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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nineteen men (mean age, 44 years) with moderately severe essential hypertension were studied invasively at rest and during exercise. After initial predrug recordings, patients received 25 mg carvedilol orally, and central hemodynamics at rest and during exercise were recorded 1 and 2 h after tablet intake to evaluate the immediate effects of carvedilol. Blood pressure decreased by 11% within 1 h, and the hemodynamic results indicated a combination beta-blocking and vasodilating effect. After 6-9 months of treatment (dose, 25-100 mg), supine hemodynamics were recorded, first 12-24 h after the last dose and then 1 and 2 h after an additional 25-mg dose. During chronic treatment (2 h after the last dose with the patient at rest and in the supine position), mean arterial pressure was reduced by 17% (p less than 0.001) and total peripheral resistance index was reduced by 6% (NS), whereas heart rate and cardiac index were reduced by 12%. Exercise hemodynamics demonstrated a decrease in blood pressure of 17% (p less than 0.001). Exercise stroke index increased by 5% (NS), in part compensating for the reduction in heart rate of 17%. Total peripheral resistance index was reduced by 5% (NS). Twenty-four-hour blood pressure monitoring (Accutracker II) demonstrated significant blood pressure reductions in awake as well as in asleep patients. Blood pressures decreased from 163/102 to 141/84 mm Hg in from 135/78 to 122/68 mm Hg in awake and asleep patients; respectively. Carvedilol is an effective antihypertensive agent, and the hemodynamic mode of action reflects alpha 1- and beta 1-blocking activities.
J Cardiovasc Pharmacol 1992
PMID:Carvedilol in hypertension: effects on hemodynamics and 24-hour blood pressure. 137 46

The effects of carvedilol, a nonselective beta-blocker with peripheral vasodilator action, on left ventricular function and mass in essential hypertension were studied in 14 patients with diastolic filling abnormalities. Treatment produced significant decreases in blood pressure (systolic: 168.4 +/- 10.5 to 154 +/- 17.2 mm Hg, p less than 0.005; diastolic: 101.6 +/- 8.6 to 95.3 +/- 11.6 mm Hg, p less than 0.025), left ventricular mass (316.7 +/- 85.8 to 276.8 +/- 84.9 g, p less than 0.05), and left ventricular mass index (157.9 +/- 42.4 to 131.6 +/- 34.6 g.m-2, p less than 0.025). There were coincident improvements in the parameters of diastolic left ventricular filling (E/A ratio: 0.66 +/- 0.14 to 0.80 +/- 0.26, p less than 0.025; mean E descent velocity: 245 +/- 130 to 264 +/- 70 cm.s-2, p less than 0.05). No significant alterations in systolic function were observed, although three patients with systolic impairment improved to normal during treatment. Two other patients, however, were withdrawn from the study because of hypotension and cardiac failure. In conclusion, carvedilol is effective in the treatment of hypertension and produces adequate blood pressure control with a percentage reduction in left ventricular mass. The associated changes in diastolic function may be due in part to the mass reduction, but no direct relation has been established, and the effect of afterload reduction on diastolic left ventricular filling remains important.
J Cardiovasc Pharmacol 1992
PMID:Effect of carvedilol on left ventricular function and mass in hypertension. 137 51

The safety and tolerability of carvedilol, a new antihypertensive agent with the combined pharmacological activities of beta-blockade and vasodilation, and of nifedipine were investigated in patients with essential hypertension and non-insulin-dependent (type II) diabetes mellitus. Twenty patients were openly randomized to receive 25 mg carvedilol once daily (five men and five women; mean age, 63 years) or 10 mg nifedipine t.i.d. (three men and seven women; mean age, 64 years) for a period of 4 weeks. Baseline mean sitting blood pressures were 168/98 and 169/95 mm Hg in the carvedilol and nifedipine groups, respectively. Baseline mean areas under the curve (AUC) of the intravenous glucose tolerance test (IVGTT) for the carvedilol and nifedipine groups were 6,136 +/- 1,195 and 6,287 +/- 1,228 mg/dl/min, respectively. Demographic and efficacy variables were not statistically different between treatment groups. After 4 weeks of therapy, mean sitting blood pressure was significantly (p less than 0.02) reduced to 144/91 mm Hg in the carvedilol group and to 149/87 mm Hg in the nifedipine group. Week 4 IVGTT AUC values of 5,735 +/- 1,464 mg/dl/min in the carvedilol group and 5,988 +/- 993 mg/dl/min in the nifedipine group, representing mean reductions of 6.14% and 3.17%, respectively, were not statistically different from baseline. Both treatments were well tolerated. No patient experienced adverse events in the carvedilol treatment group, whereas two patients in the nifedipine group reported episodes of headache (one patient) and palpitations (one patient); each episode was mild in severity and considered to be related to study medication.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1992
PMID:Comparison of the effects of carvedilol and nifedipine in patients with essential hypertension and non-insulin-dependent diabetes mellitus. 137 56

Possible counterregulatory neurohumoral and hemodynamic responses to carvedilol (a new vasodilating nonselective beta-receptor blocker) were studied in 19 men with essential hypertension (age range, 34-59 years; mean age, 44 years). Intra-arterial pressure, cardiac output (Cardio-green), heart rate, and the vasoactive peptides norepinephrine, epinephrine, and atrial natriuretic peptide (ANP) were measured at rest supine and sitting and during 100-W bicycle exercise before and 2 h after administration of 25 mg carvedilol. The same protocol was followed after 9 months of chronic carvedilol treatment (mean dose, 52 mg/day). Carvedilol induced both acute and chronic reductions (at rest supine, 11%) in mean arterial pressure, due in part to reduction in cardiac output (5%) and in part to reduction in total peripheral resistance (5%). At rest supine, carvedilol induced a reduction in ANP (27%) that could be viewed as a counterregulatory response to decrease in cardiac output, preventing excessive blood pressure reduction. ANP decreased (18%) when the patient sat up from the supine position and increased (67%) during exercise, but no further change was seen after acute or chronic carvedilol treatment. With the patient in the sitting position, norepinephrine was 110% higher than at rest supine; during 100-W exercise, norepinephrine increased 368%. A further increase (38-86% in the three situations, respectively) was seen after the first dose of carvedilol. Epinephrine showed similar but less marked changes. Neither extracellular fluid volume nor plasma volume (isotope dilution techniques) changed significantly during the study, but the acute blood pressure response to carvedilol was directly related to changes in extracellular fluid volume.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1992
PMID:Effects of carvedilol on atrial natriuretic peptide, catecholamines, and hemodynamics in hypertension at rest and during exercise. 137 57

We assessed the long-term effects of carvedilol on renal function in 10 patients with mild-to-moderate essential hypertension. After a 2- to 4-week placebo run-in period, all patients received 5 mg carvedilol once daily. If the effect was insufficient, the dosage was successively increased to 10 or 20 mg once daily. The mean +/- SEM duration of treatment was 17.3 +/- 1.0 weeks, and the final mean daily dosage was 13.5 +/- 2.2 mg/day. With treatment, systolic and diastolic blood pressures decreased significantly from 159.7 +/- 1.3 to 140.5 +/- 3.2 mm Hg (p less than 0.001) and from 98.3 +/- 1.0 to 88.2 +/- 2.7 mm Hg (p less than 0.001), respectively. Carvedilol did not cause significant changes in glomerular filtration rate, effective renal plasma flow, blood urea nitrogen, or serum creatinine. Renal vascular resistance decreased significantly from 12.7 +/- 1.4 to 11.2 +/- 1.2 dyne.s.cm-5/1.48 m2 x 10(3) (p less than 0.05). Thus, long-term carvedilol therapy was effective in reducing blood pressure in essential hypertension without causing impairment of renal function.
J Cardiovasc Pharmacol 1992
PMID:Effect of long-term carvedilol therapy on renal function in essential hypertension. 137 58

The link between arterial caliber and distensibility has been studied extensively, with conflicting results. As have other researchers, we previously showed evidence of an increase in arterial diameter and a decrease in arterial stiffness with use of nitrates at the site of the brachial artery (BA) and the aorta. Whether these results would apply to other large superficial arteries remained to be established. In the present study, by means of an original pulsed ultrasound echo-tracking system based on Doppler shift, we measured internal diastolic diameter and stroke change in diameter of the common carotid artery (CCA), the femoral artery, and the BA in patients with essential hypertension and determined the acute effects of administration of isosorbide dinitrate (ISDN 20 mg). Twenty untreated hypertensive patients entered this randomized, placebo-controlled, double-blind, parallel study. No significant change occurred during placebo. During ISDN therapy, blood pressure (BP) decreased significantly; cross-sectional compliance increased at the site of the CCA, the BA, and the common femoral artery (CFA). The increase in cross-sectional compliance was mainly due to an increase in internal diameter for CCA and to an increase in distensibility coefficient (DC) for BA. The pattern of cross-sectional compliance was intermediate for CFA. During ISDN therapy, the augmentation index of the CCA distension waveform was significantly reduced, whereas no change occurred during placebo, suggesting a reduction in wave reflection by nitrates.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1992 Apr
PMID:Mechanism of nitrate-induced improvement on arterial compliance depends on vascular territory. 138 Jun 9

This article discusses some of the mechanisms controlling the development of the vasculature. The process is complex, and the result makes it possible for the cardiovascular system to supply each tissue with the required amount of blood at the correct pressure. In general, the changes appear to be adaptive, such that the vessels perform their tasks more effectively. Increasing flow appears to be a powerful stimulus to growth, resulting in an increased lumen, whereas raised pressure is associated with an increased media: lumen ratio, which in human essential hypertension may be caused by remodeling (rearrangement of otherwise normal cells) rather than vascular growth. Thus, the physical environment (intravascular flow and pressure) plays an important role in determining vascular structure. This suggests that an important aspect of future research will be to understand more closely the mechanism by which the physical factors can stimulate growth, a process that must presumably be mediated by proto-oncogenes.
J Cardiovasc Pharmacol 1992
PMID:Vascular growth in hypertension. 138 Jun 21

The antihypertensive and hemodynamic effects of lisinopril and atenolol were evaluated in 21 patients with mild-to-moderate essential hypertension. Left ventricular systolic and diastolic performances were assessed prior to and following treatment by first-pass radionuclide cineangiography at rest and during peak upright bicycle exercise. Both lisinopril and atenolol treatment significantly reduced the blood pressure. Lisinopril therapy was associated with a reduction in systemic vascular resistance and left ventricular end-diastolic and end-systolic volumes but no change in stroke volume, cardiac output, peak ejection rate, peak filling rate, time to peak ejection rate, or time to peak filling rate. In contrast, atenolol therapy was associated with an increase in end-diastolic volume and stroke volume but no change in cardiac output; the left ventricular peak ejection and peak filling rates were decreased by atenolol treatment. Although both lisinopril and atenolol each significantly reduced the blood pressure, lisinopril had no effect on left ventricular systolic or diastolic performance; in contrast, atenolol decreased both systolic and diastolic parameters of ventricular performance. Left ventricular function may be affected in significantly different ways despite apparent similarities in blood pressure control in patients who respond to angiotensin converting enzyme inhibition or beta-adrenergic receptor blockade. Differences in hemodynamic response to an antihypertensive agent may be important in the selection of a drug for the treatment of subsets of patients with cardiac function abnormalities.
J Cardiovasc Pharmacol 1992 Aug
PMID:Comparison of the cardiac and hemodynamic effects of lisinopril and atenolol in patients with hypertension: therapeutic implications. 138 Oct 12

The determinants of cardiac output were investigated in 161 patients with essential hypertension World Health Organization (WHO) stages I and II. In multiple regression analysis, cardiac output was inversely and independently related to blood pressure and to age. In patients with more severe hypertension, the lower cardiac output was associated with a lower stroke volume and a higher peripheral oxygen extraction. When age and blood pressure were taken into account, cardiac output was not a significant predictor of total mortality and of future cardiovascular events. Clinic and casual blood pressure explain only up to about 30% of the variability of echocardiographic left ventricular mass. The relationship of electrocardiographic voltages with blood pressure at various levels of bicycle exercise was highly significant in 169 patients with essential hypertension (r = 0.29-0.38; p less than 0.001) but the relationship was not better than with pressure at rest (r = 0.39). Ambulatory blood pressure, however, may be better related to left ventricular mass than clinic pressure. Several studies indicate that left ventricular hypertrophy is a significant risk factor for future cardiovascular events, independent of age and blood pressure. Left ventricular systolic function is usually normal in established hypertension, but diastolic function is frequently impaired, which could explain the reduced peak oxygen uptake in patients with more severe hypertension.
J Cardiovasc Pharmacol 1992
PMID:Hypertensive heart disease: pathophysiology and clinical and prognostic consequences. 138 96

A primary role for the kidney in hypertension has long been recognized, but the pathogenetic interactions among renal hemodynamics, hormonal and hereditary factors, and dietary sodium intake remain ill defined. Reduction in the filtration surface area, whether acquired in the course of intrinsic renal disease or after surgical renal ablation, leads to systemic hypertension as well as to progressive renal insufficiency, sequellae made even more severe by dietary sodium excess. Moreover, hypertension and progressive renal disease occur in some individuals born with a solitary kidney, and occur almost invariably with more severe degrees of dysgenesis. Hypertension is also commonly observed in certain inbred rat strains in which the filtration surface area is congenitally deficient. Based on these and other lines of evidence reviewed herein, we postulate that a renal abnormality that contributes to essential hypertension in the general population is a reduced number of glomeruli and tubules, the consequences of which are limitations in the ability to excrete sodium and thus salt-sensitive hypertension. Furthermore, congenitally decreased filtration surface area may explain why only some, but not all, patients exposed to potentially injurious renal stimuli eventually manifest chronic nephropathy, and may also account for the susceptibility of subsets of type I and type II diabetics to develop overt glomerulopathy. Clinically, tests of renal reserve capacity may serve as a useful guide to identification of those patients at risk for the development of hypertension and progressive renal disease.
J Cardiovasc Pharmacol 1992
PMID:The interrelationships among filtration surface area, blood pressure, and chronic renal disease. 138 55


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