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

In essential hypertension ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by the organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Even the young hypertensive heart of normal size with no angiographic abnormalities appears to be prone to ischemia, because the coronary reserve is seriously limited even in the absence of coronary stenosis. Unlike ventricular distensibility, myocardial compliance may be normal even in the presence of pronounced myocardial hypertrophy. As myocardial compliance decreases, systolic wall stress increases and ventricular function is reduced. The hypertensive heart, the most common form of an irregular hypertrophy of the ventricular wall, is found in 14% of such cases. Analysis of the degree of hypertrophy shows that the hypertrophy can be inappropriately high (high mass-to-volume ratio, reduced wall stress), appropriate, or inappropriately low (normal mass-to-volume ratio, increased wall stress). Coronary reserve is reduced even in hypertensive hypertrophy without evidence of coronary artery disease. MVO2 per mass unit was directly correlated with systolic wall stress per cross-sectional area of the left ventricular wall. It is concluded that the appropriateness of left ventricular hypertrophy, as a result of mass-to-volume ratio and stress, is a major determinant of left ventricular performance, of coronary blood flow, and of myocardial oxygen consumption. Pharmacotherapeutical means of reversing cardiac hypertrophy (prazosin, clonidine, enalapril, and nifedipine) were analyzed in concentrically, as well as eccentrically, hypertrophied left ventricles. Regression of cardiac hypertrophy, i.e. therapeutic intervention on a critical precursor of hypertensive congestive heart failure, can be obtained by various antihypertensive agents. Prazosin, calcium channel blockers and angiotensin-converting enzyme inhibitors as well as a combined treatment regimen using alpha-receptor blockers together with diuretics and vasodilators can all induce regression of hypertrophy associated with an improvement in left ventricular function. Moreover, an improved coronary reserve may reduce the ischemic risk of the hypertrophied myocardium. However, not all antihypertensive drugs seem equally effective in bringing about coronary regression of left ventricular hypertrophy. No regression or little regression has been found with diuretic monotherapy despite a satisfactory reduction in blood pressure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Comparative analysis of cardiac function, geometry, energetics and coronary reserve in hypertensive heart disease. 296 4

Dispensary care was provided to 122 patients with essential hypertension. During a 3-year follow-up period BP decrease in regularly treated patients (44) was accompanied by the restoration of hemodynamic cardiac function and regression of myocardial hypertrophy and ischemia. BP stabilization, transformation of the blood circulation of hemodynamic type, an increased degree of myocardial hypertrophy and ischemia were noted in irregularly treated patients.
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PMID:[Effectiveness of long-term treatment of patients with hypertension]. 296 92

To ascertain whether or not vascular lesions lead to renoparenchymal damage through ischemia and to a deterioration of renal function in patients with essential hypertension, correlations among morphometrical findings and renal function were examined in 36 renal biopsies from Japanese patients with a benign nephrosclerosis. The following histological parameters were investigated; glomerular sclerotic index (GS), interstitial volume (IV), measured by the point-counting method, index of arteriolar hyaline change (HC) and intimal thickening (IT), determined by morphometry. Arteries were divided into two groups; those with less than 3 layers of medial smooth muscle cells (SMC less than 3) and those with more than 3 cell layers (SMC greater than or equal to 3). The mean of IT in each size was calculated. IT (SMC less than 3) showed a significant correlation with GS and IV. IT (SMC less than 3), GS and IV significantly correlated with Ccr. On the other hand, IT (SMC greater than or equal to 3) and HC showed no correlation with GS nor Ccr. IT (SMC less than 3) and HC correlated with both blood pressure and the duration of hypertension, and here, IT (SMC greater than or equal to 3) showed no correlation. These data suggest that hyaline change and intimal thickening of small arteries and arterioles (SMC less than 3) are closely related to high blood pressure and that intimal thickening of small arteries rather than hyaline change causes renoparenchymal damage through ischemia and leads to a deterioration of renal function, in those with a benign nephrosclerosis.
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PMID:Morphometrical and functional correlations in benign nephrosclerosis. 342 33

Two monocular normotensive patients with nonarteritic ischemic optic neuropathy and retinal ischemia unresponsive to steroid therapy were treated with intravenous norepinephrine. In both patients, improvement in vision began within minutes after moderate hypertension was produced. A third patient showed no response to this therapy in one eye with established ischemic optic neuropathy, but had prompt recovery of vision in the second eye early in the course of ischemic optic neuropathy. This patient returned with recurrent ischemic optic neuropathy more than 1 year later. At that time she was found to have essential hypertension. One patient could not be weaned from the norepinephrine infusion without recurrent visual loss. In the second patient, controlled hypertensive therapy restored visual acuity to 20/30 during two separate recurrences of ischemic optic neuropathy. Therapy of a later episode of ischemic optic neuropathy was delayed for 2 days, and vision did not improve with norepinephrine infusion. This eye subsequently became painful and required enucleation. Histopathological evaluation showed combined arterial and venous occlusions within the optic nerve and evidence of previous peripapillary choroidal vascular occlusion. Selected normotensive patients with ischemic optic neuropathy and retinal ischemia may benefit from controlled hypertensive therapy induced by norepinephrine infusion.
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PMID:Norepinephrine therapy of ischemic optic neuropathy. 621 76

In essential hypertension ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by the organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Even the young hypertensive heart of normal size with no angiographic abnormalities appears to be prone to ischemia, because the coronary reserve is seriously limited even in the absence of coronary stenosis. Unlike ventricular distensibility, myocardial compliance may be normal even in the presence of pronounced myocardial hypertrophy. As myocardial compliance decreases, systolic wall stress increases and ventricular function is reduced. The hypertensive heart, the most common form of an irregular hypertrophy of the ventricular wall, is found in 14% of such cases. Analysis of the degree of hypertrophy shows that the hypertrophy can be inappropriately high (high mass-to-volume ratio, reduced wall stress), appropriate, or inappropriately low (normal mass-to-volume ratio, increased wall stress). Digitalis glycosides, together with antihypertensive measures, are indicated for the dilated hypertensive heart; beta-receptor blockers are sound medication for the compensated hypertensive heart both with and without coronary stenoses. The following discussion includes classification of hypertensive heart disease based on the cardiac complications following hypertension.
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PMID:Functional dynamics of the left ventricle in hypertensive hypertrophy and failure. 624 Apr 52

Hemorheological considerations are beginning to alter routine clinical practice. A hemorheological defect may play a primary etiological role not only in classical diseases like polycythemia, but also in conditions such as essential hypertension and non-coronary angina. Hemorheological abnormalities may also play a part in arterial thrombosis through a number of mechanisms, and are a frequent accompaniment in many cases of atherosclerosis, where they carry a bad prognosis. Our new awareness of the dangers of a high hematocrit, even in the normal range, has had widespread consequences on the management of not only all kinds of ischemic disease, but also for instance on surgical practice in general. Finally, hemorheological treatment has much wider applications than simply in conditions where a hemorheological abnormality has been detected. Treatment aimed at improving the flow properties of blood, whether by drugs, hemodilution or plasmapheresis, may also be the most practical and effective therapy for ischemia due to insufficient blood flow down narrowed arteries.
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PMID:[The influence of hemorrheology on the practice of clinical medicine]. 636 97

The authors examined 40 patients with chronic ischemic pancreatitis without concomitant pathology of the alimentary organs in order to define the features of the disease clinical picture and progress. It was found that patients with disseminated atherosclerosis, especially when it is coupled with essential hypertension, and with extravasal stenosis of the celiac trunk are predisposed to the development of chronic ischemic pancreatitis. Factors promoting pancreatic ischemia include abnormalities of the blood rheological properties seen in vascular pathology and alimentary hyperlipidemia.
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PMID:[Various characteristics of chronic ischemic pancreatitis]. 652 92

Although the arterial chemoreflex exerts a powerful influence upon the cardiovascular system, this reflex has until now been a disregarded factor in hypertension research. By comparing the physiological effects of chemoreceptor excitation to disarrangements present during the early labile phase of hypertension in spontaneously hypertensive rats, we found remarkable similarities. A search through the literature as well as our experimental data fully confirm this association. Many factors, among them decreased blood flow through the glomic tissue, lead to chemoreceptor stimulation. The origins of the chemoreceptor arteries are located in areas very susceptible to atherosclerotic changes which can lead to ischemia of chemoreceptor tissue. We are led to hypothesize that arterial chemoreflex is a significant factor in the etiology of essential hypertension.
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PMID:Do arterial chemoreceptors play a role in the pathogenesis of hypertension? 721 39

22 patients (mean age 45.08 +/- 1.38 years) with essential hypertension stage II were entered in a placebo-controlled blind trial of cilazapril, angiotensin-converting enzyme. A complex of clinical-instrumental tests comprised dipidamol test, bicycle ergometry, 199Tl myocardial scintigraphy, echo-CG. A 3-month course of cilazapril reduced myocardial hypoperfusion in 15 patients, improved left ventricular relaxation: Anti-ischemia effect of the drug was also evident.
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PMID:[The effect of cilazapril on left ventricular function and myocardial perfusion in patients with essential hypertension (hypertensive disease) stage II]. 749 43

Attenuated cholinergic vasodilatation has been suggested as an endothelium-related mechanism involved in essential hypertension. We investigated the role of muscarinic (M) receptor subtypes in the forearm resistance vasculature. In eight white men with essential hypertension and eight matched normotensive control subjects (age of both groups, 47 +/- 4 years; mean +/- SEM), we infused the nonselective agonist methacholine in the presence of saline and the antagonists atropine (nonselective), pirenzepine (M1-selective), and AF-DX 116 (M2-selective) into the brachial artery and measured forearm blood flow and forearm vascular resistance using venous occlusion plethysmography. Affinity constants (pKb values) were determined from calculated plasma concentrations of the infused compounds and EC50 values. Sodium nitroprusside was given as an endothelium-independent control, and minimal forearm vascular resistance after 10 minutes of ischemia was used as a marker of structural vascular changes. Hypertensive patients showed higher minimal forearm vascular resistance, indicating structural vascular changes. However, sodium nitro-prusside- and methacholine-induced vasodilatation was similar in both groups, with apparent EC50 values (log moles per liter; mean +/- SEM) of -7.32 +/- 0.13 and -7.51 +/- 0.21 in hypertensive patients and -7.37 +/- 0.13 and -7.45 +/- 0.02 in control subjects, respectively. Atropine, pirenzepine, and AF-DX 116 caused a shift to the right of the concentration-response curve of methacholine, with apparent pKb values of 8.63 +/- 0.08, 6.81 +/- 0.13, and 5.51 +/- 0.29 in hypertensive individuals and 8.62 +/- 0.10, 6.98 +/- 0.08, and 5.49 +/- 0.09 in control subjects, respectively. Again, there were no statistically significant differences in these pharmacological parameters between hypertensive patients and normotensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vivo characterization of muscarinic receptor subtypes that mediate vasodilatation in patients with essential hypertension. 760 35


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