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

Although most workers in the field agree that salt causes hypertension, but there is no well-established mechanism(s) explaining how salt works. Vast literature exists on abnormal sodium (Na+) transport processes in human and experimental hypertension from various cell systems. We examined the recent developments in the investigation of three important sodium transport pathways: Na+/K+ pump, Na+/Li+ countertransport and Na+/K+ cotransport in hypertension. The activities of these transporters may affect vascular reactivity or may serve as genetic marker for essential hypertension. Selected reports on the abnormalities of these transporters were summarized, potential problems in the interpretation of these data were discussed, and the current view about the physiological or pathophysiological meaning of these studies were presented. The multiple sites of defects and sometime conflicting reports on Na+ transport in hypertension also lead to alternative hypothesis associating membrane abnormalities with hypertension. Two models, considering membrane lipid bilayers and cellular calcium handling as primary sites of defect and the related evidence, were introduced. Finally, the role of natriuretic hormone (or endogenous Na+ pump inhibitor) in influencing Na+ transport was briefly discussed.
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PMID:Sodium transport in hypertension. 133 8

The effects of the calcium antagonist manidipine 20 mg/day on changes in blood pressure and renal hemodynamics in response to acute stress by the mental arithmetic test (MAT) and the cold pressor test (CPT) were investigated in 14 patients with essential hypertension (median age: 50 +/- 2, WHO stage I-II). During the drug-free period, acute stress by both MAT and CPT caused an increase in the renal vascular resistance index (RVRI) [% change in RVRI, 17% for MAT (p < 0.05) and 26% for CPT (p < 0.01)] and an increase in blood pressure [% change in mean blood pressure (MBP): 17% for MAT (p < 0.001) and 16% for CPT (p < 0.001)]. CPT stress resulted in a reduction in RAFV (% change in RAFV: -12%, p < 0.05). Oral administration of manidipine resulted in hypotensive effects at rest [MBP: from 116 to 99 mmHg, p < 0.001], no change in RAFV (31.3 to 32.9 cm/sec, p = ns), and reduced RVRI (from 3.9 to 3.2 mmHg.sec/cm, p < 0.02). Manidipine inhibited the hypertensive response to acute stress by both MAT and CPT [% change in MBP: from 17% to 11% for MAT (p < 0.02) and from 16% to 11% for CPT (p < 0.01)] and also inhibited the increase in RVRI [% change in RVRI: from 17% to -1% for MAT (p < 0.05) and from 26% to 8% for CPT (p < 0.01)]. Manidipine has beneficial effects on blood pressure and renal hemodynamics at rest in patients with essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of manidipine on renal hemodynamics in essential hypertensive patients: responses to acute stress. 134 77

The effect of manidipine, a new Ca2+ antagonist, on intrarenal hemodynamics was assessed in essential hypertension and compared with nicardipine, a previously studied Ca2+ antagonist. Identical 2-week studies were repeated before and during the administration of manidipine (10 mg once daily, 2 weeks) in 3 patients with essential hypertension who were given regular- and sodium-restricted diets for 1 week each. The renal function curve (pressure-natriuresis relationship) was drawn by plotting the urinary sodium excretion rate on the y-axis as a function of the systemic mean arterial pressure (MAP) on the x-axis. Assuming that the difference between MAP and the extrapolated x-intercept of the renal function curve represents the effective filtration pressure across the glomerular capillary walls, the intrarenal hemodynamics were calculated (e.g., afferent arteriolar resistance (RA), efferent arteriolar resistance (RE), and glomerular pressure (PG)). During the regular sodium diet, MAP was lowered from 100 +/- 7 to 93 +/- 5 mmHg (p < 0.04) and the effective filtration pressure was lowered from 20 +/- 2 to 10 +/- 3 mmHg (p < 0.05); the renal plasma flow rate (pre: 560 +/- 74 vs. post: 627 +/- 108 mL/min) and glomerular filtration rate (82 +/- 10 vs. 78 +/- 5 mL/min) were not altered. RA remained unchanged (3,800 +/- 700 vs. 3,400 +/- 300 dyn.sec.cm-5; % reduction: 4 +/- 16%) whereas RE was reduced from 4,300 +/- 700 to 3,300 +/- 800 dyn.sec.cm-5 (19 +/- 15%). Thus, PG was lowered from 58 +/- 2 to 50 +/- 2 mmHg (13 +/- 3%), which parallels with the reduction in MAP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of manidipine, a new calcium antagonist, on intrarenal hemodynamics in essential hypertension. 134 78

In order to investigate the effects of manidipine, a newly developed long-acting calcium antagonist, on the diurnal variation of arterial pressure and systemic hemodynamics in patients with essential hypertension, we examined 24-h arterial pressure using a direct arterial pressure monitoring method and cardiac output using the cuvette method before and during manidipine treatment. Once-a-day administration of manidipine at daily doses of 10 to 40 mg decreased systolic and diastolic arterial pressures at almost all measurement points. The arterial pressure reductions were not significantly different between daytime and nighttime. Arterial pressure variability expressed in terms of the standard deviation of values was not affected by manidipine treatment. Thus, it appears that patients treated with manidipine can avoid the excessive decrease in arterial pressure during nighttime that may occur with the use of some other calcium antagonists. Heart rate and its variability were unaffected by manidipine treatment. A hemodynamic study revealed that manidipine did not change cardiac output, but significantly decreased total peripheral vascular resistance at rest. It is concluded that once-a-day administration of manidipine at daily doses of 10 to 40 mg brings about a safe and stable antihypertensive effect over a 24-h period, without affecting the diurnal variation of arterial pressure and heart rate. Dilation of the resistance vessels underlies the antihypertensive effect of the agent.
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PMID:A study of the effects of manidipine on the diurnal variation of arterial pressure and hemodynamics in patients with essential hypertension. 134 98

These studies were undertaken to evaluate different manifestations of structural cardiovascular changes and the effects of antihypertensive therapy in essential hypertension. A meta-analysis of 109 studies that had examined the effect of different pharmacological blood pressure lowering regimens on left ventricular structure, examined by echocardiography, was undertaken to increase the statistical power, to resolve uncertainty and to improve the accuracy of estimation of the magnitude of effect. Strict preset criteria were applied. The effect of different drugs in monotherapy and in particular first line antihypertensive therapies were compared, using an analysis of covariance (ANCOVA). ACE-inhibitors, beta-blockers and calcium antagonists all reduced left ventricular mass (LVM) through a reduction in wall hypertrophy, the effect being most pronounced with ACE-inhibitors. Conversely, diuretics reduced LVM mainly through a reduction of left ventricular volume. Previously untreated males (n = 28, 86 kg, 46 years, 27 kg/m2) with non-malignant essential hypertension (supine diastolic blood pressure (DBP) > 95 mmHg 3-4 times (in triplicate) on placebo) were randomized to long-term double-blind treatment with enalapril (E) or hydrochlorothiazide (H). There were no significant differences between the groups at baseline. Vascular alterations in the retina (eyeground photo, refined grading), cardiac morphology (M-mode echocardiography, ASE), structural vascular changes of the hand (plethysmography, minimal resistance (Rmin)), total peripheral resistance ((TPR), calculated from dye-dilution) and blood pressure (intraarterial) were significantly interrelated at baseline except LVM and Rmin. After 6 months of therapy, E reduced the signs of vascular changes in the retina as well as Rmin in the hand circulation, while H did not change or increased these structural vascular changes. The blood pressure lowering effect of E (mainly through lowering of TPR) tended to be more pronounced, measured both intraarterially and indirectly, than that seen with H (mainly through lowering of cardiac output), however, there were no significant differences. LVM decreased progressively with E while the effect of H was non-significant. E reduced wall thickness but not left ventricular diameter and also improved left ventricular distensibility significantly. The effect on cardiac morphology was significantly different between therapies when taking change in blood pressure into account. After the longest follow-up on monotherapy (18 months) E had reduced LVM by 2.7 g/mmHg and H (14 months) by 1.3 g/mmHg (significant for E only). In univariate analysis the changes in cardiovascular structure were significantly related to the changes in the Renin-Angiotensin-Aldosterone System (RAAS).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Structural cardiovascular changes in essential hypertension. Studies on the effect of antihypertensive therapy. 134 61

A 72-year-old woman with 5-year history of essential hypertension developed peritoneal tuberculosis. The patient's hypertension, which had been well-controlled by long-acting nifedipine, deteriorated after the administration of rifampicin, an antitubercular agent. During use of nifedipine and rifampicin, both the peak plasma concentration and the area under the curve of nifedipine decreased markedly to about 40% of those without rifampicin. The findings suggest that rifampicin may increase the elimination of nifedipine, presumably by induction of its hepatic metabolism. Nisoldipine, another calcium antagonist, also failed to lower the patient's blood pressure, when given in combination with rifampicin. Taken together, these findings indicate that more caution should be urged when calcium antagonist is prescribed along with rifampicin.
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PMID:Case report: nifedipine-rifampicin interaction attenuates the effect on blood pressure in a patient with essential hypertension. 134 93

In view of the likely prohypertensive effects of hyperinsulinemia and the presence of insulin resistance in primary hypertension, the effects of various antihypertensive therapies on insulin sensitivity need to be identified. The evidence strongly supports major beneficial effects of weight reduction and aerobic exercise. Deleterious effects have been shown for diuretics and most beta-blockers, whereas probable beneficial effects have been seen with alpha-blockers, one angiotensin converting enzyme inhibitor, and various calcium entry blockers. Improvement of insulin sensitivity and reduction of plasma insulin levels are desirable attributes of antihypertensive therapy that should be more carefully considered in the future.
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PMID:Effects of antihypertensive therapy on insulin resistance. 134 22

The effects of once-daily administration of calcium (Ca) channel blockers, beta-blockers and and angiotensin-converting enzyme (ACE) inhibitors on circadian rhythms of blood pressure (BP) and heart rate (HR) were studied using the cosinor method. Sixty-two recruited patients with essential hypertension (WHO stage I or II) were divided into three groups based on the class of administered drugs. In the Ca channel blocker group (n = 37, age 54 +/- 9.0 years), 18 patients were given YM 730 at a mean dose of 11 +/- 4.0 mg/day (mean +/- S.D.), 8 were given nitrendipine (11 +/- 6.7 mg/day), and 11 were given nisoldipine (8 +/- 6.4 mg/day). In the beta-blocker group (n = 15, age 42 +/- 13.5 years), 13 patients were given atenolol (44 +/- 11.0 mg/day), 1 was given nadolol (30 mg/day), and 1 was given sustained-release propranolol (60 mg/day). In the ACE inhibitor group (n = 10, age 56 +/- 8.7 years), 7 patients were given enalapril (6 +/- 2.8 mg/day), and 3 were given lisinopril (20 mg/day). Ambulatory BP monitoring (ABPM) was performed before and during treatment. Mean arterial pressure (MAP) and HR were monitored under ambulatory conditions every five minutes for 24 hr with a finger volume oscillometric device. In all three groups, the mesor of MAP decreased significantly, while the amplitude and acrophase did not change during treatment. beta-Blockers reduced the amplitude as well as the mesor of HR. Ca channel blockers increased the amplitude of HR without influencing the mesor. ACE inhibitors had no effect on the circadian rhythm parameters of HR. These results suggest that Ca channel blockers, beta-blockers and ACE inhibitors lowered BP throughout the day without changing the circadian BP rhythm. However, the three drug classes may have different influences on the autonomic nervous system that regulates circadian cardiac rhythm.
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PMID:The influence of antihypertensive agents on circadian rhythms of blood pressure and heart rate in patients with essential hypertension. 134 80

Antihypertensive drugs have differing effects on renal hemodynamics, tubular function, plasma electrolytes, and hormonal responses. Nonselective beta-blockers without intrinsic sympathomimetic activities, such as propranolol, have been reported to reduce renal blood flow and to cause a modest decrease in glomerular filtration rate. Carvedilol is a new multiple action agent displaying nonselective beta-blockade without intrinsic sympathicomimetic activity, alpha 1-adrenoceptor blockade (probably responsible for its vasodilator activity), and possibly also calcium antagonist properties. The presence of these different pharmacodynamic properties results in a different effect on the kidney as compared with, e.g., propranolol. In the dog, intrarenal infusion of carvedilol resulted in a renal vasodilator response with preservation of renal blood flow and without inducing sodium retention; in contrast, propranolol induced a renal vasoconstrictor response and sodium retention in this model. A renal vasodilator response to carvedilol was also reported in spontaneously hypertensive rats (SHR) and in DOCA-salt SHR. In contrast to labetalol, i.v. infusion of hypotensive doses of carvedilol in conscious SHR did not cause sodium retention. Carvedilol was effective in controlling hypertension and preserving renal function in a rat model of progressive hypertensive renal disease. In patients with essential hypertension, carvedilol was reported to reduce renal vascular resistance in the presence of reduced perfusion pressure, allowing for normal renal autoregulation of renal blood flow. Although a small reduction in glomerular filtration rate was seen after acute administration, renal function was preserved during chronic treatment. It is concluded from these studies that renal perfusion and renal function are well maintained during acute and chronic treatment with carvedilol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carvedilol and the kidney. 135 Apr 79

The cardinal hemodynamic disorder in established essential hypertension is increased total peripheral resistance. During exercise, the increase in stroke volume of the heart is abnormal. A 20-year follow-up study of the hemodynamics in essential hypertension demonstrated a progressive increase in total peripheral resistance and deterioration of the heart pump function. Long-term treatment with antihypertensive agents modifies the circulatory system in different ways. Vasodilators (angiotensin converting enzyme inhibitors, alpha 1-blockers, and calcium antagonists) all reduce total peripheral resistance, and in general, cardiac output, heart rate, and stroke volume remain unchanged. Calcium antagonists like verapamil and diltiazem reduce the heart rate approximately 10% during exercise, but since stroke volume increases, cardiac output is unchanged. Chronic treatment with conventional beta-blockers induces a permanent reduction in cardiac output and heart rate during exercise. In contrast, carvedilol--a beta 1,beta 2-blocker with alpha 1-blocking activity--prevents the immediate increase in total peripheral resistance during acute beta-blockade. In 19 patients followed by hemodynamic measurements over 6-9 months, blood pressure was well controlled by carvedilol. During exercise, total peripheral resistance decreased 6% (P less than 0.05), and the reductions in heart rate and cardiac index were less than on conventional beta-blockade. Echo-Doppler studies showed a significant reduction in the intraventricular septum of 13%.
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PMID:Long-term hemodynamic effects of antihypertensive treatment. 135 Apr 86


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