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M Marin-Grez

Publications and source records attributed to M Marin-Grez.

60 records · Page 4Linked to original sources
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Atrial natriuretic peptide causes pre-glomerular vasodilatation and post-glomerular vasoconstriction in rat kidney.

Atrial natriuretic peptide (ANP) can be extracted from rat hearts, and is found to increase fluid excretion by the kidneys when injected into test animals. The mechanism of ANP action is still unclear. ANP may reduce sodium reabsorption in the renal tubules, but it is also known that it increases the rate of glomerular filtration in the kidney, and relaxes preparations of smooth muscle, including one made from arteries that supply the kidney. To clarify its mode of action, we have studied directly the effects of semi-purified and synthetic ANP on blood vessels in the kidney of anaesthetized rats. We found that ANP causes a vasodilatation of the blood vessels which supply the glomeruli and a vasoconstriction of the arterioles which drain them. This substantiates the finding that increased filtration pressure participates in the natriuretic response.

Animals↗
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Evidence for an inhibitory effect of kallikrein on collecting duct bicarbonate secretion in rats and rabbits.

The luminal membrane of collecting duct cells, especially the intercalated cells, is normally exposed to active kallikrein. This is the consequence of the specific localization of this renal enzyme in the connecting tubule cells and its principal route of secretion being into the tubular lumen. It is conceivable that kallikrein acts downstream on a transporter involved in distal bicarbonate handling. To investigate this possibility, we estimated bicarbonate concentration and measured kallikrein amidolytic activity in urine fractions collected after a classical stop-flow experiment in rabbits. A highly significant inverse correlation was found between these parameters (r = -0.94, p < 0.001) in the peak kallikrein fractions. Neither sodium nor potassium concentration were correlated to kallikrein. This suggests that the physiological role of renal kallikrein may be to regulate extracellular fluid pH by inhibiting collecting duct bicarbonate secretion. To test the hypothesis that tubular fluid kallikrein activity and bicarbonate secretion are causally related, we developed a novel in vivo stop-flow injection model ('orthograde stop-flow'). A hog-kallikrein containing solution (0.5 microgram/ml) was injected through the abdominal aorta into the renal tubular system of one kidney of barbiturate-anesthetized rats, while the renal blood supply was interrupted. The ureter was then occluded and renal blood perfusion reinitiated. After a 2-min contact time five 125-microliters urine fractions were collected. Bicarbonate secretion was clearly detected in the second and third fractions (i.e. those coming from the collecting ducts) of the control animals, which had received only the vehicle. There was no bicarbonate secretion peak in the corresponding urine fractions collected from kallikrein-injected animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗