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Biomedical subjects

A Iaina

Publications and source records attributed to A Iaina.

At least 109 records · Page 6Linked to original sources

Beneficial effect of verapamil in ischemic acute renal failure in the rat.

To investigate the possible protective effect of Ca2+ blockers in ischemic acute renal failure (ARF), verapamil, in a dose of 10 micrograms/kg body wt/min was administered for 100 min, starting 15 min before the total occlusion of the left renal artery after right nephrectomy in rats. Mean 24-hr creatinine clearance, blood urea, and serum creatinine levels, 24 hr after declamping, were used as a measure of kidney function. These values which were 135 +/- 1.9 microliter/min, 231 +/- 22 mg%, and 2.25 +/- 0.22 mg%, respectively, in the untreated rats, were found to be significantly different, i.e., 326.3 +/- 33.2 microliter/min, P less than 0.001, 112 +/- 25 mg%, P less than 0.001, and 1.26 +/- 0.28 mg%, P less than 0.01, respectively, in the verapamil-treated animals. Increased 24-hr total urine creatinine, sodium, osmolality, and a lower fractional excretion of sodium were also observed in the verapamil-treated rats with ARF. The combination of propranolol 1 mg/kg body wt/min and verapamil 10 micrograms/kg body wt/min for 100 min had no additive effect on renal function. In another group of ARF rats in which verapamil was started after declamping, no alleviating effect was observed. It is concluded that verapamil, an inhibitor of cellular membrane transport, when given prior to the renal ischemia, offers a partial but significant protection in this model of ischemic ARF.

Acute Kidney Injury↗

Treatment of hypertension in dialysis and essential hypertension patients with nifedipine.

The immediate antihypertensive effect of 10 mg nifedipine sublingually (nifedipine test), was measured in 19 chronic renal failure hypertensive patients on dialysis and 34 essential hypertensive patients with normal kidney function. The blood pressure decreased significantly in both groups. The minimal values were observed between 30 and 60 minutes after the sublingual administration of nifedipine. The blood pressure decreased from 178 +/- 3.3/104.0 +/- 3.9 to 136.0 +/- 4.7/87.5 +/- 5.1 mm Hg (p less than 0.001) in dialysis patients and from 176.8 +/- 4.5/107.1 +/- 2.4 to 133.0 +/- 3.0/81.7 +/- 2.2 mm Hg in essential hypertension patients (p less than 0.001). The decrease in blood pressure during the test had a significant positive correlation with the pre-test values. Thirteen hypertensive patients on dialysis and 20 essential hypertensive patients completed 2 weeks of daily oral nifedipine therapy, with a dose of 30 to 40 mg per day. The mean blood pressure at the end of the 2 weeks of treatment decreased from 179.5 +/- 4.5/108.5 +/- 5.3 mm Hg to 154.4 +/- 6.3/82.3 +/- 2.6 mm Hg (p less than 0.001) in dialysis patients, and from 176.8 +/- 5.8/110.3 +/- 2.9 to 151.3 +/- 5.3/93.5 +/- 2.6 mm Hg (p less than 0.001) in essential hypertension patients. The present results reveal that nifedipine has a powerful immediate as well as a long-term antihypertensive action in dialysis patients with high blood pressure. This effect is similar to that obtained in essential hypertensive patients.

Humans↗

Lithium prevents saline deoxycorticosterone acetate (DOCA) hypertension in the rat.

Uni-nephrectomized rats drinking 1% saline instead of water, were given Doca intramuscularly, 50 mg/kg BW per week for 2 weeks. The mean blood pressure in the control group was 105 +/- 4 (+/- S.E.) mm Hg, whereas in the Doca-saline group it rose to 152 +/- 5.1 (p less than 0.001). Rats, similarly treated, were placed on daily intraperitoneal lithium injections of either of two doses: 1.5 or 3.0 mEq/kg BW per day. Their blood pressures, at the end of 2 weeks of treatment, were 117 +/- 2 mm Hg and 103 +/- 2.1, respectively (p less than 0.001 vs. lithium-untreated Doca-saline rats). Water-drinking rats, receiving daily intraperitoneal lithium (3 mEq/kg BW) for 2 weeks, had normal blood pressures, not different from the controls (104 +/- 11 mm Hg). The Doca-saline and Doca-saline-lithium (1.5 mEq/kg/day) groups had similar changes in mean daily body weight, plasma sodium, osmolality, and GFR. The renal beta-adrenergic receptor density in the Doca-saline-lithium rats was in the normal range, 51 +/- 4.5 mol/mg of protein. In the Doca-saline hypertensive rats, it was significantly lower, being 27.2 +/- 3 fmol/mg of protein, p less than 0.05. These renal plasma cell membrane beta-adrenergic receptors were characterized by direct tissue binding with (-)[3H]dihydroalprenolol. These results show that lithium prevents the development of hypertension in the Doca-saline rats. The effect of lithium on the sympathetic nervous system is a possible mechanism in the prevention of the Doca-saline hypertension.

Animals↗

Evidence for an extrarenal action of chlorothiazide on serum potassium.

The effects of chlorothiazide and furosemide on serum potassium were studied in fasting anuric patients maintained by chronic hemodialysis and compared to a control period when no drug was administered. Serum potassium levels were significantly lower following oral chlorothiazide (15 mg/kg body weight) than during the control period. After intravenous furosemide (1 mg/kg body weight), potassium levels were midway between those of the chlorothiazide and control periods, but statistical significance was not attained. Comparing the three study periods, there were no significant differences in the changes in body weight, blood pressure, blood pH, hematocrit, urea, glucose, sodium, albumin, insulin, plasma renin activity and aldosterone. This suggests that an extrarenal action of chlorothiazide on the cell membrane promotes cellular uptake of potassium.

Chlorothiazide↗

Continuous ambulatory peritoneal dialysis- a new dimension in the treatment of end-stage renal disease.

Thirty-five patients treated with continuous ambulatory peritoneal dialysis (CAPD) were followed over a 2-yr period. Serum levels of protein metabolites were maintained at stable and satisfactory levels. Blood hemoglobin was higher during CAPD treatment than during hemodialysis. At the end of the follow-up period, 45.7% of the patients were still on CAPD, 25.7% of them had been transferred to another mode of dialysis because of complications, and 28.6% of the patients had died. In half of the latter, death was directly related to CAPD. The high incidence of peritonitis (one infection per 2.4 patient months) is the main drawback and reason for mortality in CAPD. Reduction in the incidence of peritonitis would make CAPD the preferred mode of dialytic therapy.

Adult↗

Sodium, potassium and age: possible determinants of plasma renin activity and aldosterone during childhood (age 4-16).

The renin-angiotensin-aldosterone system was studied in fifty healthy children aged 4-16 years under normal sodium and potassium intake. The plasma renin activity (PRA) and plasma aldosterone (PA) decreased with age: r = -0.30, P less than 0.05 for plasma renin activity and r = -0.33, P less than 0.05 for plasma aldosterone. Significant negative correlation was obtained between plasma renin activity and the 24-h urinary sodium excretion; r = -0.40, P less than 0.01. This relationship remained significant when the daily urinary sodium excretion was corrected for 1.73 m2 body surface area (BSA); r = -0.40, P less than 0.01. Using the multivariance analysis, plotting the plasma renin activity against the two combined parameters (24-h urinary sodium excretion and age), no improvement was obtained (r = 0.38, P greater than 0.05). This finding suggests that during childhood, sodium rather than age has a major modulatory role on plasma renin activity. With advancing age the plasma aldosterone showed a significant positive correlation coefficient with plasma renin activity(r = 0.29, P less than 0.05). Multivariance analysis between plasma aldosterone and the two combined parameters, Plasma renin activity and age, significantly improved the correlation coefficient (r = 0.42, P less than 0.05) suggesting that both plasma renin activity and age play a dominant modulatory role in the control of plasma aldosterone during childhood. Neither 24-h urinary sodium excretion, nor 24-h urinary potassium excretion, improved the multiple correlation coefficient with plasma aldosterone when added to plasma renin activity and age.

Adolescent↗

Body weight reduction necessary to attain normotension in the overweight hypertensive patient.

All 212 patients with essential hypertension and an overweight of at least 10 per cent in excess of ideal body weight, referred to out clinic in the years 1975-1979, were included in this study. The patients were advised to take a balanced low-calorie (about 1080 kcal/day) diet containing 83 g carbohydrates, 41.5 g fat and 85 g proteins. They were advised to eat salt freely. There were 40 patients who had four clinic visits or less and 49 others who could not follow their diet. Therefore the compliance-failure rate was 89/212, ie 42 per cent. Decrease in body weight resulted in a significant decrease in blood pressure, despite free ingestion of salt and with 24-h urine sodium which was not different from that obtained before dietary therapy was started. Over two-thirds of the compliant patients will achieve normal blood pressure with a loss of only one-half of their weight excess, even if at this point they are still overweight. In the group receiving no diuretic or any other anti-hypertensive therapy, 82.6 percent reached normal systolic blood pressures and 78.3 per cent reached normal diastolic blood pressures, but only 31/38 reached a body weight within 10 per cent of ideal body weight. It is concluded that most of overweight hypertensive patients can attain a normal blood pressure by reducing body weight, long before achieving the ideal weight.

Blood Pressure↗

Hereditary renal-retinal dysplasia.

Juvenile nephronophthisis and medullary cystic diseases are inherited kidney disorders leading to end stage uremia. As these diseases appear to be identical, they were grouped together in nephronophthisis-cystic renal medulla complex. Among its extrarenal manifestations, tapeto-retinal degeneration is the most frequent allied condition. This specific association of the renal and retinal conditions, suggesting a genetic background, is called hereditary renal-retinal dysplasia and is transmitted as an autosomal recessive trait. There are some variations in the type of the retinal degeneration in renal-retinal dysplasia and similar basic genetic mechanisms may results in Leber's congenital amaurosis, or retinitis pigmentosa, central retinal degeneration or stationary congenital night blindness. Pleiotropism seems to be responsible for the spectrum of these anomalies. Occasional expression in the heterozygous state by urinary concentrating disabilities or electroretinographic impairments were documented. The nature and pathogenesis of renal-retinal dysplasia remain a debated issue, but some evidence supports the possibility of an inborn error of metabolism causing the basic defects.

Adolescent↗

beta 1-Adrenergic receptors in kidney tubular cell membrane in the rat.

We used a beta-adrenergic antagonist, (-) 3H-dihydroalprenolol, to demonstrate binding sites in purified rat kidney preparations that consistsed of plasma membranes of cells from tubules. The tubular origin of these plasma membranes was shown by electron microscopy and Na-K-ATPase enrichment. The binding was rapid (t1/2, 78 sec) and rapidly reversible (t1/2, 48 sec). The binding sites were saturable and bound 69.8 +/- (SD) 29.1 fmoles/mg of membrane protein. The binding was stereospecific with the isomers of beta-adrenergic agonists and beta-adrenergic antagonist propranolol, the (-) isomers being about 40 times more potent than the (+) isomers incompeting for these sites. (-) 3H-dihydroalprenolol had a high affinity for the binding sites, expressed by the mean equilibrium dissociation constant (KD) (KD, 7.1 nM). The beta-adrenergic antagonist (-) propranolol also showed high affinity (KD, 62.8 nM). The order of potency for inhibition of binding by beta-adrenergic agonists was: (-) isoproterenol (KD, 0.66 microM) greater than (-) epinephrine (KD, 4.3 microM) greater than or equal to (-) norepinephrine (KD, 13.5 microM). Conclusion. The (-) 3H-dihydroalprenolol binding sites in the rat kidney tubular cell membrane are beta-adrenergic receptor of the beta1 subgroup.

Alprenolol↗

Sector retinitis pigmentosa in juvenile nephronophthisis.

In a patient with juvenile nephronophthisis, sector retinitis pigmentosa was found as an extrarenal manifestation, establishing a hitherto undescribed variety of retinal degeneration occurring in this disorder. The retinal function in this case was identical with that in the classic type of sector retinitis pigmentosa, namely, subnormal ERG amplitudes but normal cone and rod implicit times. The range of the retinal findings and their autosomal recessive transmission are discussed. Paucity of information makes it difficult to elucidate the basic genetic defect operating in this condition.

Adolescent↗

Exercise tolerance in patients on chronic hemodialysis.

Twenty-two patients on chronic hemodialysis were tested on a bicycle ergometer to determine their near-maximal physical work capacity. The patients were found to have low physical work capacity that averaged 51.6 +/- 3.8 (SE)% predialysis and 50.3 +/- 3.7% postdialysis, when compared with the physical work capacity of healthy control subjects. The exercise was stopped when patients complained of muscular fatigue, and the work load at this point was considered their subjective maximal work capacity. At this stage the patients had high blood lactic acid levels and an increased double product (systolic blood pressure x heart rate), the latter indicating a high stage of cardiac output. The oxygen consumption and oxygen pulse were similar to those obtained from control individuals at the same work load. This study suggests that limited physical work capacity of chronic hemodialysis patients is due to early muscular fatigue. This phenomenon is associated with the rapid onset of anaerobic metabolism and may thus be caused by limited maximal oxygen uptake.

Adult↗