Renal excretion of calcium and sodium in acute nephritis

Hypocalciuria was found in the early stages of illness in six patients aged 12 to 30 with acute nephritis. The hypocalciuria does not appear to be due to hypocalcaemia, lowered glomerular filtration rate, or hypoparathyroidism. It is suggested that the hypocalciuria is due in part to decreased intestinal absorption of calcium, though possibly there is also a primary alteration in renal tubular handling of calcium.     

Renal reflexes in the regulation of blood pressure and sodium excretion

The rich innervation of the kidney is distributed to all structures of renal parenchyma thus providing important anatomical support to the functional evidence that the renal nerves can control kidney functions and send signals on the kidney environment to the central nervous system. Efferent renal nerve fibres are known to influence renal haemodynamics by modifying arteriolar vascular tone, renin release by a direct action on juxtaglomerular cells, and the excretion of sodium and water by changing tubular reabsorption of sodium and water at the different tubular levels. Mechano- and chemo-receptors have been shown in the kidney. Afferent fibres connected with renal receptors convey signals to the central nervous system both at spinal and supraspinal levels. The central areas receiving inputs from the kidney are those involved in the control of cardiovascular homeostasis and fluid balance. Activation of renal receptors by the electrical stimulation of renal afferent fibres were found to elicit both excitatory and inhibitory sympathetic responses. Although the existence of excitatory renorenal reflexes has been suggested, electrophysiological and functional data demonstrate that neural renorenal reflexes exert a tonic inhibitory influence on the tubular sodium and water reabsorption and on the secretion of renin from the juxtaglomerular cells.     

Effects of methacholine on the carotid chemoreceptors.

The present electrophysiological study shows that methacholine (MCh), generally regarded as a muscarinic agonist, stimulates the carotid chemoreceptors in pentobarbitone anaesthetized cats. The response consisted of a primary increase in discharge, attributable to nicotinic actions of MCh since it was unaffected by atropine but abolished by mecamylamine, and a delayed secondary increase in discharge, due mainly to bronchoconstriction evoked by MCh. Physostigmine caused similar potentiation of responses to acetylcholine and MCh which implies that acetylcholinesterase is located close to the site(s) at which the drugs act to stimulate chemoreceptor activity. The findings are in agreement with the general principle that chemosensory activity is increased by nicotinic agonists but not by muscarinic agonists.     

Hypoxic modulation of systolic blood pressure and urinary sodium excretion in spontaneously hypertensive rats after carotid body denervation

To explore the role of arterial chemoreceptors, the effect of hypobaric hypoxia on urinary sodium excretion and systolic blood pressure was investigated in conscious spontaneously hypertensive rats (SHR) with carotid body denervation (CBD) or after sham-operation (SO). Denervation of the carotid bodies was performed by section of the carotid sinus nerves. Exposure to hypobaric hypoxia equivalent to high altitude of 4000 m led to a more pronounced decrease in systolic blood pressure in CBD-rats than in SO-rats. The pattern of urinary sodium excretion observed on the first two days of hypoxia in both groups was not affected by the chemodenervation. It is being suggested that arterial chemoreceptors do not play a critical role in blood pressure and natriuretic responses to hypobaric hypoxia in conscious SHR.     

Renal protein excretion after exercise in man

Thirteen men were submitted to graded exhaustive cycle exercise to determine the kinetics of proteinuria in the recovery period. Venous blood samples were analysed for haematocrit, lactate, creatinine, total protein and albumin for 1 h following exercise. Urine samples were collected during a 3-h recovery period. Total protein, albumin, and creatinine levels were determined for these samples. Total protein and albumin urinary excretion increased to 581 and 315 micrograms min-1, respectively, at the end of the 1st h of recovery as compared to 42 and 15 micrograms.min-1 for resting values. Plasma volume returned to pre-exercise levels between 30 and 60 min after cessation of exercise, while urinary total protein and albumin content still remained above the resting values for the following 2 h. Both post-exercise urinary total protein and albumin excretion followed a logarithmic decline with the same half-life of 54 min, thus requiring about 4 h to regain resting values. The reduction of plasma volume and the degree of dehydration do not seem to be involved in the process. The present study indicates the delayed recovery of protein handling by the kidney, as compared with other biochemical parameters, and provides accurate information on the kinetics of post-exercise proteinuria.     

Oxygen sensing by the carotid body chemoreceptors.

Carotid bodies are sensory organs that detect changes in arterial blood oxygen, and the ensuing reflexes are critical for maintaining homeostasis during hypoxemia. During the past decade, tremendous progress has been made toward understanding the cellular mechanisms underlying oxygen sensing at the carotid body. The purpose of this minireview is to highlight some recent concepts on sensory transduction and transmission at the carotid body. A bulk of evidence suggests that glomus (type I) cells are the initial site of transduction and that they release transmitters in response to hypoxia, which causes depolarization of nearby afferent nerve endings, leading to an increase in sensory discharge. There are two main hypotheses to explain the transduction process that triggers transmitter release. One hypothesis assumes that a biochemical event associated with a heme protein triggers the transduction cascade. The other hypothesis suggests that a K(+) channel protein is the oxygen sensor and that inhibition of this channel by hypoxia leading to depolarization is a seminal event in transduction. Although there is body of evidence supporting and questioning each of these, this review will try to point out that the truth lies somewhere in an interrelation between the two. Several transmitters have been identified in glomus cells, and they are released in response to hypoxia. However, their precise roles in sensory transmission remain uncertain. It is hoped that future studies involving transgenic animals with targeted disruption of genes encoding transmitters and their receptors may resolve some of the key issues surrounding the sensory transmission at the carotid body. Further studies are necessary to identify whether a single sensor or multiple oxygen sensors are needed for the transduction process.     

Function of the rat carotid body chemoreceptors in ageing

Some age-related deficits in the ventilatory responses have been attributed to a decline in the functionality of the carotid body (CB) arterial chemoreceptors, but a systematic study of the CB function in ageing is lacking. In rats aged 3-24 months, we have performed quantitative morphometry on specific chemoreceptor tissue, assessed the function of chemoreceptor cells by measuring the content, synthesis and release of catecholamines (a chemoreceptor cell neurotransmitter) in normoxia and hypoxia, and determined the functional activity of the intact organ by measuring chemosensory activity in the carotid sinus nerve (CSN) in normoxia, hypoxia and hypercapnic acidosis. We found that with age CBs enlarge, but at the same time there is a concomitant decrease in the percentage of chemoreceptor tissue. CB content and turnover time for their catecholamines increase with age. Hypoxic stimulation of chemoreceptor cells elicits a smaller release of catecholamines in rats after 12 months of age, but a non-specific depolarizing stimulus elicits a comparable release at all ages. In parallel, there was a marked decrease in the responsiveness to hypoxia, but not to an acidic-hypercapnic stimulus, assessed as chemosensory activity in the CSN. We conclude that in aged mammals chemoreceptor cells become hypofunctional, leading to a decreased peripheral drive of ventilation.