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Biomedical subjects

R A Reeves

Publications and source records attributed to R A Reeves.

54 records · Page 3Linked to original sources
PubMed1988

Cardiovascular effects of indapamide in hypertensive patients with or without renal failure. A dose-response curve.

Fifteen patients with mild-to-moderate hypertension (10 with normal and five with decreased renal function) were studied after treatment with placebo and low (1 mg), intermediate (2.5 mg), and high (5.0 mg per day) doses of indapamide, each for four weeks. Six patients--five with normal renal function--were classified as nonresponders (decrease in diastolic blood pressure less than 5 mm Hg). The remaining nine patients had dose-related decreases in blood pressure. Patients with or without renal failure showed similar decreases in blood pressure. Blood pressure reduction was associated with a significant decrease in cardiac index in the responders at the highest dose, related to a decrease in left ventricular end-diastolic dimension and stroke volume, whereas heart rate did not increase. This apparent decrease in venous return was associated with a significant decrease in body weight but not plasma volume in the responders. Indapamide did not change plasma norepinephrine levels, but decreased pressor responsiveness to exogenous norepinephrine. Responders had lower initial plasma renin activity and a smaller absolute increase in plasma renin activity while receiving indapamide, whereas angiotensin II pressor responsiveness was decreased more. The results presented indicate that the blood pressure lowering effect of indapamide in the present patient population is observed with or without renal failure and is associated with a decrease in pressor reactivity. In nonresponders, compensatory mechanisms (e.g., renin) may negate the antihypertensive effect of indapamide.

Cardiovascular System↗
PubMed1988

Epinephrine and left ventricular function in humans: effects of beta-1 vs nonselective beta-blockade.

Changes in cardiac performance in response to epinephrine administered by graded infusion were assessed by M-mode echocardiography in normotensive healthy subjects after pretreatment with placebo, the beta 1-selective blocker atenolol, or the nonselective beta-blocker propranolol. Epinephrine alone increased heart rate and left ventricular end diastolic dimension and decreased left ventricular end systolic dimension. Left ventricular performance as assessed by fractional shortening and systolic blood pressure/end-systolic volume (P/V) ratio was also increased. Atenolol pretreatment did not significantly affect the increase in heart rate by epinephrine. However, atenolol did prevent the effects of epinephrine on left ventricular dimensions and left ventricular performance at the lower infusion rates and significantly blunted these effects at the highest infusion rate. After propranolol, epinephrine significantly decreased left ventricular end diastolic dimension despite decreasing heart rate and left ventricular emptying (associated with a high afterload). P/V ratio remained unchanged. These results indicate that beta 2-receptors may play a major role in the increase in heart rate caused by epinephrine. In contrast, epinephrine's positive inotropic effect appears to be mediated primarily via beta 1-receptors and, at higher concentrations, possibly also through beta 2-receptors. The pattern of changes in left ventricular end diastolic dimension suggests that epinephrine increases venous return via both beta 1- and beta 2-receptor stimulation and that alpha-receptor stimulation (epinephrine after propranolol) may actually decrease venous return.

Adrenergic beta-Antagonists↗
PubMed1987

Vasodilators and regression of left ventricular hypertrophy. Hydralazine versus prazosin in hypertensive humans.

Long-term treatment of hypertensive rats with arterial vasodilators may further increase left ventricular hypertrophy. Since left ventricular hypertrophy may be an important determinant of outcome in hypertension, the long-term effects of arterial vasodilation with hydralazine on left ventricular mass and function were compared with those of an alternative third-line drug, the alpha1 blocker prazosin, in patients still hypertensive despite combined diuretic and beta blocker therapy. A single-blind, randomized, two-group parallel design was employed. Both treatments induced a sustained antihypertensive effect, with hydralazine showing more effect on supine blood pressure, and prazosin having more effect on standing pressure. Heart rate, cardiac output, and volume status showed only minor changes. Plasma norepinephrine showed a sustained increase when measured in both the supine and standing positions, but the increases were similar for the two treatments. Supine and standing plasma renin activity increased only during long-term treatment with hydralazine. Prazosin induced a progressive decrease in left ventricular mass over time (-34 +/- 15 g/m2 at 12 months), but hydralazine did not (-9 +/- 10 g/m2 after 12 months). Stepwise regression indicated that a decrease in systolic blood pressure was associated with a decrease in left ventricular mass with both treatments, but an increase in plasma norepinephrine was associated with an increase in left ventricular mass only with hydralazine, suggesting that increased sympathetic activity may affect left ventricular mass via cardiac alpha1 receptors. Thus, if regression of left ventricular hypertrophy is a worthwhile therapeutic goal, hydralazine and analogous arterial vasodilators are not drugs of choice.

Adult↗
PubMed1987

Hemodynamic interaction of nonselective vs. beta-1-selective beta-blockade with hydralazine in normal humans.

To assess the effects of nonselective vs. beta 1-selective beta-blockade on the hyperdynamic circulation induced by hydralazine, eight healthy volunteers received placebo, propranolol, 20 and 40 mg, and atenolol, 25 and 50 mg, on 5 separate days, followed by hydralazine (range 75 to 150 mg). Hydralazine decreased afterload (end-systolic wall stress) and increased venous return and left ventricular performance (by M-mode echocardiography). Both beta-blockers blunted the increases in heart rate, cardiac output, and venous return similarly, although heart rate and cardiac output were not completely normalized. Atenolol did not affect the hydralazine-induced decrease in afterload, whereas propranolol significantly opposed this change (P less than 0.03). The hyperdynamic circulation seen with hydralazine is mostly beta mediated, primarily beta 1. When given with hydralazine the two beta-blocker types differ primarily in their effects on afterload.

Adolescent↗
PubMed1987

Beta-receptor-mediated increase in venous return in humans.

To assess the involvement of beta 1- and beta 2-receptors in the regulation of venous return in humans, changes in left ventricular end-diastolic (LVED) dimension were determined during beta-receptor stimulation either by exogenous catecholamines or by increased endogenous sympathetic activity after hydralazine, after placebo and during nonselective versus beta 1-selective blockade. Taking changes in heart rate and LV emptying into account, the three beta-agonists (isoproterenol, terbutaline, and epinephrine) as well as hydralazine increased venous return as inferred from LVED dimension. After hydralazine, nonselective and beta 1-selective blockade were equally effective in blunting the increases in venous return, in heart rate, and in positive inotropic response. Beta 1-Selective blockade did not affect the increase in heart rate caused by epinephrine and partially inhibited the positive inotropic effect and the increase in venous return. Nonselective blockade not only blocked the increase in venous return owing to epinephrine but actually led to a decrease, as evidenced by a decrease in LVED dimension despite the marked bradycardia and high afterload with this combination. The present findings in healthy humans indicate that stimulation of both beta 1- and beta 2-receptors increases venous return, heart rate, and myocardial contractility. Beta 1-Receptors appear to predominate in the response to neuronal sympathetic activity.

Adult↗
PubMed1987

Relevance of echocardiographic left ventricular hypertrophy in mild hypertension.

The current diagnostic criteria for uncomplicated mild hypertension inadequately distinguish the subgroup actually at increased risk for cardiovascular sequelae, from the large group not at increased risk, and therefore unlikely to benefit from current pharmacological intervention. Although finding of electrocardiographic left ventricular hypertrophy indicates increased risk, the ECG lacks sufficient sensitivity to be diagnostically useful in mild hypertension. It can be argued that echocardiographic screening for LV hypertrophy may better detect the subpopulation of mildly hypertensive patients at increased risk. The known relationships between ambulatory BP, LV hypertrophy and prognosis support this hypothesis. Further study is required, however, before echocardiography can be advocated for routine application to the diagnosis and management of mild hypertension.

Blood Pressure Determination↗
PubMed1986

Relaxation therapy for hypertension. Comparison of effects with concomitant placebo, diuretic, and beta-blocker.

We compared the effects of relaxation therapy in hypertensive patients taking placebo, a beta-blocker (atenolol, 100 mg/d), or a diuretic (chlorthalidone, 50 mg/d), and we also compared the effects of relaxation therapy with the effects of the latter two drugs alone. Blood pressures were measured not only in the relaxation therapists' office and at a hypertension clinic, but also in the patient's environment by means of 24-hour ambulatory blood pressure recordings. The effect of relaxation therapy, while statistically significant, was modest. There was no generalization of effect to ambulatory blood pressure. Atenolol was significantly more effective than relaxation in reducing both systolic and diastolic pressure. Chlorthalidone was significantly more effective than relaxation in reducing systolic but not diastolic pressure in the hypertension clinic only. The long-term effects of relaxation were independent of concomitant drug use, but within the actual relaxation sessions blood pressure dropped further during chlorthalidone than during placebo or atenolol treatment.

Adrenergic beta-Antagonists↗
PubMed1986

The role of cardiac beta-1 receptors in the hemodynamic response to a beta-2 agonist.

The role of beta 1-receptors in the hemodynamic response to beta 2-stimulation was assessed in seven healthy subjects by infusion of the selective beta 2-agonist terbutaline both with and without selective beta 1-blockade by atenolol (50 mg). Infusion of terbutaline increased heart rate (+28 bpm) and indices of left ventricular (LV) performance associated with a marked decrease in LV end-systolic wall stress. The LV end-diastolic dimension remained unchanged despite the tachycardia, suggesting that venous return had increased. Systolic blood pressure increased, whereas total peripheral resistance and diastolic blood pressure decreased. Atenolol pretreatment caused the hemodynamic changes expected of beta 1-blockade but did not blunt the effects of terbutaline on heart rate, peripheral resistance, or venous return. Increases after terbutaline in LV performance and systolic blood pressure were significantly blunted by atenolol. Stimulation of beta 1-receptors therefore appears to play no role in the chronotropic and only a moderate role in the inotropic response after infusion of a beta 2-agonist. Alternative mechanisms for the cardiac changes with terbutaline include (1) withdrawal of vagal tone, (2) decrease in afterload, and (3) stimulation of cardiac beta 2-receptors.

Adult↗
PubMed1986

Loss of nocturnal decline in blood pressure after cardiac transplantation.

Twenty-four hour noninvasive ambulatory blood pressure and heart rate monitoring was performed on patients who underwent orthotopic cardiac transplantation, as part of the investigation of the de novo hypertension that developes in such patients. Patients with essential hypertension served as control subjects. The results demonstrated a highly significant loss of the usual decline in blood pressure and heart rate during sleep in the transplant patients. A similar loss of nocturnal decline in blood pressure was noted in a group of 10 patients with autonomic neuropathy secondary to diabetes mellitus. The de novo hypertension associated with cardiac transplantation is probably multicausal. Impairment of renal function by cyclosporin-A with associated salt and water retention and persistent elevation of the systemic vascular resistance in the presence of a restored normal cardiac output by the "new" heart are major factors. In addition, loss of the normal nocturnal decline in blood pressure and heart rate, which probably is related to the denervated state of the transplanted heart, may play an important role in blood pressure control.

Adult↗
PubMed1985

Nadolol, propranolol, and thyroid hormones: evidence for a membrane-stabilizing action of propranolol.

Ten normal subjects participated in a placebo-controlled, randomized, parallel study to determine the effects on thyroid hormones of chronic (4 wk) propranolol or nadolol, including observation for 2 wk after their discontinuation. Subjects took placebo for 1 wk, then propranolol or nadolol doses increased weekly to 240 mg/day by 3 wk. After 1 wk of placebo, after 2 wk of the highest dose of propranolol or nadolol, and 2, 4, 6, 9, and 13 days after their discontinuation, thyroid hormone levels were measured by radioimmunoassay and heart rate responses to exercise were assessed. Both drugs induced equal and high degrees of exercise tachycardia inhibition. Propranolol decreased 3,3'5-triiodothyronine (T3) levels, increased 3-3'-5'-triiodothyronine (rT3) levels, tended to increase thyroxine levels, but did not increase thyroid-stimulating hormone levels. After discontinuation of propranolol, rT3 levels slowly (day 6) returned to values after placebo, suggesting delayed recovery of 5'-deiodination. There was no evidence of any rebound in T3 levels after withdrawal of propranolol. Nadolol induced no significant changes in the thyroid hormones measured. The data agree with the known effects of propranolol on thyroid hormones in normal man and show that nadolol does not have these effects when given chronically at an equivalent beta-blocking dose. The likely explanation is that the membrane-stabilizing activity of propranolol alters thyroid physiology by interfering with 5'-deiodinase.

Adult↗
PubMed1984

Nonselective beta-blockade enhances pressor responsiveness to epinephrine, norepinephrine, and angiotensin II in normal man.

Nonselective beta-blockers increase peripheral vascular resistance and, sometimes, blood pressure (BP); increased responsiveness to circulating pressor agents could be one of the underlying mechanisms. Heart rate (HR) and BP responses to graded intravenous infusions of epinephrine, norepinephrine, and angiotensin II were recorded after placebo and then after 4 wk of beta-blocker treatment (nadolol or propranolol, 240 mg/day) in 10 healthy young men. Adequacy of beta-blockade was demonstrated by a mean 31% decrease in HR response to bicycle exercise, with no differences between the two beta-blockers. Under placebo conditions epinephrine lowered diastolic BP and raised HR; these effects were reversed during treatment with beta-blockers. beta-Blockade potentiated BP responses to norepinephrine and angiotensin II: Thirty-five percent less norepinephrine and 52% less angiotensin II were required to increase mean BP by 15 mm Hg. A final study 2 wk after beta-blocker cessation revealed the absence of lasting effect. These results confirm the concept of unopposed alpha-constriction for epinephrine and also demonstrate increased BP responses to norepinephrine and angiotensin II during chronic beta-blockade.

Adult↗
PubMed1983

Pseudopseudohypoparathyroidism and pheochromocytoma. Association or coincidence?

We saw a patient who had a pheochromocytoma producing hypertension along with clear evidence of pseudopseudohypoparathyroidism (PPHP). Although PPHP does not have the biochemical features of hypocalcemia and elevated parathyroid hormone levels as seen in pseudohypoparathyroidism, it seems from this case to share the potential for multiple endocrine neoplasia seen in a number of metabolic disorders in which pheochromocytoma may be a prominent manifestation.

Adrenal Gland Neoplasms↗
PubMed1978

Effects of color and trait anxiety on state anxiety.

A 2 (trait anxiety) X 4 (color) factorial design was used to determine the effects of red, green, yellow, and blue on state anxiety as a function of high and low trait anxiety. The State-Trait Anxiety Inventory was used to assess both traint (A-Trait) and state (A-State) anxiety for the 10 students assigned to each of the eight treatment combinations. High A-Trait students were significantly more anxious while viewing blue, red, and green than were the low A-Trait students and blue produced significantly more state anxiety than did either yellow or green. These results are consitent with state-trait theory and indicate that the effects of color on state anxiety may be confounded with trait anxiety unless the levels of A-Trait are equivalent for each color condition. The role of cultural and individual differences in the relationship between color and emotion and implications for research are discussed.

Anxiety↗
PubMedDate not supplied

Omapatrilat provides long-term control of hypertension: a randomized trial of treatment withdrawal.

Omapatrilat simultaneously inhibits neutral endopeptidase and angiotensin-converting enzyme, increasing levels of vasodilatory peptides while decreasing production of angiotensin II. This study evaluated the clinical effects of withdrawal of omapatrilat after a patient's hypertension had been controlled (seated diastolic blood pressure <90 mm Hg) on omapatrilat for at least 6 months, with or without adjunctive antihypertensive medications. This double-blind study randomized 83 patients to receive either their established omapatrilat dose or placebo for 8 weeks; any concomitant antihypertensive medications were kept constant. Patients continuing on omapatrilat had no change in blood pressure. Patients whose chronic omapatrilat treatment was replaced by placebo had clinically important increases in both systolic (+16.5 mm Hg) and diastolic ((+9.6 mm Hg) blood pressures (both p<0.001). An increase in blood pressure was also seen in patients who were taking adjunctive antihypertensive medications prior to withdrawal of omapatrilat. This study demonstrates that when compared to withdrawal placebo, omapatrilat maintains clinically and statistically significant blood pressure reductions.

Adult↗