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Biomedical subjects

S Julius

Publications and source records attributed to S Julius.

227 records · Page 13Linked to original sources
PubMedDate not supplied

Plasma norepinephrine variations with dietary sodium intake.

Plasma catecholamine and renin activity levels were measured across a range of dietary sodium intakes (10--300 mEq/day) in 20 normal male volunteers. Supine plasma norepinephrine levels presented a triphasic pattern in relation to urine sodium, whereas epinephrine levels were not significantly altered by sodium intake, and renin showed the well-known hyperbolic relationship to urine sodium excretion. Highest supine norepinephrine values occurred at low salt intakes, the lowest when sodium excretion was between 100 and 180 mEq/day, and intermediate when sodium excretion was greater than 180 mEq/day. These findings show that sodium intake is an important consideration in the interpretation of plasma norepinephrine levels.

Adult↗
PubMedDate not supplied

Sustained blood pressure elevation to lower body compression in pigs and dogs.

Inflatable suits were constructed for lower body compression in pigs and dogs. The suit for pigs encompassed hindquarters and part of the abdomen, and the smaller suit for dogs compressed only the hindquarters, leaving free the abdominal cavity. In conscious, diazepam-pretreated pigs, the compression lasted 30 minutes; during that period the blood pressure increased 50/38 mm Hg over the baseline. In chloralose-anesthetized dogs, the compression was extended to 3 hours; the blood pressure increase was 44/53 mm Hg. Blood pressure fell to the baseline immediately after decompression in both animals. In both species the substantial blood pressure increase was due to an increase of vascular resistance; this did not induced the expected baroreceptor-mediated bradycardia. In dogs, the blood pressure increase was accompanied by a large increase of plasma norepinephrine (from 179 to 975 pg/ml). To test whether the increase of vascular resistance reflected the mechanical compression of the vessels under the suit, animals were pretreated with trimethaphan. In pigs the trimethaphan substantially decreased the vascular resistance and the blood pressure response. This indicated that a portion of the vasoconstriction occurred in areas outside the suit. Lower body compression is a new model to cause prolonged blood pressure elevation by noninvasive and nonpharmacologic means. The mechanism of the blood pressure elevation requires further investigation.

Abdomen↗
PubMedDate not supplied

Role of cardiovascular receptors on the neural regulation of renin release in normal men.

Although factors influencing renin release have been studied extensively, one facet of renin release remains controversial, namely, neural regulation by arterial high-pressure receptors and cardiopulmonary low-pressure receptors. We therefore designed four studies to investigate systematically the separate and combined effects of unloading (decreased stretch) high- and low-pressure receptors on renin release in normal men. Selective unloading of cardiopulmonary receptors was induced by impeding the venous return with tourniquets around the thighs. A predominant unloading of arterial (carotid) baroreceptors was elicited with upright posture and simultaneously preventing the venous pooling in the legs. Unloading of both high- and low-pressure receptors was achieved by both upright standing and tilting. During postural experiments to predominantly unload arterial baroreceptors, the heart rate increased and the veins constricted, but renin failed to increase. The postural increase of renin occurred only if we allowed venous pooling in the legs. Selective unloading of cardiopulmonary receptors elicited substantial increases of renin. When both the cardiopulmonary and arterial baroreceptors were unloaded, renin increased more than with isolated unloading of cardiopulmonary receptors. We conclude that: 1) in intact humans it is possible to demonstrate an independent role of cardiopulmonary receptors in the control of renin release; 2) there Is evidence for interaction between the two receptor systems in renin control; but 3) an independent role for arterial baroreceptors in the control of renin release could not be demonstrated under the conditions of this experiment.

Adolescent↗
PubMedDate not supplied

Racial differences in erythrocyte cation transport.

Erythrocyte contents and ouabain-insensitive transport pathways were measured in 120 white and black normotensives and hypertensives. Mean maximal sodium-stimulated lithium-sodium countertransport rate was higher in white hypertensives than in white normotensives, and countertransport was significantly positively correlated with mean arterial pressure in whites. Values similar to those in white normotensives were found in both black normotensives and hypertensives, and countertransport was not significantly correlated with blood pressure in blacks. The rate constant for passive lithium efflux was greater in whites as compared to blacks, and the difference was not related to blood pressure level or sex. Ouabain-insensitive, furosemide-sensitive sodium and potassium effluxes were not found to be altered in hypertension. Furosemide-sensitive sodium efflux rate was lower in blacks but furosemide-sensitive potassium efflux was not similarly depressed. While white subjects demonstrated a close correlation between sodium and potassium effluxes, blacks did not. Further study of these differences in the cellular metabolism of sodium and potassium may provide clues to the pathogenesis of racial dissimilarities in total body sodium handling.

Adolescent↗
PubMedDate not supplied

Role of cardiopulmonary mechanoreceptors in ADH release in normal humans.

Although animal studies have shown that cardiopulmonary receptors regulate the release of antidiuretic hormone (ADH), human studies have produced conflicting results. Consequently, we studied 17 normal healthy men to determine the ADH response to selective unloading (decreased stretch) of cardiopulmonary low-pressure receptors by thigh cuff inflation in the supine position. Thigh cuff inflation of 30 to 40 mm Hg decreased the central blood volume and right atrial pressure (cardiopulmonary receptor load), while mean arterial pressure and pulse pressure were unchanged (arterial baroreceptor load). Thigh cuff inflation to this level did not alter plasma osmolality or cardiac output. Plasma ADH increased an average of 67% (p less than 0.01) following thigh cuff inflation compared to the preceding supine baseline. After thigh cuff deflation (n = 6), the ADH decreased toward preinflation values. We conclude that selective unloading of the cardiopulmonary receptors in humans increases plasma ADH levels.

Adolescent↗
PubMedDate not supplied

The defense reaction: a common denominator of coronary risk and blood pressure in neurogenic hypertension?

In addition to high blood pressure, patients with hypertension often have insulin resistance, dyslipidemia and increased sympathetic tone. An increased sympathetic tone can negatively affect glucose utilization through three distinct mechanisms; a direct beta-adrenoreceptor-mediated insulin resistance, through conversion to more insulin resistant fast twitch fibers and through alpha-adrenergic vasoconstriction which may decrease the delivery of insulin and glucose to the skeletal muscle cells. The insulin resistance in turn may be responsible for the observed dyslipidemia in hypertension. The sympathetic overactivity in hypertension reflects a chronic activation of defense/vigilance reaction. The increase of cardiac output, blood pressure and insulin resistance in the course of the defense reaction are viewed as an appropriate preparatory response to facilitate muscular exercise (through higher cardiac output and increased pressure) and preserve (through insulin resistance) the optimal supply of glucose to the brain. The defense reaction may have been useful in evolution and may have offered survival advantage. In modern times with prolonged life expectancy the previously useful response (in evolutionary terms) contributes to a faster and deleterious wear and tear of the cardiovascular system.

Arousal↗
PubMedDate not supplied

The evidence for a pathophysiologic significance of the sympathetic overactivity in hypertension.

Interest for the role of the sympathetics in the genesis of hypertension has come full circle from early enthusiasm, through a period of neglect, to present understanding that strong evidence cannot be ignored. Sympathetic overactivity starts in childhood and is easily evident in 30% of patients with incipient hypertension. Later, in advanced hypertension, altered cardiovascular responsiveness obscures the obvious signs of sympathetic overactivity but the brain maintains its decisive pathophysiologic role. The early onset, the bimodal distribution of the neurogenic "hyperkinetic" pattern and familial aggregation suggest a genetic component in sympathetic overactivity. Patients with hypertension are at high risk for coronary disease and some of that risk is not directly related to blood pressure elevation. High sympathetic tone explains the pathophysiology of "pressure-independent" risk for premature coronary atherosclerosis in hypertension and for excess mortality/morbidity in patients who had already developed coronary heart disease.

Adult↗
PubMedDate not supplied

Borderline hypertension.

Borderline hypertension is a widespread condition and because of its large prevalence, it has a major impact on the cardiovascular mortality of the population. A modest elevation of blood pressure in borderline hypertension is closely associated with multiple rheologic, hemodynamic, humoral and metabolic abnormalities. Many of these abnormalities, independently of the blood pressure, increase the coronary risk in patients with borderline hypertension. There is no sufficient evidence in the literature to propose a well structured algorithm of management and treatment of borderline hypertension. Establishing a reliable baseline blood pressure (by ambulatory or home blood pressure monitoring) is the first step in the management of borderline hypertension. One year of intensive nonpharmacologic treatment is recommended as the first therapeutic modality. If this fails to decrease the blood pressure, pharmacologic treatment with small doses of antihypertensive medication is recommended in patients with dyslipidemia or in patients whose out of office blood pressure remains elevated.

Cardiovascular Diseases↗
PubMedDate not supplied

Role of cardiac factors in the initial hypotensive action by beta-adrenoreceptor blocking agents.

The blood pressure decrease after beta-blockade is delayed and there are little data on the hemodynamic events associated with the initial decrease in blood pressure. The present study measured the hemodynamics of the initial hypotensive action of timolol maleate, a nonselective beta-adrenoreceptor blocking agent, in 10 patients with essential hypertension. Frequent measurements were made for the first 30 hours of treatment, and follow-up measurements made at 3 and 6 weeks. Before treatment, mean arterial blood pressure, cardiac output, and arteriovenous oxygen difference were 115.9 +/- 9.1 mm Hg, 4.65 +/- 1.05 liter/min, and 55.0 +/- 9.6 ml/liter, respectively. At 3 hours after the first dose of timolol, blood pressure had fallen 13.5 +/- 8.2 mm Hg (p less than 0.05). This was preceded by an initial decrease in cardiac output, which was not associated with a simultaneous decrease in blood pressure, and by an increase of arteriovenous oxygen difference. The early, statistically significant, decrease in cardiac output was followed by a return to normal output, which coincided with the onset of blood pressure reduction. The magnitude of the initial decrease of cardiac output and of the initial increase in arteriovenous oxygen difference was significantly correlated to the later decrease in blood pressure (7 hours after first dose). These hemodynamic observations are consistent with the notion that early underperfusions of tissue play a role in the initial hypotensive action of beta-blockers. After 6 weeks, the blood pressure remained lower but the cardiac output was again decreased at that point. As with many antihypertensive agents, there was a difference between the early and late hemodynamic pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗