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Biomedical subjects

J F Burris

Publications and source records attributed to J F Burris.

At least 55 records · Page 3Linked to original sources
PubMed1989

Humoral Na+-K+ pump inhibitory activity in essential hypertension and in normotensive subjects after acute volume expansion.

Plasma from black male patients with essential hypertension was bioassayed for vascular Na+-K+ pump inhibitory activity. Halves of the same rat tail artery were incubated for two hours in boiled plasma supernates from a hypertensive patient and a paired age-, sex-, and race-matched normotensive subject and then ouabain-sensitive 86Rb uptake was measured. Ouabain-sensitive 86Rb uptake by their leukocytes was also measured. Eighteen pairs of subjects were studied. The uptakes were not significantly different in the hypertensive patients and control subjects. However, when we selected from the eighteen hypertensive patients, nine with low plasma renin activity on the day of the study, uptakes were reduced in the hypertensive patients relative to the paired control subjects. We also assayed plasma supernates from normotensive black and white male subjects before and after acute volume expansion (2.5 L saline IV + 1.5 L distilled water orally over a three-hour period) and from paired normotensive subjects before and after sham volume expansion and obtained a positive bioassay in the expanded subjects both on intraindividual and interindividual comparisons. These studies demonstrate increased vascular Na+-K+ pump inhibitory activity in the plasma of black male patients with low renin essential hypertension and in the plasma of normotensive subjects after acute volume expansion. The findings suggest that the inhibitory activity in the hypertensive subjects' plasma is related to volume expansion, relative or absolute.

Adult↗
PubMed1989

Comparison of the antihypertensive effects of betaxolol and chlorthalidone as monotherapy and in combination.

In this multicenter, double-blind, parallel study, the antihypertensive effects of betaxolol (20 mg once daily) and/or chlorthalidone (25 mg once daily) were analyzed in 186 patients with essential hypertension. Following a 2- to 4-week placebo baseline period, patients were randomized to one of two treatment groups (betaxolol or chlorthalidone) and studied for 6 weeks while receiving single therapy and an additional 6 weeks with a combination of the two agents. Significant decreases from baseline supine diastolic blood pressure (SDBP) were observed in both groups at the end of the single-therapy phase (11 mm Hg in SDBP for betaxolol and 12 mm Hg in SDBP for chlorthalidone); a further significant decrease (7 mm Hg for betaxolol and 8 mm Hg for chlorthalidone in SDBP) was observed from the end of the single-therapy phase to the end of the combination-therapy phase. Changes in supine systolic blood pressure (SSBP) from baseline to the end of the single-therapy phase were 10 mm Hg for the betaxolol and 16 mm Hg for the chlorthalidone group. In all cases, within-group changes were statistically significant. From the end of single therapy to end of combination therapy there was an additional 14-mm Hg and 13-mm Hg reduction in SSBP in the betaxolol and chlorthalidone groups, respectively. Overall, 89% of the randomized patients completed the single-treatment phase (phase I), and 89% of those patients completed the combined therapy phase (phase II). There was no significant difference between treatment groups in the clinical response rate (SDBP at or below 90 mm Hg or a decrease from baseline of at least 10 mm Hg). A substantial percentage of patients completing phase I responded to either single agent (58% for betaxolol and 65% for chlorthalidone). Among patients completing phase II therapy, the combination of the two agents produced a greater response rate (83% for the betaxolol-first group and 85% for the chlorthalidone-first group). In conclusion, both agents were effective and well tolerated. The most frequent adverse events in the single-therapy phase were headache, arthralgia, and dizziness, while bradycardia, rhinitis, arthralgia, and dizziness were most frequent in the combination-therapy phase. The combination of betaxolol (20 mg) and chlorthalidone (25 mg) once daily produced an additive antihypertensive effect regardless of which drug was administered first.

Betaxolol↗
PubMed1988

Comparison of the antihypertensive effects of betaxolol to atenolol.

A randomized double-blind multicenter study compared a new oral beta 1-adrenergic antagonist, betaxolol 10 to 40 mg (n = 71), with atenolol 25 to 100 mg (n = 75). Each drug was administered once daily for 24 weeks in patients with mild to moderate hypertension. Blood pressure (BP) measurements were taken 24 hours after dosing. Each drug produced significant (p less than 0.01) reductions in mean supine diastolic BP. The mean decrease in supine diastolic BP with betaxolol was significantly greater at weeks 4, 6, 10 and 12 (p less than 0.05). Throughout the remainder of the trial (weeks 14 to 24), no significant differences in BP reduction were noted between treatment groups. Normotension (supine diastolic BP less than or equal to 90 mm Hg) was achieved in 72% of those given betaxolol compared with 52% of those given atenolol (p less than 0.05). The most common side effects noted were bradycardia, fatigue and headache. The incidence of these and of central nervous system side effects was similar between the betaxolol and atenolol groups. Both agents were well tolerated. At recommended doses, betaxolol once daily may be more effective than atenolol once daily in patients with mild to moderate hypertension.

Adrenergic beta-Antagonists↗
PubMed1988

Long-term efficacy and safety of nitrendipine in severe essential hypertension.

This multicenter study evaluated nitrendipine, a dihydropyridine calcium antagonist, alone or in combination with hydrochlorothiazide and/or propranolol in severe essential hypertension (baseline supine diastolic BP greater than or equal to 115 mm Hg). After an initial 3- to 7-day drug-free run-in, a 2- to 5-week titration phase, and a 4- to 6-week maintenance period, patients with supine diastolic less than or equal to 90 mm Hg entered long-term maintenance. Four centers enrolled 57 patients initially; 43 qualified for the extended therapy trial, and 30 had completed greater than 2 years of therapy (mean duration of 756 days) at the time of analysis. Supine BP fell from 186/122 +/- 5/2 mm Hg at baseline (group mean +/- SEM) to 139/89 +/- 3/2 mm Hg after 2 years (p less than 0.001/0.001). Standing BP fell from 185/126 +/- 5/2 to 138/90 +/- 3/2 mm Hg (p less than 0.001/0.001). Supine pulse rate changed from 82 beats/min at baseline to 74 beats/min (p less than 0.01) and standing pulse rate from 88 to 78 beats/min (p less than 0.01). Seventeen patients received nitrendipine alone, 4 received nitredipine plus HCTZ, 2 received nitrendipine plus propranolol, and 7 patients received all three drugs. Response was similar in patients less than 50 years old and in those greater than or equal to 50 years, and also in black and nonblack patients. Three patients were lost to follow-up, six were terminated for inadequate BP control, and four terminated for side effects. Twenty-four patients completed greater than 2.5 years treatment (mean duration of 933 days).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

A double-blind evaluation of the effect of amlodipine on ambulatory blood pressure in hypertensive patients.

Amlodipine is a new long-acting calcium antagonist that has a long half-life and appears to be suitable for once-daily administration. A double-blind, randomized, parallel, placebo-controlled study was conducted to evaluate the effect of amlodipine on ambulatory blood pressures in hypertensive patients. The study consisted of a 4-week single-blind placebo run-in phase, followed by 4 weeks of double-blind therapy. Ambulatory blood pressure was measured for 24 h at the end of the placebo run-in phase and after double-blind therapy. Sixteen patients were randomized to receive either amlodipine 5 mg or placebo in a 2:1 ratio. Amlodipine 5 mg daily significantly reduced supine and standing blood pressure 24 h postdose. Ambulatory blood pressure recordings revealed adequate blood pressure control throughout the 24-h dosing interval. Amlodipine was well tolerated and only two patients reported side effects--neither was withdrawn from therapy. No treatment-related abnormalities were noted. It was concluded that amlodipine 5 mg daily was effective antihypertensive therapy throughout the 24-h dosing period in the patients studied, and it was well tolerated.

Amlodipine↗
PubMed1988

Double-blind comparison of amlodipine and hydrochlorothiazide in patients with mild to moderate hypertension.

Amlodipine, a new long-acting dihydropyridine calcium antagonist, was compared with hydrochlorothiazie (HCTZ) in 145 patients with mild to moderate hypertension. After 4 weeks of single-blind placebo runin, patients were randomly allocated to receive amlodipine (2.5-10 mg once daily, n = 97) or HCTZ (25-100 mg once daily, n = 48). At study week 12 response rates for amlodipine and HCTZ were 61.5 and 60.5%, respectively. There were clinically significant reductions in 24-h postdose blood pressures with both amlodipine (-18/-11 mm Hg supine: -14/-10 mm Hg standing) and HCTZ (-18/-10 mm Hg supine, -18/-9 mm Hg standing). After study week 12, atenolol (50-100 mg once daily) was added to the regimen of those patients whose hypertension was not controlled with monotherapy. Neither amlodipine nor HCTZ produced clinically significant changes in pulse rate, electrocardiogram, or chest x-ray film. Although amlodipine increased and HCTZ decreased the high-density lipoprotein (HDL)/total cholesterol ratio and the HDL/(low-density lipoprotein + very-low-density lipoprotein) ratio, the difference between the two treatments was not statistically significant. The incidence of side effects and the rate of patient withdrawal was comparable in the two groups. The incidence of laboratory abnormalities was 56% with HCTZ (mainly hypokalemia and hyperuricemia) and 16% with amlodipine. Amlodipine was an effective, well-tolerated agent for treatment of mild-to-moderate hypertension in this study, as single-daily-dose monotherapy and in combination with atenolol.

Adolescent↗
PubMed1988

Nitrendipine in severe hypertension. Satellite symposium on calcium antagonists.

We report the results of a multicenter trial in which nitrendipine, alone or in combination with a diuretic, a beta-blocker, or both, was administered to 114 patients with severe hypertension (greater than or equal to 115 mm Hg). Nitrendipine was titrated in doses of 5 to 30 mg b.i.d. If blood pressure was not controlled with nitrendipine alone, hydrochlorothiazide or propranolol or both were added. After a mean of 29 days in the study, 96 (90%) of 107 patients reached the initial goal of therapy; in 44 (41%) given nitrendipine alone the mean decrease in supine blood pressure was 38/25 mm Hg. After a mean of 91 days, 69 (72%) of 96 patients achieved the final goal of therapy; in 24 (25%) patients given nitrendipine alone the mean supine blood pressure decrease from baseline was 49/33 mm Hg. Falls in blood pressure were comparable in the patients given drug combinations. Seventy-two of 114 patients given study drug(s) had adverse experiences; headache and edema were the most frequent complaints. Only four patients dropped out of the study because of adverse effects. Most abnormal laboratory values occurred when nitrendipine was given with hydrochlorothiazide or propranolol or both. Analysis of severely hypertensive patients followed up in our Virginia center revealed continued control of blood pressure after long-term follow-up (43 +/- 3 [SD] months). Average supine blood pressure was reduced from 180/121 +/- 21/5 to 140/90 +/- 16/9 (SD) mm Hg (p less than 0.001). It was concluded that the calcium antagonist nitrendipine, alone or in combination with a diuretic or beta-blocker or both, is effective in the treatment of severe hypertension.

Adrenergic beta-Antagonists↗
PubMed1988

Thiazide therapy is not a cause of arrhythmia in patients with systemic hypertension.

Forty-four patients with uncomplicated systemic hypertension underwent 48-hour electrocardiographic monitoring before and after four weeks of treatment with hydrochlorothiazide, 100 mg daily. Plasma potassium concentration decreased from 4.07 +/- 0.26 mmol/L (4.07 +/- 0.26 mEq/L) to 3.36 +/- 0.44 mmol/L (3.36 +/- 0.44 mEq/L). The average number of premature ventricular contractions, couplets, or ventricular tachycardia episodes did not change significantly. Twenty patients had more than minimal ventricular ectopy (class 2 to 5) before and 17 after diuretic therapy. Further analysis revealed that following diuretic therapy, neither patients with plasma potassium levels of 3.4 mmol/L or less (less than or equal to 3.4 mEq/L) nor patients with left ventricular hypertrophy had increased ectopy as compared with baseline. At baseline, patients with left ventricular hypertrophy had more arrhythmias than patients without. We conclude that the results of this study provide no evidence that diuretic therapy or diuretic-induced hypokalemia results in increased ventricular ectopy, and that patients with left ventricular hypertrophy may have more ventricular ectopy than patients without, but these arrhythmias are not adversely effected by diuretic therapy.

Cardiac Complexes, Premature↗
PubMed1988

Remission of mild to moderate hypertension after treatment with carteolol, a beta-adrenoceptor blocker with intrinsic sympathomimetic activity.

Previous studies have indicated that some hypertensive patients, following a period of effective treatment with certain antihypertensive drugs, may experience prolonged normotension after drug withdrawal. We have studied the ability of carteolol, a nonselective beta-adrenoceptor antagonist with intrinsic sympathomimetic activity, to produce such remissions of hypertension. Thirty-four patients whose diastolic blood pressure was controlled at 90 mm Hg or less with carteolol monotherapy (2.5 to 5.0 mg/d for an average of 328 days) were randomized to a nine-month, double-blind, placebo-controlled drug-withdrawal trial. Those patients randomized to continue carteolol therapy had initially responded to carteolol treatment with reduction in blood pressure from 151 +/- 4/99 +/- 2 to 132 +/- 4/80 +/- 2 mm Hg. Those randomized to treatment with placebo had initially responded with blood pressure reductions from 154 +/- 4/97 +/- 2 to 137 +/- 4/81 +/- 2 mm Hg. Changes in mean systolic and diastolic blood pressure (mm Hg +/- SEM) from baseline during carteolol therapy to the final visit at nine months were not different for patients receiving placebo (13 +/- 5/6 +/- 4 mm Hg, recumbent; 11 +/- 6/4 mm Hg, standing) or carteolol (11 +/- 5/7 +/- 3 mm Hg, recumbent; 12 +/- 6/7 +/- 3 mm Hg, standing). The final mean recumbent diastolic blood pressure (86.9 mm Hg) was the same in both groups. Prolonged normotension may follow a period of carteolol treatment, again suggesting the potential importance of periodic withdrawal of antihypertensive medication.

Blood Pressure↗
PubMed1988

Effects of a nonpressor dose of neuropeptide Y on cardiac output, regional blood flow distribution and plasma renin, vasopressin and catecholamine levels.

Neuropeptide Y (NPY) is a peptide with vasoconstrictor properties known to be present in the central nervous system as well as in sympathetic nerve endings and the adrenal medulla. The purposes of this study were to investigate in normotensive conscious rats the effects of nonpressor doses of NPY on cardiac output and regional blood flow distribution (using radiolabeled microspheres) as well as on plasma renin activity, plasma catecholamine and vasopressin levels. NPY (0.1 microgram/min) infused i.v. for 30 min modified neither blood pressure nor heart rate. Cardiac index was at comparable levels in NPY- as in vehicle-treated rats (17.7 +/- 1.6, n = 8, vs. 21.3 +/- 0.9 ml/min/100 g, n = 8, mean +/- S.E.M.). There was no significant difference in regional blood flow distribution between the two groups of rats, except for the large intestine (0.42 +/- 0.06 vs. 0.71 +/- 0.1 ml/min/g in NPY- and vehicle-treated rats, respectively, P less than .05). Basal plasma renin activity and catecholamine levels were not modified by NPY whereas plasma vasopressin levels were lower (P less than .05) in rats given NPY (0.76 +/- 0.3 pg/ml, n = 8) than in those having received the vehicle (2.2 +/- 0.4 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Nitrendipine monotherapy in severe hypertension.

Nitrendipine is a new dihydropyridine derivative developed specifically for the treatment of hypertension. Oral nitrendipine was administered to twelve patients with severe hypertension (diastolic blood pressure greater than 114 mm/Hg). All antihypertensive drugs were discontinued at least 72 hours prior to nitrendipine administration. The initial dose of nitrendipine was 5 mgs. orally twice daily which was titrated at 2 to 5 day intervals up to a maximum dose of 40 mgs. twice a day. Average pretreatment blood pressure (+/- SD) was 194/118 (28/3) mm/Hg and was 191/122 (25/9) mm/Hg standing. After 7 to 10 days of nitrendipine monotherapy, the average blood pressure had decreased to 170/102 (20/9) mm/Hg supine and 167/106 (19/8) mm/Hg standing. Thirty days of nitrendipine therapy resulted in a further decrease of average blood pressure to 159/96 (18/7) mm/Hg supine and 154/99 (12/12) mm/Hg standing. Average supine pulse (+/- SD) increased from 79.0 (13.9) to 90 (15.7) beats/min. after 7-10 days and to 82 (17) beats/min. after 30 days of therapy. The average total daily dose of nitrendipine was 47.5 mgs. after 30 days. Side effects were minimal and the medication was well tolerated by most patients. It was concluded that nitrendipine is a potent and effective antihypertensive agent in patients with severe hypertension.

Administration, Oral↗
PubMed1987

Postpropranolol vasodilation in adrenalectomized glucocorticoid hypertensive rats.

Acute beta-adrenoreceptor blockade results in an enhanced blood pressure-lowering effect in glucocorticoid hypertensive rats in the absence of the adrenals. To evaluate the possible mechanism of this enhanced blood pressure-lowering effect, systemic and regional hemodynamics were determined by the radioactive microsphere technique before and after propranolol administration in bilaterally adrenalectomized (AX) and sham-operated (SH) glucocorticoid hypertensive rats. Propranolol decreased mean blood pressure (BP) and heart rate (HR) to a greater extent in the AX animals. In response to propranolol, cardiac output (CO) decreased equally in both the AX and SH animals. Regional vascular responses to propranolol were similar between the AX and SH animals, except in muscle. In muscle propranolol significantly decreased blood flow and increased resistance in the SH animals. In marked contrast, in the AX animals propranolol significantly increased blood flow and decreased vascular resistance. The results of this study show that in adrenalectomized glucocorticoid hypertensive rats, the enhanced BP lowering effect of acute beta-adrenoreceptor blockade is not mediated by changes in CO. Additionally, in glucocorticoid hypertensive rats acute beta-adrenoreceptor blockade causes selective vasodilation in skeletal muscle.

Adrenalectomy↗