Biomedical subjects

B Egan

Publications and source records attributed to B Egan.

At least 37 records · Page 2Linked to original sources

PubMed1988

Vascular structure enhances regional resistance responses in mild essential hypertension.

Forearm blood flow (FABF) and forearm vascular resistance (FAVR) responses to sequential regional infusions of norepinephrine (NE) and angiotensin II (Ang II) were examined in 24 hypertensive and 18 matched normotensive subjects. Sensitivity to both vasoconstrictors, defined as the percentage increase in FAVR in response to the lowest dose of each agonist, was similar in the two groups. Also, the FABF response curve to the full range of both agonists did not differ between hypertensives and normotensives by analysis of variance (ANOVA). While the FAVR responses at the lowest doses of both NE and Ang II were similar in hypertensives and normotensives, FAVR responses in hypertensives diverged progressively from the normotensive response pattern, P less than 0.01 according to ANOVA. The hypertensives achieved greater maximum FAVR levels at the highest doses of both agonists, P less than 0.05 according to repeated measures ANOVA. After 10 min of ischaemic exercise, FAVR was higher in hypertensives than in normotensives (2.24 +/- 0.10 versus 1.87 +/- 0.08; P = 0.02, respectively). This value for FAVR was termed the minimum FAVR (mFAVR). The overall response pattern characterized by increased mFAVR, unchanged threshold sensitivity, steeper slope, greater maximum response and similarity of responses to both NE and Ang II is most consistent with a structural augmentation of resistance responses. A model was used in an effort to increase understanding of the vessel morphology. This model suggested that an increased wall/lumen ratio, perhaps without an actual increase in vascular smooth muscle mass, played an important role in the observed FAVR pattern.

Adult↗

PubMed1987

Mechanism of increased alpha adrenergic vasoconstriction in human essential hypertension.

Multiple components of vascular alpha adrenergic responsiveness were investigated in twenty-four men with mild hypertension and eighteen age- and weight-matched normotensive controls. Arterial plasma norepinephrine (paNE), an index of sympathetic drive, was increased in hypertensives compared to normotensives (mean +/- SE), 199 +/- 24 vs. 134 +/- 11 pg/ml, P less than 0.02. The effective concentration of intra-arterial (iaNE) increasing forearm vascular resistance (FAVR) 30% (NE-EC30, an index of vascular alpha-receptor sensitivity) was similar in normotensives and hypertensives, 9 +/- 1 vs. 13 +/- 3 ng/100 ml per min, respectively, P greater than 0.3. The phentolamine induced reduction in FAVR, an index of vascular alpha-tone, was greater in hypertensives, -21.3 +/- 1.8 vs. normotensives, -14.9 +/- 1.2 U, P less than 0.02. We interpret these data as evidence for normal vascular alpha-receptor sensitivity to norepinephrine in mild hypertensives. Consequently, the increased sympathetic drive in mild hypertensives explains the elevated vascular alpha-tone. Although vascular alpha-receptor sensitivity to iaNE was normal, the FAVR responses at high doses (reactivity) were greater in hypertensives to regional infusion of both NE and angiotensin II. This "nonspecific" enhancement of vascular reactivity is probably explained by structural vascular changes in hypertensives.

Adult↗

PubMed1987

The heart and the regulation of renin.

The cause of the low-renin state in hypertension is unknown. To consider our hypothesis that cardiopulmonary mechanoreceptors suppress renin release in these patients, it was necessary to prove that "low pressure" receptors affected renin levels in man. A series of experiments was performed to selectively alter the stretch (load) on carotid and cardiopulmonary baroreceptors in healthy human volunteers. These studies showed that selectively altering high-pressure baroreceptor load did not affect plasma renin activity. Selectively unloading the low-pressure receptors increased plasma renin activity. Simultaneous unloading of both baroreceptors caused the largest increases in renin activity. While the data indicated an interaction of high- and low-pressure receptors on the neural regulation of renin release, we interpreted these results as evidence for a predominant influence of cardiopulmonary mechanoreceptors on the neurogenic regulation of renin secretion in man.

Arteries↗

PubMed1986

Management of the patient with borderline hypertension.

A clinical definition of borderline hypertension is offered that includes increased risk of complications but no proof that interventions will be effective in reducing those complications. Defining an average blood pressure level permits improved prediction of individual risk. Simple clinical assessment permits definition of overall risk for hypertension and atherosclerosis. The vigor of intervention should be matched to the level of overall absolute risk. Pharmacologic treatment is appropriate for patients with borderline pressure elevation who have hypertensive target organ changes or a history of hypertensive complications. Patients with borderline hypertension deemed to be at intermediate to high risk but without target organ injury should receive nonpharmacologic (NP) instruction to reduce overall cardiovascular risk. The average blood pressure level, other atherosclerosis risk factors, and the effects of NP measures on these variables should be reevaluated at 6-12-month intervals in this group. Those at low risk should be cautioned about excessive weight gain and should have annual blood pressure measurements.

Aerobiosis↗

PubMed1985

Pharmacologic reduction of sympathetic drive increases platelet alpha-2-receptor number.

Several lines of evidence implicate sympathetic nervous system involvement in the pathophysiology of essential hypertension in man. Extrapolations are frequently made from in vitro measurements of plasma catecholamine levels to the physiologic role of the sympathetic system in hypertension. We assessed the utility and validity of such extrapolation from in vitro to in vivo measures of adrenergic function. Addition of guanadrel to diuretic therapy in 11 patients with essential hypertension reduced supine intra-arterial blood pressure from 135 +/- 14/76 +/- 9 to 127 +/- 13/67 +/- 5 mm Hg (P less than 0.02). Supine heart rate was also reduced, from 77 +/- 14 to 63 +/- 13 bpm (P less than 0.001). Plasma norepinephrine levels fell from 303 +/- 107 to 170 +/- 46 pg/ml (P less than 0.01). Platelet alpha 2-receptor number ([3H]yohimbine maximal binding) increased from 204 +/- 77 to 301 +/- 150 fmol/mg (P less than 0.02). The pupillary mydriatic response to phenylephrine and the forearm arterial vasoconstrictor response to intra-arterial norepinephrine did not change. Thus guanadrel reduced blood pressure by decreasing sympathetic tone. In this milieu of low sympathetic activity the platelet alpha 2-receptor number increased, but physiologic responses to exogenous alpha-agonists did not change. Caution is therefore advised when extrapolating from in vitro measurement of plasma catecholamine levels and platelet alpha 2-receptor number to the in vivo physiologic significance.

Adult↗

PubMed1985

Methods for measuring vascular and nonvascular alpha-receptor sensitivity in humans.

Since increased alpha-adrenergic reactivity may participate in the pathophysiology of essential hypertension, methods for accurately assessing in vivo alpha-receptor sensitivity in humans might be useful. The goals of this study were to employ previously used methods, namely pupillometry and local forearm intraarterial infusions, to assess alpha-receptor sensitivity, create an in vivo environment of decreased sympathetic drive (plasma norepinephrine) and increased alpha-receptor number (platelet alpha 2), in which increased alpha-receptor sensitivity to exogenous agonists might occur. Five patients with minimally elevated blood pressure (139 +/- 5/90 +/- 4 mm Hg) while on diuretic monotherapy completed assessment of biochemical and physiologic variables on diuretic alone and again on diuretic and guanadrel. Guanadrel plus diuretic compared with diuretic alone lowered the seated diastolic and standing systolic and diastolic blood pressure. Heart rate was decreased about 10 beats/min. Baseline supine norepinephrine was reduced an average of 40% (from 281 +/- 23 to 168 +/- 16 pg/ml, p = 0.03), and platelet alpha 2-receptors were increased roughly 40% (from 178 +/- 34 to 250 +/- 54 fmol/micrograms, p = 0.07). Despite the expected decrease in sympathetic drive and increase in alpha-receptors (platelet alpha 2), the pupillary mydriatic response to phenylephrine and the forearm vasoconstrictor response to intraarterial norepinephrine were not augmented. The failure to detect increased physiologic responsiveness in the presence of decreased norepinephrine and increased alpha 2-receptor number lends itself to multiple explanations which need to be tested in future research.(ABSTRACT TRUNCATED AT 250 WORDS)

Arm↗

PubMed1985

Vascular hypertrophy in borderline hypertension: relationship to blood pressure and sympathetic drive.

While borderline hypertension increases the chance for cardiovascular disease, most with borderline hypertension will not experience problems. Thus, the risk of intervening probably outweighs benefit for the majority. However, those with target organ damage are probably at higher risk and might benefit from more aggressive management. Therefore, we assessed vascular hypertrophy and average home blood pressures in patients with borderline hypertension which might be of value in therapeutic planning. Minimum forearm vascular resistance (mFAVR) was used as an index of vascular hypertrophy. Comparing ten normotensive controls to twenty individuals with borderline hypertension revealed a significant difference in mFAVR (1.7 +/- 0.06 vs 2.1 +/- 0.1, p less than .05). There were obvious differences in blood pressure between normotensives and borderlines which contributed to differences in mFAVR. However, within the group with borderline hypertension, no relationship was apparent between mean blood pressure and mFAVR, r = 0.13, NS. Among the borderline hypertensives, baseline plasma norepinephrine correlated with mFAVR, r = 0.48, p less than .05, suggesting that the sympathetic nervous system contributes to vascular hypertrophy in this group. In a separate group of individuals with nine normotensives and nine borderline hypertensives we wished to find if average home blood pressure would correlate better with mFAVR than a single laboratory measurement. While both the home (r = 0.56, p less than .05) and laboratory (r = 0.66, p less than .01) MBP correlated significantly with mFAVR, the data did not confirm the hypothesis that the average home blood pressures would better predict the degree of vascular hypertrophy. These data show that a substantial proportion of patients with borderline hypertension have evidence for vascular hypertrophy, sympathetic drive might contribute to vascular hypertrophy in borderline hypertension, average home blood pressures did not aid in separating those with and without evidence for vascular hypertrophy.

Adult↗

PubMed1985

Nutritional and lifestyle approaches to the prevention and management of hypertension.

We have been encouraged by the growing interest in nutrition and lifestyle for the prevention and treatment of hypertension. While no proven means for preventing hypertension exist, epidemiologic data have identified risk factors for hypertension. We have attempted to outline a reasonable program based on knowledge of risk factors for hypertension on one hand vs. the lack of data that hypertension can be prevented on the other. Managing patients who have hypertension with nondrug strategies is a different matter. First, more evidence is available indicating effectiveness for reducing a high pressure than for preventing a normotensive person from becoming hypertensive. Secondly, hypertension is a risk factor for premature cardiovascular morbidity and mortality. Thus, the risk-to-benefit ratio from intervening is tipped toward probability of benefit. Many of the nondrug therapies have been presented. It is unreasonable to expect a patient to adhere to every one. Therefore, patients with uncomplicated, newly diagnosed borderline and mild hypertension are given the range of modalities available and assisted in choosing those best suited to their lifestyle. The nondrug efforts are tried for three to six months in patients with uncomplicated mild hypertension. We advocate evaluating responses to the nondrug approaches with blood pressures measured both in and outside the office. Blood pressures measured by the patient at work and rest have been very valuable in our practice. If no antihypertensive benefit is seen, then most of these patients receive standard antihypertensive drugs. For those who have complete or partial success, the nondrug efforts are continued or reinforced with follow-up every three to six months.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Drinking↗

PubMed1983

Cardiopulmonary mechanoreceptors and renin release in humans.

We investigated the hemodynamic determinants of the reflex release of renin to changes in posture and blood volume distribution in healthy humans to determine the relative contribution of arterial and cardiopulmonary mechanoreceptors to the reflex release of renin under physiological circumstances. In the first experiments, we induced a selective decrease of right atrial pressure by inflation of cuffs around the thighs. Renin increased and returned toward baseline on decompression. The renin increase was neurogenic because plasma norepinephrine increased, the response was abolished by beta blockade, and renin did not increase in patients with denervated transplanted kidneys. The second experiments were performed with tilting and later filling a pressure suit to counteract the effect of tilting on gravitational pooling of the blood. Tilting elicited increases of renin and norepinephrine; filling the suit abolished these increases. Right atrial pressure fell with tilting and rose after filling the suit. Because the neck was elevated above the heart equally in both conditions, it is concluded that the increase and decrease of renin reflected decrease and increase of the stretch of cardiopulmonary receptors. The third experiments were performed by elevating the upper trunk with the legs remaining in a horizontal position (sitting). This caused a heart-to-neck pressure difference and an increased sympathetic outflow through unloading arterial baroreceptors. Norepinephrine increased but renin did not. Cardiopulmonary receptors exhibit an important influence on the reflex release of renin.

Blood Pressure↗

PubMed1983

Borderline hypertension.

Blood pressures over 130 mm Hg systolic and 80 mm Hg diastolic are associated with a significantly increased risk of cardiovascular morbidity and mortality as well as an increased risk of progression to later established hypertension. An average blood pressure based on repeated determinations is a better predictor of target organ damage in hypertensive individuals than an isolated casual clinic blood pressure. Careful clinical assessment of the patient with borderline hypertension can identify those at highest risk for progression to established hypertension and those at greatest risk for cardiovascular morbidity and mortality. We cannot currently recommend pharmacologic therapy for the vast majority of patients with blood pressures between l30/80 and l140/90 mm Hg. Although nonpharmacologic therapy is frequently met with a high degree of noncompliance, there is evidence that modest reductions in salt intake and weight often result in significant reductions in blood pressure. Many patients with borderline hypertension, when appraised of these facts, will comply and attempt to reach these limited goals. Repeated self-determination of blood pressures at home is ideally suited to many patients with borderline hypertension in defining current average blood pressure, detecting future progression, and evaluating the effects of nonpharmacologic interventions.

Alcohol Drinking↗

PubMed1981

The transient inability of the conjugating female cell to host 186 infection explains the absence of zygotic induction for 186.

In an Hfr(186) X F- cross, the 186 prophage on the incoming male chromosome is not induced, despite the fact that prophage 186 can be induced by other means (W. H. Woods and J.B. Egan, J Virol. 14:1349-1356, 1974). We show here that the conjugating female is temporarily inhibitory to infection by 186, and this delay, we postulate, enables cI repression to be reestablished before the female cell recovers its 186 sensitivity.

Chromosomes, Bacterial↗

PubMed1981

Coliphage 186 Replication is delayed when the host cell is UV irradiated before infection.

In contrast to results with injections by lambda and P2, the latent period for infection by coliphage 186 is extended when the host cell is UV irradiated before infection. We find that 186 replication is significantly delayed in such a cell, even though the phage itself has not been irradiated. In contrast, replication of the closely related phage P2 under the same conditions is not affected.

Bacteriophage lambda↗

PubMed1968