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Biomedical subjects

E J Zambraski

Publications and source records attributed to E J Zambraski.

53 records · Page 3Linked to original sources

Renal prostaglandin E2 secretion and excretion in conscious dogs.

Renal prostaglandin E2 (PGE2) secretion and excretion rates were determined in nine conscious dogs. Renal venous (RV) and urine PGE2 concentrations were measured by radioimmunoassay. In 21 controls tests RV PGE2 ranged from 37 to 215 pg/ml, with a mean concentration of 97 +/- 11 pg/ml. Basal left kidney PGE2 secretion was 317 +/- 42 pg.g-1.mm-1. Urine PGE2 concentration averaged 8,320 +/- 1,510 pg/ml with a PGE2 excretion rate of 3,260 +/- 480 pg/min from both kidneys. Indomethacin (2 mg/kg) reduced RV and urine PGE2 concentrations by 60 and 77%, respectively. Meclofenamate (2 mg/kg) decreased RV and urine PGE2 concentrations by 36 and 48%, respectively. PG inhibition had no significant influence on blood pressure or renal blood flow (RBF). PG inhibition reduced urine flow rate and increased urine osmolality. Indomethacin had no effect on urine sodium concentration or sodium excretion; meclofenamate increased urine sodium concentration and slightly diminished sodium excretion. These data demonstrate that PGE2 is released from the kidney in a conscious animal and that both indomethacin and meclofenamate significantly reduce the renal secretion and excretion of PGE2. In a normal, conscious animal prostaglandins do not control blood pressure or RBF but are involved in the excretion of water.

Animals↗

Proteinuria in the exercising dog.

Exercise proteinuria is a transient condition often observed following heavy exercise in man. A general belief is that exercise proteinuria in man is partially due to the decline in renal blood flow (RBF) associated with exercise. The purpose of this study was to determine if exercise proteinuria occurs in the dog, an animal whose RBF is constant during exercise. Chronic bladder cannulas were surgically implanted in four female mongrel dogs. Urine from both kidneys was collected prior to, during, and after heavy treadmill exercise (30 minutes duration, 5mph, and 15% grade). Urine protein concentration was determined by the biuret method. When compared to resting control urine, protein concentration during exercise increased by 47 percent (P less than .01). Urine flow rate at rest, .17 +/- .02 ml/min, decreased to .09 +/- .01 ml/min (P less than .01) during exercise, resulting in a small but not statistically significant decline in protein excretion. In twenty-six tests, when comparisons were made between resting and post-exercise periods, urine flow rate was identical, urine protein concentration was significantly highently elevated (P less than .01). These data indicate that exercise proteinuria may occur in the absence of changes in RBF.

Animals↗

Mechanism of intrarenal blood flow redistribution after carotid artery occlusion.

Bilateral carotid artery occlusion results in an increase in mean arterial pressure, an increase in renal sympathetic nerve activity, and a redistribution of renal blood flow from inner to outer cortex. To elucidate the mechanism of the renal blood flow redistribution, carotid artery occlusion was performed in anesthetized dogs with the left kidney either having renal perfusion pressure maintained constant (aortic constriction) or having alpha-adrenergic receptor blockade (phenoxybenzamine); the right kidney of the same dog served to document the normal response. When renal perfusion pressure was maintained constant, renal blood flow distribution (microspheres) was unchanged by carotid artery occlusion. In the presence of renal alpha-adrenergic receptor blockade, carotid artery occlusion elicited the usual redistribution of renal blood flow from inner to outer cortex. The redistribution of renal blood flow observed after carotid artery occlusion is mediated by the increase in renal perfusion pressure rather than the increase in renal sympathetic nerve activity.

Adrenergic alpha-Antagonists↗

Neurogenic control of renal tubular sodium reabsorption in the dog: a brief review and preliminary report concerning possible humoral mediation.

The evidence supporting a role for direct neurogenic control of renal tubular sodium reabsorption is reviewed. Electron microscopic and fluorescence histochemical studies have demonstrated adrenergic nerve terminals in direct contact with basement membranes of mammalian renal tubular epithelial cells. Low level direct or baroreceptor reflex stimulation of renal sympathetic nerves produces an increase in renal tubular sodium reabsorption without alterations in glomerular filtration rate, renal blood flow, or intrarenal distribution of blood flow. The antinatriuresis was prevented by prior treatment of the kidney with guanethidine or phenoxybenzamine. Rat kidney micropuncture studies have localized the site of enhanced tubular sodium reabsorption to the proximal tubule. Possible indirect mediation of the antinatriuresis by other humoral agents known to be released from the kidney upon renal nerve stimulation was explored. Renal blockade to circulating angiotensin II did not alter the antinatriuretic response to low level direct renal nerve stimulation. Indomethacin was used to inhibit prostaglandin synthesis; this resulted in a rise in mean arterial pressure, a fall in renal blood flow, no significant change in glomerular filtration rate, and a variable fall in urinary sodium excretion. Despite inhibition of prostaglandin synthesis, low level direct renal nerve stimulation produced an increase in renal tubular sodium reabsorption in the absence of changes in renal hemodynamics. Thus, the antinatriuresis of low level direct renal nerve stimulation is not mediated by either circulating angiotensin II or prostaglandin.

Adrenergic Fibers↗

Angiotensin II in antinatriuresis of low-level renal nerve stimulation.

Low-level direct renal nerve stimulation increases both renal tubular sodium reabsorption and renal renin secretion rate without changing arterial pressure, glomerular filtration rate, renal blood flow, or intrarenal blood flow distribution. The possibility was considered that intrarenal angiotensin II formation might mediate the antinatriuretic effect by directly enhancing renal tubular sodium reabsorption. Low-level direct renal nerve stimulation was performed in anesthetized saline-loaded dogs before and after intrarenal blockade to angiotensin II with [1-sarcosine, 8-alanine]angiotensin II. The antinatriuretic response to low-level direct renal nerve stimulation was not altered by intrarenal blockade to angiotensin II. Renal renin secretion rate was increased by low-level direct renal nerve stimulation in the absence of changes in systemic or renal hemodynamics. The antinatriuretic effect of low-level direct renal nerve stimulation does not depend on the intrarenal action of angiotensin II.

Angiotensin II↗

Specificity of neural effect on renal tubular sodium reabsorption.

Low level direct renal nerve stimulation increases renal tubular sodium reabsorption in the absence of changes in glomerular filtration rate, renal blood flow, or intrarenal distribution of blood flow. Blockade of this response with phenoxybenzamine (or guanethidine) supports the interpretation that it is mediated by direct adrenergic innervation of the renal tubule.

Animals↗

A device for the cutaneous exteriorization of chronic intravascular catheters.

A device has been designed which permits the cutaneous exteriorization of chronically implanted intravascular catheters. From one to three catheters may be exteriorized for withdrawing blood samples or for connecting to a pressure transducer. The device is uniquely suited for studying animals in a conscious and unrestrained state such as during exercise.

Animals↗

Effect of sympathetic blocking agents on the antinatriuresis of reflex renal nerve stimulation.

To evaluate the effects of reflex renal sympathetic nerve stimulation on renal tubular sodium handling, clearance studies were performed in anesthetized dogs. With renal perfusion pressure held constant, baroreceptor reflex renal sympathetic nerve stimulation was produced by controlled arterial hemorrhage or carotid sinus perfusion. Significant decreases in urinary sodium excretion occurred in the presence of minor insignificant alterations in renal blood flow and no changes in glomerular filtration rate. Renal alpha adrenergic receptor blockade (phenoxybenzamine) or adrenergic blockade (guanethidine) completely reversed the fall in urinary sodium excretion; this could not be attributed to alterations in glomerular filtration rate or renal blood flow. These studies support the interpretation that adrenergic innervation of the renal tubules is involved in the regulation of renal tubular sodium reabsorption.

Adrenergic alpha-Antagonists↗

Iowa wrestling study: weight classification systems.

Many wrestlers lose a large amount of weight in a relatively short period of time to become certified for interscholastic competition. In most states, there are twelve certified weight classes with intervals ranging from 6 to 18 pounds. Using anthropometric data obtained from 834 "average" wrestlers that were measured 5-8 weeks before competition, we predicted their "minimal" body weights and assigned them into arbitrarily designated weight classes of 6, 8 and 10 pound intervals. In addition, the 1973-74 and the 1974-75 certifying records for Iowa wrestlers were examined with regard to frequency distribution patterns. The results indicated that the majority of students were certifying for a weight classes. In fast, forty percent of the more than 8900 students were certified for the 119-138 classes and 57% of the population were located within the 112-145 weight classes. Inspection of the frequency distribution patterns of wrestlers assigned to the arbitrary classes also showed a marked concentration of wrestlers who weighed between 120 and 140 pounds and this relationship became more apparent when ten pound intervals were considered. From these findings we recommended that state high school associations consider: 1) allowing more than one wrestler per team to compete in a single weight class; 2) porviding more weight classes than the current twelve; and 3) promoting body composition assessments during the pre-season period in order to minimize the problems created by the "making of weight."

Body Composition↗

Iowa wrestling study: weight loss and urinary profiles of collegiate wrestlers.

A longitudinal study was conducted with various members of the 1975 University of Iowa NCAA championship wrestling team to determine if excessive weight loss, accompanied by signs of dehydration, occurred at the college level of competition. Body weight changes from September to December indicated a mean loss of 6%, while skinfold totals (6 sites) changed from a mean of 58 mm to 37 mm. During a four-month period, mean weight losses of 10.2, 9.5, 8.0, 7.5 and 7.0 lbs occurred in intervals of 12, 4, 3, 2 and 1 day, respectively. Basal urines analyzed throughout the season usually contained 2-3 times the potassium excreted before the season started. Analyses of urines at various intervals during a 2-day time period prior to weigh-in showed a .003 increase in specific gravity, 160 mosm/1 increase in osmolarity, .10 decrease in pH, 45.3 mEq/1 decrease in Na+ concentration, and a 71.3 mEq/1 increase in K+ concentration which suggested that the wrestlers were dehydrated prior to competition. Total urinary electrolyte loss during the 2 days amounted to 3.7% of estimated total body Na+ stores and 3.0% of total body K+ stores. These data were similar to what had been reported for Iowa high school finalists and indicated that collegiate wrestlers were also competing while in a dehydrated state.

Body Weight↗

Renal neuroadrenergic transmission.

To study the role of the renal sympathetic nerves in the regulation of sodium excretion, we examined the renal functional response to left renal nerve stimulation before (group I) and after (group II) left renal adrenergic blockade with guanethidine. In group I dogs, absolute sodium excretion from the left kidney fell markedly after left renal nerve stimulation; the decreases in glomerular filtration rate and renal blood flow were of a similar magnitude. Using the radiolabeled microsphere technique, distribution of renal blood flow to the outer cortex was diminished after left renal nerve stimulation. In group II dogs, guanethidine blocked all of these effects of left renal nerve stimulation. In group iii studies, a low level of left renal nerve stimulation was used which resulted in a decrease in sodium excretion in the absence of changes in glomerular filtration rate, renal blood flow, or intrarenal distribution of blood flow; this effect was blocked by renal adrenergic blockade with guanethidine in group iv studies. These data support a role for the renal sympathetic nerves to directly influence renal tubular sodium transport in the absence of alterations in renal hemodynamics.

Animals↗

Iowa wrestling study: changes in the urinary profiles of wrestlers prior to and after competition.

During the 1973 and 1974 state high school wrestling championships, urine samples were obtained from wrestlers prior to the weigh-in, immediately before they wrestled, and immediately after the subjects had completed their match. Specific gravity, osmolarity, pH, sodium and potassium determinations, as well as qualitative tests for protein and ketones, indicated that the wrestlers were in a dehydrated state at the time of weigh-in. After the five hour interim between the weigh-in and the first match, all but the pH measure remained essentially unchanged. This absence of significant changes in the urinary profile suggests that the wrestlers were unable to rehydrate during the five hour time period between the weigh-in and the first match and that they were competing in a dehydrated state. Urine samples collected after competition were significantly lower in specific gravity, osmolarity and potassium concentration than samples obtained before the match. The urinary potassium levels were of interest because at the three conditions (weigh-in, before the first match, after competition) they were 73-182% higher than values reported for high school students who were nonwrestlers.

Dehydration↗

Baroreflex control of renal sympathetic nerve activity in hypertensive miniature swine.

The baroreceptor reflex control of renal nerve activity was examined in seven normotensive and 14 deoxycorticosterone acetate-treated anesthetized Yucatan miniature swine. Pressor responses evoked by the administration of phenylephrine were used to assess reflex control. The mean absolute threshold for inhibition of renal nerve activity was higher but not significantly different between the deoxycorticosterone acetate-treated and normotensive group. However, the mean relative threshold for inhibition of renal nerve activity was significantly greater in the deoxycorticosterone acetate-treated group (p less than 0.05). Responses from five deoxycorticosterone acetate-treated and five normotensive swine were used to examine the time course of the baroreflex inhibition of renal nerve activity. During the initial rise in pressure the percent inhibition of renal nerve activity was similar for the two groups. During the recovery phase of the response, renal nerve activity in the deoxycorticosterone acetate-treated group returned to baseline while renal nerve activity remained attenuated below baseline in the normotensive group. The gain of the reflex was significantly lower in the deoxycorticosterone acetate-treated group compared with the control group (p less than 0.05). The results of this study clearly indicate that baroreceptor reflex control of renal nerve activity is altered in anesthetized deoxycorticosterone acetate-treated hypertensive swine.

Animals↗

Physical activity in human hypertension. A mechanisms approach.

The concept of treating hypertension without medication is seen as an attractive alternative to the problems that can arise with the use of drug therapy. Weight loss, salt restriction, relaxation therapy, and exercise have been the non-pharmacological treatments for hypertension. The role of long term exercise in lowering resting arterial pressure in hypertension, and its use as a non-drug therapy have been studied. Epidemiological studies of athletic ability, occupation, and leisure-time activities have provided equivocal findings and the effect of training on chronic high blood pressure of hypertensives is still unclear. Further well-controlled studies (with respect to training intensities, weight loss, concurrent hypotensive medication, salt restriction, and hypertensive classification), with an emphasis on elucidating the physiological mechanisms involved, are required so that the contribution of exercise to hypertensive therapy can be determined.

Blood Pressure↗