Showing papers by "Joseph L. Izzo published in 1983"
TL;DR: Age accentuates and moderate prior caffeine use attenuates the cardiovascular effects of oral caffeine; these effects are not mediated solely through the sympathoadrenal system.
Abstract: The effects of age and chronic caffeine use (approximately 300 mg/day) on the cardiovascular and humoral responses to 250 mg of oral caffeine (the equivalent of 2 to 3 cups of coffee) were examined. Older subjects had greater increases in blood pressure than younger subjects (p
96 citations
TL;DR: It was concluded that increased ICP induces sustained increases in CAs which adversely affect pulmonary pressures and shunting and selective β blockade reverses these effects and may be useful in patients with evidence of sympathetic overactivity and progressive hypoxemia after head injury.
Abstract: Intracranial pressure (ICP) was increased by hyperosmolar intracerebral infusion in dogs and the cardiopulmonary and catecholamine (CA) responses followed for 4 h Increased ICP evoked persistent increases in endogenous CAs, pulmonary vascular pressures, pulmonary blood volume, and venous admixture Other dogs similarly monitored were treated with a beta-blocking dose of propranolol 25 min after the onset of increased ICP Although catecholamines were increased, elevated pulmonary pressures and venous admixture returned to control levels CO and heart rate (HR) were reduced after beta blockade but systemic vascular resistance increased It was concluded that increased ICP induces sustained increases in CAs which adversely affect pulmonary pressures and shunting Selective beta blockade reverses these effects and may be useful in patients with evidence of sympathetic overactivity and progressive hypoxemia after head injury
19 citations
TL;DR: At physiologic concentrations, circulating norepinephrine should be considered to be a cardiovascular hormone as well as an index of sympathetic nervous activity.
Abstract: The hormonal effects of circulating norepinephrine (NE) were evaluated with two-step NE infusion studies in normal volunteers. At an infusion rate that increased plasma NE 2.5-fold (approximately equivalent to the change from supine to upright posture), there were small but consistent increases in diastolic pressure (+5 mm Hg) and plasma renin activity (+13%). At the high extreme of the physiologic range (a 9-fold increase over supine basal), circulating NE caused major changes in blood pressure (+22/15 mm Hg), heart rate (-7 bpm), and plasma renin activity (+67%). Thus, at physiologic concentrations, circulating NE should be considered to be a cardiovascular hormone as well as an index of sympathetic nervous activity.
18 citations
TL;DR: An adaptation of the single-isotope radioenzymatic catecholamine assay technique allows simultaneous quantitation of free dihydroxyphenylglycol (DHPG), diHydroxymandelic acid (DOMA), and dihydrophilic acid (DOPAC) in small volumes of plasma.
11 citations
TL;DR: Pretreatment supine plasma norepinephrine correlated with blood pressure changes during fludrocortisone dosing, which suggests participation of the sympathetic nervous system in the blood pressure elevations reported during exogenous steroid administration or primary aldosteronism.
Abstract: Fludrocortisone depressed plasma norepinephrine in normal subjects but to a lesser degree than it depressed renin activity or urinary aldosterone excretion. Sympathetic nervous reactivity (defined as upright/supine plasma norepinephrine) was decreased more than supine plasma norepinephrine. Pretreatment supine plasma norepinephrine (but not plasma renin activity or aldosterone excretion) correlated with blood pressure changes during fludrocortisone dosing, which suggests participation of the sympathetic nervous system in the blood pressure elevations reported during exogenous steroid administration or primary aldosteronism. Suppression of sympathetic nervous activity and reactivity by fludrocortisone tends to explain its limited usefulness in patients with autonomie dysfunction and postural hypotension.
Clinical Pharmacology and Therapeutics (1983) 33, 102–106; doi:10.1038/clpt.1983.15
9 citations
Journal Article•
TL;DR: The data suggest that circulating NE may normally suppress sympathetic nervous activity, but that this negative feedback mechanism is impaired in uremia.
8 citations
TL;DR: It is reported that another A II receptor blocker, sarcosine-1 threonine-8 angiotensin II ([Sar 1 , Thr 8 ]A II), is not superior to saralasin in predicting the response of renovascular hypertension to surgical correction.
Abstract: Recent experiences with the angiotensin II (A II) receptor blocker sarcosine-1 alanine-8 angiotensin II (saralasin) 1 and the angiotensin-converting enzyme (ACE) inhibitor captopril 2 have served to reemphasize the importance of the renin-angiotensin axis in cardiovascular homeostasis. In this issue ofThe Journal(p 368), Fouad and her colleagues report that another A II receptor blocker, sarcosine-1 threonine-8 angiotensin II ([Sar 1 , Thr 8 ]A II), is not superior to saralasin in predicting the response of renovascular hypertension to surgical correction. However, despite the fact that depressor responses to angiotensin blockers are not specific for renovascular hypertension, it would be a mistake to assume that interruption of the renin-angiotensin system is not a useful diagnostic or therapeutic measure. Correct interpretation of various BP responses to reninangiotensin interruption is sometimes difficult but generally possible. Despite some controversy, the most important overall determinant of response to renin-angiotensin blockade is the baseline activity
5 citations