Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The safety and efficacy of ketanserin, a competitive serotonin blocking agent, and propranolol were compared in 33 patients with mild to moderate hypertension (sitting diastolic blood pressure [DBP] 95-115 mm Hg) using a placebo run-in, randomized, double-blind parallel study design. All patients received placebo for 4 weeks, then were randomized to receive increasing doses of either ketanserin (20, 40 mg twice daily) or propranolol (40, 80 mg twice daily) to achieve a goal sitting DBP less than 90 mm Hg. Patients not achieving the goal blood pressure with either drug as monotherapy, received the other drug in combination. At the end of the active monotherapy phase (week 10 of the study), propranolol demonstrated a greater decrease in DBP from baseline, as compared to ketanserin (-7.9 +/- 10.9 mm Hg with propranolol, P less than 0.05; -1.0 +/- 7.2 mm Hg with ketanserin, P = NS). Four out of 16 patients achieved goal response on propranolol, compared to 3/17 for ketanserin. With combination treatment, 9/18 patients reached the goal response; the addition of propranolol to ketanserin in non-responders resulted in further reduction of sitting DBP of -10.3 +/- 6.3 compared to monotherapy (P less than 0.001), while the addition of ketanserin to non-responders produced no significant response in sitting DBP. Propranolol showed a consistent effect in slowing heart rate. Ketanserin displayed less frequent side effects than propranolol. Propranolol used twice daily appears to be more effective than twice daily ketanserin use in patients with mild to moderate hypertension.
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PMID:Serotonergic blockade compared with beta-adrenergic blockade in systemic hypertension: a double-blind comparison of ketanserin with propranolol. 290 19

In an open crossover comparison of propranolol and nitrendipine, 19 patients with hypertension received 40 to 160 mg propranolol and 5 to 20 mg nitrendipine twice a day. Mean (+/- SD) predose supine blood pressure fell from 145/98 +/- 11/7 to 132/88 +/- 12/8 mm Hg with propranolol and to 135/92 +/- 11/9 mm Hg with nitrendipine. Resting heart rate was reduced by propranolol but was unchanged 12 hours after nitrendipine dosing. Neither propranolol nor nitrendipine altered plasma glucose or insulin after oral glucose. Propranolol significantly increased fasting triglyceride levels and reduced high-density lipoprotein cholesterol levels, but nitrendipine induced no change. Propranolol reduced and nitrendipine increased plasma renin activity after exercise. Peak plasma nitrendipine levels were dose proportional and occurred at 1 to 2 hours after dosing, whereas peak blood pressure reductions occurred 4 hours after the last dose of nitrendipine and were associated with mean increases in heart rate. Nitrendipine is almost equivalent in hypotensive effect to propranolol, but nitrendipine increases plasma renin activity after exertion and may produce transient tachycardia. However, nitrendipine does not cause unwanted metabolic effects.
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PMID:Hemodynamic and metabolic effects of the calcium channel blocking agent nitrendipine. 293 98

The effect of celiprolol at a daily dosage of 300 mg (19 patients) was compared with that of propranolol at a daily dosage of 120 mg (14 patients) on peripheral blood flow of the calf and foot in a randomized double-blind trial. Altogether 33 patients (47 extremities) suffering from arterial occlusive disease (stage II according to Fontaine) and hypertension, were treated for 25 days. Blood flow was measured by strain-gauge plethysmography. Celiprolol led to a small, insignificant increase in resting blood flow of the muscle. Propranolol produced a small decrease in resting blood flow of the muscle, and a significant fall in resting blood flow of the skin of the foot. At the completion of treatment with celiprolol there was a small increase in the initial value of reactive hyperaemia of the calf. Propranolol led to a decrease in the initial, and in the maximum values of reactive hyperaemia of the calf and foot. Celiprolol and propranolol led to a comparable decrease in resting blood pressure.
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PMID:[Comparative studies of the effect of a cardioselective and a noncardioselective beta-blocker on peripheral circulation in patients with arterial occlusive disease]. 293 41

We studied the control of forearm vascular resistance (FVR) by cardiopulmonary receptors in seven patients with hypertension and left ventricular hypertrophy (LVH) and in seven normotensive control subjects. Increasing levels of lower body negative pressure (LBNP) (-10 and -40 mm Hg) induced a progressive decrease in central venous pressure (CVP) and an increase in FVR. The changes in these two variables were correlated both in normal subjects and patients with hypertension (slope for normal subjects = -29.9, for patients with hypertension = -40.3, NS). After propranolol, there was a significant reduction in the increase in FVR induced by -40 mm Hg LBNP in normal subjects (+107 +/- 5 vs +129 +/- 15 mm Hg/ml/sec, p less than .05) but not in patients with hypertension. Consequently, the slope of the delta CVP/delta FVR regression was reduced in normal subjects (-20.6, p less than .01) but not in patients with hypertension. In another seven normal subjects and seven patients with hypertension and LVH we assessed the effects of -10 and -40 mm Hg LBNP on left ventricular filling pressure (LVFP). LBNP induced similar changes in CVP, LVFP, and total peripheral resistance both in normal subjects and in patients with hypertension. Propranolol failed to modify the effects of LBNP on CVP and LVFP in both groups and reduced the response of total peripheral resistance to -40 mm Hg LBNP only in normal subjects. Propranolol did not reduce the response of FVR to the cold pressor test and sustained handgrip or the arterial baroreflex response to the injection of phenylephrine and increased neck tissue pressure. Thus, hypertension-induced LVH seems to be associated with a selective impairment of the left ventricular sensory receptors.
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PMID:Impaired responsiveness of the ventricular sensory receptor in hypertensive patients with left ventricular hypertrophy. 294 75

The antihypertensive efficacy of timed-release diltiazem was compared with propranolol in a randomized, double-blind study of 40 patients with mild to moderate hypertension. Patients (diltiazem = 17; propranolol = 9) had echocardiograms at baseline and after 6 months of therapy to determine left ventricular mass, end-systolic stress, total peripheral resistance, and cross-sectional area index. Diltiazem lowered the blood pressure (152/98 to 134/83), as propranolol did (155/98 to 150/85). Diltiazem caused a significant reduction in left ventricular mass (215.1 +/- 56.3 to 175.7 +/- 54.7 g; p less than 0.0007) and in cross-sectional area index (5.7 +/- 1.0 to 4.8 +/- 1.1 cm2; p less than 0.002). Propranolol caused no change in mass (227.5 +/- 45.6 to 227.4 +/- 54.0) and no change in cross-sectional area index (5.3 +/- 0.8 to 5.5 +/- 1.2). Comparisons between diltiazem and propranolol showed a significantly greater decrease in mass with diltiazem (p less than 0.03) and cross-sectional index (p less than 0.015). Diltiazem proved to be safe and equally efficacious in blood pressure control and significantly better in reducing indices of mass hypertrophy than propranolol.
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PMID:Diltiazem-induced left ventricular mass regression in hypertensive patients. 295 72

The effects of graded lower body negative pressure (-10 and -40 mm Hg) on vascular resistance and plasma vasopressin, norepinephrine, and renin activity were assessed in seven hypertensive subjects with left ventricular hypertrophy and seven sex-matched and age-matched normotensive subjects. In both groups increasing levels of lower body negative pressure induced a progressive decrease in right atrial pressure and an increase in vascular resistance. In normal subjects plasma vasopressin, norepinephrine, and renin activity were progressively raised, whereas only the higher level of stimulation increased plasma renin activity, norepinephrine, and vasopressin in hypertensive subjects. Propranolol induced a significant increase in plasma vasopressin in normal subjects (from 1.3 +/- 0.1 to 2.0 +/- 0.1 pg/ml; p less than 0.05) but not in hypertensive subjects. In this latter condition -10 mm Hg lower body negative pressure failed to increase plasma vasopressin, norepinephrine, and renin activity in normal subjects. Propranolol abolished the change in plasma renin activity in both groups, reduced the increase in vascular resistance induced by -40 mm Hg lower body negative pressure in normotensive subjects, but did not modify the rise in vasopressin elicited by this stimulus in normal subjects or the humoral and hemodynamic reflex responses evoked in hypertensive subjects. These results suggest that cardiopulmonary receptors are involved in the control of vasopressin release in normal subjects, whereas in hypertensive subjects with left ventricular hypertrophy, this control is altered because of an impaired function of cardiopulmonary receptors.
Hypertension 1987 Dec
PMID:Impaired control of vasopressin release in hypertensive subjects with cardiac hypertrophy. 296 89

Previous studies have suggested that dopamine may have an important role as an inhibitor of aldosterone secretion in humans. Recent studies have also suggested that the adrenergic nervous system may have an important role in controlling aldosterone secretion. The present study investigated the effects of dopamine on aldosterone secretion in response to angiotensin II, with and without pretreatment with propranolol, and to adrenocorticotropic hormone, another known stimulator of aldosterone secretion. Nine normal subjects in balance at 10 mEq sodium intake received dopamine (4 micrograms/kg/min) or vehicle for 270 minutes on 2 consecutive days on three separate occasions. After 120 minutes of dopamine infusion, the subjects received a 30-minute intravenous infusion of angiotensin II (in cumulative doses of 0.5, 1, 2, 4, and 6 pmol/kg/min), angiotensin II after oral pretreatment with propranolol, or adrenocorticotropic hormone (in cumulative doses of 0.5, 1, 2, and 5 U/hr). Aldosterone responses to 2, 4, and 6 pmol/kg/min of angiotensin II (without propranolol) were greater in vehicle-treated than in dopamine-treated subjects (p less than 0.05), as was the slope of the angiotensin II-vehicle dose-response curve (0.46, p less than 0.05). Propranolol suppressed the aldosterone response to angiotensin II, but dopamine still inhibited the response. Aldosterone and cortisol secretion were stimulated equally by adrenocorticotropic hormone in dopamine-treated and vehicle-treated groups. These results suggest that dopamine selectively inhibits the aldosterone response to angiotensin II and that this response is not mediated by teh activity of dopamine at beta-adrenergic receptors.
Hypertension 1986 May
PMID:Dopamine selectively inhibits aldosterone responses to angiotensin II in humans. 300 25

Propranolol is a commonly used drug; of new and refilled prescriptions, it ranked no. 1 in 1984 and no. 2 in 1985. Medical conditions for its use include angina pectoris, myocardial infarction, hypertension, cardiac dysrhythmias, hypertrophic subaortic stenosis, migraine headache, hyperthyroidism, and pheochromocytoma. Almost all dental practitioners will treat a patient receiving propranolol for one of these conditions. The following recommendations seem appropriate at this time: The patient should continue to receive propranolol during dental treatment. Sudden withdrawal of the beta-blocker will cost the patient the benefit of propranolol therapy and may lead to acute myocardial ischemia. Acute stress should be minimized, as hypertensive responses may also be caused by endogenously released epinephrine. Short appointments scheduled in the morning, possibly with conscious sedation, should be considered. The dosage of adrenergic vasoconstrictors should be limited and gingival retraction cord containing epinephrine avoided entirely. The blood pressure should be taken approximately 5 minutes after local anesthesia is administered to determine if a systemic response has occurred. In the unlikely event of a hypertensive emergency, a rapidly acting, short-duration antihypertensive drug, such as the alpha-blocker phentolamine (Regitine, 5 mg intravenously) should be administered. Sublingual nitroglycerin (Nitrostat, 0.4 mg) may be useful as a nonparenteral alternative. These recommendations apply to other nonselective beta-blockers, including nadolol (Corgard) and timolol (Blocadren). They may also apply to labetalol (Normodyne, Trandate), a nonselective beta-antagonist with some alpha-blocking activity and to pindolol (Visken), a beta-blocker with some intrinsic beta 2-agonistic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertensive response to levonordefrin in a patient receiving propranolol: report of case. 327 28

A double-blind parallel group study was conducted to examine the effects of oral labetalol, in doses from 100 to 800 mg BID, and propranolol, 40 to 320 mg, in patients with mild to moderate hypertension. The doses of labetalol (n = 74) and propranolol (n = 79) were titrated weekly to achieve a sitting diastolic blood pressure (DBP) of less than 90 mmHg or at least a 10-mmHg decrease from placebo baseline on two consecutive visits. A 2-month fixed-dose maintenance phase followed in which a diuretic could be added if the sitting DBP was greater than or equal to 100 mmHg on maximum doses of either drug. BP and heart rate were measured 8-12 hours after a dose in the sitting and standing positions. Labetalol was significantly more effective at the end of monotherapy than propranolol was in lowering both the sitting (p less than .05) and standing (p less than .04) DBP. The reduction in the systolic, although more pronounced for those on labetalol, was not significantly different; 53% of patients had a "good" response to labetalol compared with 30% of the propranolol group. Propranolol significantly (p less than 0.01) lowered heart rate compared with labetalol. Nine patients in the labetalol group and 10 in the propranolol group required a diuretic. The decrease in BP after the addition of a diuretic was comparable. Changes in plasma lipids were not significant, but HDL increased 9% with labetalol and decreased 2% with propranolol. Triglycerides increased 25% with labetalol and 31% with propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Labetalol compared with propranolol in the treatment of black hypertensive patients. 331 2

The efficacy and safety of nifedipine in a gastrointestinal therapeutic system (GITS) push-pull osmotic pump formulation was compared with long-acting propranolol in 49 patients with mild to moderate hypertension already receiving diuretics. Using a two-week placebo run-in, double-blind study design, patients were randomly assigned to receive nifedipine GITS (n = 24) in doses of 30 mg, 60 mg, or 90 mg once daily; or long-acting propranolol (n = 25) in doses of 80, 160, or 240 mg once daily. Previous diuretic therapy was continued. Sitting and five-minute standing blood pressure and heart rate measurements were made 24 hours after dosing. At the endpoint of treatment, both nifedipine GITS and sustained-release propranolol reduced blood pressure compared with placebo (p less than 0.001) in the sitting and standing positions. Nifedipine GITS was more effective in lowering standing systolic blood pressure than was propranolol (p less than 0.02). Propranolol caused a greater reduction in resting heart rate than did nifedipine GITS (p less than 0.003). Both drugs were well tolerated. Nifedipine GITS is an effective and safe once-daily drug for use in patients with hypertension who are already receiving diuretics, may be more effective than sustained-release propranolol, and may be better tolerated than conventional nifedipine capsules.
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PMID:Multicenter comparison of the nifedipine gastrointestinal therapeutic system and long-acting propranolol in patients with mild to moderate systemic hypertension receiving diuretics. A preliminary experience. 333 74


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