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Biomedical subjects

J L Cuche

Publications and source records attributed to J L Cuche.

At least 19 recordsLinked to original sources

Arterial effects of salt restriction in hypertensive patients. A 9-week, randomized, double-blind, crossover study.

OBJECTIVE: To investigate the hemodynamic effects of a moderately low-salt diet in a 9-week, randomized, double-blind, crossover study in 20 hypertensive, ambulatory patients. METHODS: All subjects followed a 9-week, low-salt diet. During this period, they received capsules containing either lactose or salt in 4-week treatment periods, separated by a 1-week washout period. Hemodynamic and biological parameters were evaluated on the day of randomization and at the end of weeks 4 and 9. We defined a low-sodium diet (LSD) as a salt-restriction period with lactose capsules, and a normal-sodium diet (NSD) as a salt-restriction period with capsular salt supplementation. RESULTS: Blood pressure was significantly lower during LSD compared with NSD. This fall in blood pressure was associated with a decrease in peripheral resistance in carotid and forearm circulation. Brachial artery diameter was larger during LSD whereas carotid artery diameter remained unchanged. The changes in brachial artery were: (1) not related to blood pressure changes; (2) positively related to age, and (3) negatively correlated with baseline intracellular sodium content. CONCLUSIONS: These results suggest that moderate low-salt restriction is capable of decreasing blood pressure and peripheral resistance in carotid and forearm circulation. The increase in brachial, but not carotid, artery diameter following salt restriction suggests a difference in salt dependence among different arteries.

Adult

[Renovascular hypertension and beta blockers. Theoretical and practical implications].

Beta blockade was instituted in 10 patients with renovascular hypertension due to renal artery stenosis or thrombosis. The treatment was very effective in unilateral stenosis with a normal contralateral kidney (2 kidney Goldblatt) and in fibromuscular dystrophy of the renal artery. On the other hand many failures were observed in hypertension with a single kidney (1 kidney Goldblatt) and in renovascular hypertension with complex lesions or associated renal failure. Although a clear relationship was often observed between the increased plasma renin activity and the antihypertensive effect of beta blockade, this association was sometimes completely erroneous. Beta blockade, which is easy to perform, should be tried out systematically in renovascular hypertension, but, when no result is observed, this therapeutic test should not exclude surgical management thereafter.

Adrenergic beta-Antagonists

Catecholamines, cyclic AMP and renin in two contrasting forms of essential hypertension.

Essential hypertension (EH) can be subdivided according to the sympathetic and renin activity into two contrasting forms: (1) borderline beta-hyperadrenergic renin hyperresponsive and (2) stable beta-hypoadrenergic renin hyporesponsive EH. These two forms probably represent two expreme poles in the spectrum of EH in which sympathetic and renin hyper- or hyporeactivity cannot be accounted for by catecholamine determinations solely. beta-Adrenergic responsiveness monitored by plasma cyclic AMP determinations revealed plasma cyclic AMP, renin and circulatory hyperresponsiveness to isoproterenol in borderline hyperadrenergic EH while the opposite, cyclic AMP and renin hyporesponsiveness to insulin-induced hypoglycemia have been described in low renin stable EH. The kidney is in the center of the adrenergic abnormality in the two forms of EH with the borderline one excreting into the urine catecholamines not accounted for by their glomerular filtration. Catecholamines solely, however, do not account for the differences in both forms of EH which can probably be attributed to their different beta-adrenergic responsiveness.

Adrenergic beta-Antagonists

Catecholamine excretion in "idiopathic" edema: decreased dopamine excretion, a pathogenic factor?

In 16 women with idiopathic edema, urinary dopamine excretion was decreased when compared to control women (146 +/- 13 SE ng/ml/m2 vs. 212 +/- 32, P less than 0.05 in the supine position and 140 +/- 9 vs. 199 +/- 20, P less than 0.005 combined values of supine and recumbent positions) and was also lower when pooled values for urinary dopamine excretions both before and after furosemide were compared in idiopathic edema patients and in control subjects (270 +/- 30 ng/ml vs. 480 +/- 70, P less than 0.05). These patients have lower basal sodium excretions, decreased tubular rejection fractions of sodium in the upright position and lower urinary sodium excretions following furosemide administration. The urinary sodium and dopamine excretions before and following furosemide are positively correlated in control (P less than 0.05), idiopathic edema patients (P less than 0.02) and in both groups combined (P less than 0.005). Idiopathic edema patients have normal urinary noradrenaline and adrenaline excretions but, as previously observed, elevated: 1) plasma renin activity while either recumbent or upright, and 2) plasma aldosterone concentrations while upright. These results suggest that a decrease in urinary dopamine, a catecholamine recently recognized to have natriuretic action, possibly reflects a suppression of the renal dopaminergic system and may contribute to the excessive sodium retention in idiopathic edema either directly or indirectly through the renin-aldosterone system.

Adult

Circadian variations of the urinary excretion of catecholamines and electrolytes.

Concomitant measurements of circadian variations in the urinary excretion of dopamine (DA), homovanillic acid (HVA), norepinephrine (NE), epinephrine (E) as well as of creatinine, sodium and potassium under controlled dietary conditions during relative physical and emotional rest in 13 volunteers have shown that maximum excretion of all these substances occurred in the afternoon period between 14:30h and 18:00h, and minimum excretion in the morning between 4:00h and 5:00h. The changes were in some cases progressive from one collection period to the other, and synchronized for NE and E. DA and HVA excretions fluctuated from subject to subject. Excretory rhythms of sodium and potassium were found to be similar to those of the catecholamines. This can be explained by diurnal changes in renal blood flow and different renal excretory mechanisms of catecholamines. None of the catecholamines correlated with the urinary volume but urinary NE and E positively correlated with urinary creatinine, urinary NE and E with urinary DA and urinary sodium with urinary E. There are some common patterns in the diurnal rhythms of catecholamines and electrolytes but their interrelationship is different for individual catecholamines.

Adult

Intrarenal calcium in phosphate handling.

The intrarenal role of plasma ionized calcium (Ca), on fractional phosphate excretion (FE PO4) was investigated in dogs with control of parathyroid hormone (PTH). In series 1, acute thyroparathyroidectomy was immediately followed by a constant infusion of bovine PTH (0.01 U/kg per min). Subsequent calcium chloride infusions increased Cai in plasma phosphate and decreased in the percentage of ultrafiltrable phosphate. A 20% increase in Cai significantly increased FE PO4 by +3.82 +/- 0.97% (P less than 0.01) when infused intravenously and by +2.62 +/- 1.06% (P less than 0.05) when infused in the renal artery. In contrast, a 75% increase in Cai did not significantly change FE PO4. In series 2, dogs were thyroparathyroidectomized 18 h before experiments, and no PTH infusion was initiated. A bolus of bovine PTH (30 U/kg) increased FE PO4 + 8.9 +/- 0.9% (P less than 0.001) in hypocalcemic dogs, +19.1 +/- 4.4% (P less than 0.001) in normolcalcemic dogs, and +15.5 +/- 1.5% (P less than 0.001) in hypercalcemic dogs. We conclude that increases in plasma calcium potentiate the phosphaturic effect of PTH. This potentiating effect is attenuated in marked hypercalcemia by superimposed hemodynamic and/or metabolic changes.

Animals

Sodium balance and the natriuresis of hypertonic saline infusion in dogs.

Recently, a paradoxical effect of dietary salt intake on the natriuresis following hypertonic saline infusion was observed in rats. In these experiments the effects of alterations in dietary sodium on the natriuretic response to a hypertonic saline load was studied in dogs. Dogs maintained on a high-sodium diet did not have a significantly different natriuresis than those on a low-sodium diet. When differences in sodium balance were amplified by the use of deoxycorticosterone, furosemide, and manipulation of dietary sodium, dogs in positive sodium balance showed a significantly enhanced initial excretion of sodium followed by a reversal of the pattern. Consequently, the cumulative sodium excretion was not different between low- and high-sodium groups. Since the cumulative natriuretic response to isotonic saline infusion was larger in dogs in positive sodium balance compared to those in negative sodium balance, the failure to detect a difference following hypertonic saline infusion was probably because of the increased plasma sodium concentration.

Animals

Comparison of proximal tubule fluid-to-plasma ultrafiltrate chloride ratio in rats and dogs.

Previous studies in rats have demonstrated that the concentration of chloride in proximal tubule fluid is greater than that in plasma. The gradient reaches a free-flow steady-state level in the early proximal tubule and is maintained throughout the accessible proximal tubule. On the other hand, studies in dogs are in conflict regarding either the existence of a gradient or the development of a free-flow steady-state level. Since a species difference of tubule fluid to plasma chloride (TF/PC1) may exist, the present study was done to systematically compare the tubule fluid to ultrafiltrate chloride ratio (TF/UFC1) in hydropenic rats and dogs during normal acid-base balance. Chloride was analyzed by microelectrometric titration. In the rat the TFC1 and UFC1 concentrations were 139 +/- 1.4 and 120 +/- 1.2 meq/1, respectively. In the dog the TFC1 and UFC1 concentrations were 138 +/- 1.3 and 121 +/- 1.5 meq/1, respectively. Thus, there was no significant difference in the TF/UFC1 ratio between the rat (1.17 +/- 0.02) and the dog (1.14 +/- 0.01). Furthermore, regression analysis indicates that there is no correlation between TF/UFC1 and TF/PIn in either the rat or dog, which suggests that the gradient originates early in the proximal tubule and is maintained throughout the accessible proximal tubule in both species.

Animals

Phosphaturic effect of dopamine in dogs. Possible role of intrarenally produced dopamine in phosphate regulation.

A possible role for dopamine in phosphate handling by the dog kidney was investigated by intrarenal artery infusions of dopamine. Dopamine increased fractional phosphate excretion both in the presence and absence of control of parathyroid hormone and calcitonin. In addition, dopamine increased both renal blood flow and sodium excretion, however, the phosphaturia was independent of these changes; since 30 min after completion of dopamine infusion, renal blood flow and sodium excretion returned to control levels and phosphate excretion remained elevated. For comparison, the vasodilator isoproterenol increased renal blood flow and sodium excretion without a significant change in fractional phosphate excretion. Thus, the phosphaturic effect of dopamine is probably independent of its vasodilator effect. The phosphaturic effect of dopamine could not be accounted for by subsequent conversion to norepinephrine, since norepinephrine was antiphosphaturic in the dog. The effect of endogenous dopamine on renal phosphate excretion was investigated by intrarenal infusion of the precursor dopa. Dopa was phosphaturic both in the presence and absence of parathyroid hormone and calcitonin. In dogs pretreated with carbidopa, which blocks conversion of dopa to dopamine, dopa was no longer phosphaturic, although the kidney remained responsive to dopamine. It is postulated that dopamine may play a role in the intrarenal regulation of phosphate excretion.

Animals

Lack of effect of hypocalcemia on renal phosphate handling.

A possible effect of decreased plasma ionized calcium concentration on renal phosphate handling was investigated in dogs with control of parathyroid hormone. Intrarenal artery infusion of either EDTA or sodium citrate decreased ionized calcium concentration 25 per cent in renal vein blood but had no significant effect on fractional phosphate excretion. Similarly, intravenous infusion of chelators had no significant effect on fractional phosphate excretion. It is concluded that acute decreases in ionized calcium have no significant effect on the renal handling of phosphate.

Animals

Urinary homovanillic acid, dopamine and norepinephrine excretion in patients with essential hypertension.

Urinary excretion of dopamine, norepinephrine and homovanillic acid was measured in normotensive subjects and in patients with either labile of stable hypertension under conditions controlled for posture, sodium and potassium intake and time of day. Mean homovanillic acid excretion was 313.5 plus or minus 77.7 (SE) mug/4h in the normotensive patients. Mean values for the patients with labile or stable hypertension were significantly greater, at 2506 plus or minus 476 mug/4 h (P smaller than 0.001) and 795 plus or minus 170 mug/4 h (P smaller than 0.01), respectively. Urinary excretion of dopamine and norepinephrine tended to be elevated in patients with labile hypertension when compared with values in the control subjects and the patients with stable hypertension. The data are compatible with the hypothesis of adrenergic hyperactivity in labile hypertension and underline the biochemical heterogeneity of essential hypertension. Because the overlapping of values between control subjects and patients with labile hypertension was minimal, it is proposed that an elevated valve for urinary homovanillic acid could be used as a biochemical marker to identify the patients with labile hypertension.

Adolescent

Effects of extracellular fluid volume contraction and expansion on the bicarbonaturia of parathyroid hormone.

To evaluate the effect of extracellular fluid volume alterations on the bicarbonaturia of parathyroid hormone, thyroparathyroidectomized dogs were made alkalotic and volume-contracted or expanded through hemodialysis. Clearance studies were performed before and after infusion of purified bovine parathyroid extract (PTE). Glomerular filtration rate and blood bicarbonate concentrations were kept constant throughout the experiments. A significant increase in fractional bicarbonate excretion was observed following PTE infusion in both the volume-contracted (8.67 +/- 3.25 to 14.70 +/- 3.63%, P less than 0.010) and the volume-expanded state (22.80 +/- 3.04 to 37.26 +/- 3.38%, P less than 0.050). It is concluded that PTE decreases reabsorption of bicarbonate independent of the volume state of the animal.

Alkalosis

Sex differences in the urinary catecholamines.

Urinary excretion of dopamine, norepinephrine and epinephrine was measured in a group of adult men and women of comparable age during recumbency and then during stimulation by upright posture. Urinary norepinephrine was found to be significantly higher in women (30.3 +/- 4.4 ng/min/m2 B.S.) than in men (18.3 +/- 2.7 ng/min/m2 B.S.) during recumbency; there was no significant sex difference in dopamine and epinephrine excretion. There was no apparent trend indicating a difference in urinary catecholamine excretion during the follicular or luteal phase of the menstrual cycle. In response to upright posture, there was a significant decrease in the urinary dopamine-norepinephrine ratio in both sexes; the magnitude of the decrease was, however, significantly higher in men (-9.9 +/- 3.0) than in women (-2.05 +/- 0.72). The mechanisms of the sex differences in urinary catecholamine excretion are unknown. Clinical studies involving catecholamines have to take these sex differences into account.

Catecholamines

Measurement of renal interstitial fluid pressure with polyethylene matrix capsules.

The renal interstitial fluid pressure was measured in dogs from small chronically implanted solid capsules made of porous polyethylene matrix material (pore size approximately 60 mum). Tissue does not grow into the polyethylene and the matrix creates a permanent fluid-filled space in communication with the interstitium. The fluid pressure in the capsule matrix was measured from a tube leading from the capsule with an active servo-null pressure-measuring device. Renal interstitial fluid pressure measured from 28 hydropenic dogs averaged 6.1 plus or minus 0.51 mmHg (SE). Increasing oncotic pressure inside the capsule to 90 mmHg resulted in a small but significant increase in hydrostatic pressure inside the capsule of 3.3 plus or minus 0.46 mmHg. However, the hydrostatic pressure returned to control levels within 30 min. In vitro studies indicated that the pressure measured from the capsule was highly sensitive to change in surrounding hydrostatic pressure, but insensitive to change in surrounding oncotic pressure. Histological studies showed a small layer of connective tissue surrounding the capsule less than 100 mum thick in many areas. There was no evidence of inflammation or tissue rejection. It is concluded that the small chronically implanted polyethylene capsule is a reliable method for the measurement of renal interstitial fluid pressure.

Animals