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

Functional platelet characteristics were studied in hypertensive subjects having episodes of silent myocardial ischemia. A total of 36 patients with essential hypertension (EH) stage II (WHO criteria, 1979) underwent echocardiography and 24-h ECG monitoring. Platelet aggregation induced by adenosine diphosphate was assessed by laser aggregation analyzer. It is demonstrated that platelet aggregation in EH patients with silent ischemia was increased 5-fold as compared to healthy subjects and 2-fold versus EH patients without ischemia. No significant differences existed between the two groups by such parameters as systolic or diastolic pressure and left ventricular myocardial mass. An involvement of elevated platelet aggregation can be suggested in the genesis of coronary insufficiency in EH associated with episodes of silent myocardial ischemia.
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PMID:[The functional characteristics of the thrombocytes in patients with hypertension and "silent" myocardial ischemia]. 790 27

The regression of structural and functional alterations in the hypertrophic left ventricle was measured in the course of long-term correction of arterial pressure with a new inhibitor of angiotensin-converting enzyme ingibeis (chilasapril) in 23 patients with essential hypertension stage II-III. The results were for the most part obtained at echocardiography providing basic hemodynamic parameters and those of left ventricular diastolic function. Adaptability of the hypertrophic myocardium in response to physical loading was studied dynamically under isometric exercise test. The findings proved high efficacy of chilasapril in monotherapy of arterial hypertension. Long-term (6 months) therapy of left ventricular hypertrophy provides regression of the latter and improves left ventricular diastolic function, pumping capacity. In the course of arterial hypertension correction relevant patients with associated coronary heart disease improved their condition, demonstrated less frequent ECG changes indicative of ischemia.
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PMID:[The regression of the structural-functional changes in the hypertrophic left ventricle during the long-term correction of the arterial pressure with Inhibace (cilazapril)]. 799 12

The microcirculation of the subcutaneous tissue and muscles of the extremities is changed already in the early stage of essential hypertension. Insight into the effect of celiprolol, a beta blocker of the third generation, on tissue microcirculation is of both pathogenetic and therapeutic value. On using the method of Na131I tissue clearance, the effect of celiprolol on the microcirculation of subcutaneous tissue and muscles of the extremities was studied in 21 patients with essential hypertension. Celiprolol was administered orally in the daily dose of 300 mg. After one-week administration celiprolol significantly reduced mean arterial pressure and significantly increased the microcirculation in the subcutaneous tissue of the hand and crus as well as in the calf muscle. Celiprolol was thus found to increase the microcirculation in those tissues of the extremities in which its decrease was recorded before onset of the treatment. The obtained results may be of therapeutic value particularly in patients suffering from ischemia of the lower extremities. (Fig. 2, Ref. 19.).
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PMID:[Celiprolol increases the microcirculation in subcutaneous tissue and calf muscles in essential hypertension]. 835 37

Among hypertensive patients, blacks are more likely than whites to have ischemia by electrocardiographic and 201Tl-myocardial stress imaging, possibly due to racial differences in the regulation of coronary blood flow or velocity. This investigation was undertaken to determine whether intensive antihypertensive therapy with two or more drugs can correct or reduce ischemia in black hypertensive patients. Thallium myocardial stress imaging and electrocardiographic and echocardiographic studies were performed on 13 black patients with essential hypertension and ischemic heart disease due to hypertensive heart disease (without significant obstructive epicardial coronary artery disease). The studies were made at baseline and after 4 to 48 months of intensive treatment, with a calcium antagonist and an angiotensin converting enzyme (ACE) inhibitor as the main components of the antihypertensive drug regimen. The majority of the patients with abolition or reversal of myocardial ischemia documented by 201Tl-myocardial imaging also had a significant reduction in left ventricular mass (LVM). However, some patients either did not have LV hypertrophy at baseline or had changes in LVM beyond the precision of the echocardiographic M-mode mass calculations. The finding indicated that factors other than reduction of LVM were involved in the reversal of the ischemia. The most likely factor was a change in the regulation of coronary blood flow. Reduction in LVM and reversal of myocardial ischemia determined either by electrocardiography or by thallium myocardial imaging studies may be considered indicators of the effectiveness of treatment.
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PMID:Correction of left ventricular ischemia in blacks with hypertensive heart disease. 839 11

Nephrosclerosis is the most typical and widespread renal manifestation of hypertension and can be judged as the pathological hallmark of essential hypertension. Nephrosclerosis is an important and frequent cause of progressive renal disease, however, information in the literature on the risk of developing renal failure in the course of essential hypertension is sparse. Traditionally, nephrosclerosis was thought to result from glomerular ischemia. Alternatively, glomerular sclerosis in hypertension may result from glomerular hyperperfusion or hypertension. Studies in experimental models of renal disease have identified a promising intervention with either Ca antagonists or angiotensin-converting enzyme inhibitors. Application of these therapies to patients with nephrosclerosis should await the results of careful clinical trials.
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PMID:[Nephrosclerosis: current status]. 841 83

Hypertension is associated with an altered design of resistance vessels and decreased endothelium-dependent vasodilator response to acetylcholine. A role of angiotensin II in both defects is suggested by animal experiments in which angiotensin-converting enzyme inhibition reverted structural and functional changes. We investigated the effects of 20 weeks of therapy with the angiotensin-converting enzyme inhibitor cilazapril (5 mg twice daily) on the endothelium-dependent response to brachial artery infusions of acetylcholine and the endothelium-independent vascular relaxation after sodium nitroprusside in 22 subjects with mild to moderate essential hypertension. In addition, we measured minimal forearm vascular resistance (ratio of mean arterial pressure and forearm blood flow after heating, ischemia, and ischemic exercise) as an indirect estimate of vascular structure. Cilazapril decreased blood pressure (151 +/- 14/99 +/- 7 mm Hg during placebo to 138 +/- 17/89 +/- 8 mm Hg after cilazapril treatment, P<.01) and baseline (42.2 +/- 12.6 to 37.1 +/- 10.6 U, P<.05) and minimal (3.0 +/- 1.1 to 2.4 +/- 0.7 U, 15.9 +/- 20.2%; P<.05) forearm vascular resistances. The change in minimal forearm vascular resistance was unrelated to age, duration of hypertension, or changes in blood pressure. Sodium nitroprusside increased forearm blood flow from 2.6 +/- 1.0 to 11.4 +/- 5.9 mL/min per 100 mL and acetylcholine to 21.5 +/- 17.8. Both responses did not change after cilazapril. The data provide indirect evidence that cilazapril therapy may improve vascular structure in human hypertension. The lack of relationship between vascular and blood pressure changes would be compatible with experimental evidence supporting a role for angiotensin II in the development and regression of vascular changes, but this needs further study. Therapy with cilazapril for 20 weeks, like other antihypertensive therapy, does not seem to influence endothelial vasodilator function in humans to a significant degree.
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PMID:Effects of cilazapril on vascular structure and function in essential hypertension. 869 40

Increased vascular resistance in essential hypertension occurs mainly in microvessels with luminal diameters < 100 microm. It is not known whether abnormalities in these vessels are a cause or consequence of high blood pressure (BP). We studied 105 men (aged 23-33 yr) in whom predisposition to high blood pressure has been characterized by both their own BP and those of their parents. Factors that are secondary to high BP correlate with offspring BP irrespective of parental BP, but factors that are components of the familial predisposition to high BP are more closely associated with higher BP in offspring whose parents also have high BP. Offspring with high BP whose parents also have high BP had impaired dermal vasodilatation in the forearm following ischemia and heating (289+/-27 [n = 25] versus 529+/-40 [n = 26], 476+/-38 [n = 30], and 539+/-41 flux units [n = 24] in other groups; P < 0.0001) and fewer capillaries on the dorsum of the finger (23+/-0.8 capillaries/0.25 mm2 versus 26+/-0.8 in all other groups; P < 0.003). Except for BP, other hemodynamic indices (including cardiac output and forearm vascular resistance) were not different. The dermal vessels of men who express a familial predisposition to high BP exhibit increased minimum resistance and capillary rarefaction. Defective angiogenesis may be an etiological component in the inheritance of high BP.
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PMID:Impaired microvascular dilatation and capillary rarefaction in young adults with a predisposition to high blood pressure. 910 31

The purpose of this study was to evaluate the influence of different factors, among them left ventricular hypertrophy (LVH) on long-term heart rate variability (HRV) in patients with hypertension. 38 patients with arterial hypertension of different genesis were included in the study. Ischemia was excluded in all the patients by the data of clinical and instrumental methods of investigation. LVH data obtained from HRV of 20 healthy subjects was used as control. HRV was evaluated by estimating variations for short intervals of a rhythmogram (VSI). A HRV decrease did not depend on sex, but essentially depended on patients'a age, disease duration and the form of hypertension. A marked tendency leading to the rate variability decrease was observed only in moderate LVH. In cases of original LVH variability data did not differ from those in patients without signs of LVH. Low or marginal HRV was more often observed in patients with essential hypertension and in those with hypertension of endocrine genesis. As far as renal hypertension is concerned low variability was less frequent. There were a lot of factors which affect the change of HRV. The more significant of them were the patients' age, hypertension genesis and form of hypertension. Factors leading to the rate variability decrease were the following age above 40, endocrine or essential hypertension and moderate form of hypertension.
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PMID:[The effect of different factors on cardiac rhythm variability in patients with arterial hypertension]. 922 34

Short-acting calcium antagonists have a deleterious effect on the prognosis for patients with myocardial ischemia, possibly caused by overactivation of sympathetic nerves due to vasodilatation, negative inotropism, or coronary steal. However, there is considerable debate about whether long-acting calcium antagonists as well as the short-acting calcium antagonists have the same effect. Barnidipine-HCl is a newly-developed calcium antagonist with 1:2 short- and long-acting particles. This study evaluated the changes of autonomic tone due to barnidipine. Both the short- and long-acting effect of the calcium antagonist was evaluated. Eleven patients with primary hypertension underwent 24-hour ambulatory electrocardiogram and blood pressure monitoring before and after the treatment with barnidipine. Heart rate and blood pressure were compared before and after the medication. Heart rate variability was analyzed with a Marquette 8000/T. High frequency power (HF), as a parameter of vagal tone, and the ratio to low frequency power (LF), as a parameter of sympathetic tone, were obtained. Twenty-four-hour average blood pressure decreased significantly during the day, but nocturnal hypotension was not observed. Heart rate did not increase. HF decreased at the peak of the short- and long-acting components. LF/HF increased at the peak of the short-acting component. Short-acting particles of barnidipine had a deleterious effect on the autonomic tone, that is overactivation of sympathetic tone and suppression of vagal tone. Long-acting particles of barnidipine suppressed the vagal tone. These findings suggest that short-acting calcium antagonists may cause arrhythmia or deterioration of coronary ischemia.
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PMID:[Effect of barnidipine hydrochloride on the autonomic nervous system: difference between short- and long-acting components of calcium antagonist]. 925 91

We present a new hypothesis to explain the development of salt-dependent hypertension in humans. We propose that hypertension has two phases: an early phase in which elevations in blood pressure (BP) are mainly episodic and are mediated by a hyperactive sympathetic nervous or renin-angiotensin system, and a second phase in which BP is persistently elevated and that is primarily mediated by an impaired ability of the kidney to excrete salt (NaCl). We propose that the transition from the first phase to the second occurs as a consequence of catecholamine-induced elevations in BP that preferentially damage regions of the kidney (juxtamedullary and medullary regions) that do not autoregulate well to changes in renal perfusion pressure. The catecholamine response is associated with both an increase in peritubular capillary pressure and a reduction in peritubular capillary plasma flow, resulting in injury to the peritubular capillaries with ischemia to the tubules and interstitium. The local injury triggers the release or activation (angiotensin II, adenosine, renal sympathetic nerves) or inhibition (nitric oxide, prostaglandins, dopamine) of vasoactive mediators that further augment ischemia and result in abnormal tubuloglomerular feedback and enhanced NaCl reabsorption. The peritubular capillary injury with rarefaction simultaneously blunts the pressure natriuresis mechanism. The combined effect of enhanced tubuloglomerular feedback and impaired pressure natriuresis results in a defect in NaCl excretion which, on the exposure to salt, results in the development of persistent hypertension. Evidence is provided to suggest that this may be the major mechanism for the development of salt-dependent hypertension, and particularly for the hypertension associated with blacks, aging and obesity. Thus, essential hypertension may be a type of acquired tubulointerstitial renal disease.
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PMID:Hypothesis: the role of acquired tubulointerstitial disease in the pathogenesis of salt-dependent hypertension. 935 Jun 40


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