that originates in or is influenced by the AV3V area of the brain. (Hypertension 3 (suppl II): II-96-II-101, 1981)

Demonstration of a humoral inhibitor of the Na+-K+ pump in some models of experimental hypertension.

Electrical stimulation of helically cut strips of rabbit carotid artery, mounted so as to allow development of tension isometrically, causes a contraction-relaxation cycle which remains reproducibl...

Alteration of contractile response of artery strips by a potassium-free solution, cardiac glycosides and changes in stimulation frequency.

Regulation of ammonia excretion in the rat.

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Alteration of contractile response of artery strips by a potassium-free solution, cardiac glycosides and changes in stimulation frequency.

Regulation of ammonia excretion in the rat.