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

Severe essential hypertension in a subset of American black subjects is associated with marked stenosis of interlobular arteries and arterioles of the kidneys, observed by renal biopsy and binephrectomy specimens. The interlobular arterial stenosis is caused by marked thickening of the intima due mainly to the presence of smooth muscle cells, basement membrane material, and acid mucopolysaccharide. Because of this makeup, we propose the term "musculo-mucoid intimal hyperplasia" for this lesion. The media of these arteries appears maximally dilated, and by electron microscope displays degenerative changes of the smooth muscle cells. The arterioles are thickened, due mainly to hyalinization, but also due to the musculo-mucoid change (onionskin effect). The smooth muscle cells are degenerated and atrophic. These patients do not exhibit fibrinoid necrosis of the arteries, arterioles, and glomeruli, presumably because of the rapidity of the development of the arterial stenotic lesion. Accordingly, the glomeruli are destroyed by ischemia, and there is no evidence of glomerulitis (no "Kombinations" form of Fahr). A unifying hypothesis concerning renal hypertensive arterial disease is suggested by these studies. This hypothesis places the main emphasis for all the morphological expressions of the intrinsic visceral vasculature on changes involving the main functional unit of the vessel wall, the medical smooth muscle.
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PMID:Malignant hypertension due to musculo-mucoid intimal hyperplasia of intrarenal arteries. Absence of renal fibrinoid necrosis. 4 31

Hypertension during pregnancy and its complications are the most important cause of maternal and foetal death and morbidity. The chronic primary hypertension can be differentiated from the dysgravidia by anamnestic, biological, clinical and technical investigations. However the diagnosis remains difficult and the renal needle biopsy can help to ascertain it. The pathogenesis of dysgravidia is still obscure: the placental ischemia leads to a slow disseminated intravascular coagulation state with renal injury, while a vascular hyperreactivity leads to an increase of the resistance, a relative hypovolemia and lowering of cardiac output. The treatment and remote prognosis of the hypertensive disease associated with the pregnancy are summarized. The antihypertensive drugs improve the maternal prognosis while jeopardize the foetal outcome.
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PMID:[Hypertension and pregnancy]. 30 56

Renovascular hypertension can result from renal artery lesions involving the main renal artery, or its branches. It is generally felt that the elevation of blood pressure results from excessive systemic vasoconstriction secondary to enhanced renin secretion by one or part of one kidney. Renin secretion is enhanced because of constriction of the renal artery and resultant intrarenal ischemia. Clinically patients cannot be distinguished from those with essential hypertension and diagnosis must be made with arteriography although urography and isotope renography may suggest the diagnosis. Surgical cure can be predicted if differential renal vein renin ratios lateralize but a non-lateralizing study does not necessarily mean that surgery will fail. In properly selected patients, surgical results are excellent.
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PMID:Renovascular hypertension: pathophysiology, diagnosis, and treatment. 37 21

Endothelium-dependent vasodilation is reduced in essential hypertensive subjects. To evaluate whether this abnormality is a primary defect or is a consequence of blood pressure increment, in offspring of essential hypertensive and normotensive subjects (n = 13 subjects for each group) matched for age, sex, body weight, and blood pressure, we studied the response of forearm vasculature to acetylcholine (ACh) (an endothelium-dependent vasodilator), sodium nitroprusside (a direct vasodilator of vascular smooth muscle), and forearm ischemia (13 min plus 1 min of exercise) to induce maximal vasodilation. Drugs were infused into the brachial artery at cumulative doses (ACh: 0.15, 0.45, 1.5, 4.5, and 15 micrograms/100 ml of forearm tissue/min; sodium nitroprusside: 1, 3, and 10 micrograms/100 ml of forearm tissue/min) while forearm blood flow was measured by strain-gauge venous plethysmography. The intra-arterial blood pressure and heart rate were continuously monitored. Despite a comparable forearm vascular response to sodium nitroprusside and to forearm ischemia, the effect of ACh was significantly (p < 0.001) reduced in offspring of hypertensive subjects compared to the offspring of normotensive subjects. These data indicate that ACh-mediated forearm vasodilation is reduced in normotensive subjects with a familial history of essential hypertension, a finding that suggests that endothelium dysfunction can precede the appearance of hypertension and that this abnormality might play a role in the pathogenesis of essential hypertension.
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PMID:Endothelium-dependent forearm vasodilation is reduced in normotensive subjects with familial history of hypertension. 128 67

Diabetes mellitus (DM)-linked metabolic alterations and hypertension concomitantly accelerate or precipitate cerebrovascular and coronary heart disease, nephropathy, retinopathy and widespread macroangiopathy, thereby conferring to diabetic patients a very high risk of morbidity, disability and early death. Therefore, the long-term care for diabetic patients should be aimed at concomitant metabolic and blood pressure (BP) control. Dietary measures are indispensable; a high fibre, low fat, low salt diet is recommended, complemented with caloric restriction and physical exercise when body weight is above the ideal. Antidiabetic pharmacotherapy involves an unresolved dilemma. The desired achievement of euglycemia necessitates effective levels of insulin, but hyperinsulinemia (due to parenteral [over]treatment in insulin-dependent DM) is suspected to promote atherogenesis and represents a coronary risk factor and perhaps even facilitates hypertension. Considering antihypertensive pharmacotherapy, thiazide-type or loop diuretics are problematic drugs in DM because they can aggravate metabolic alterations. These agents also seem to exert only a limited preventive or regressive effect on left ventricular hypertrophy (LVH); beta-blockers are also not considered ideal, since they decrease the awareness of hypoglycemia and tend to promote glucose intolerance. Unselective beta-blockers in particular promote peripheral ischemia and insulin-induced hypoglycemia, while beta-blockers without intrinsic sympathomimetic activity lower serum HDL-cholesterol. Calcium antagonists and ACE inhibitors have equivalent antihypertensive efficacy, do not impair carbohydrate and lipid homeostasis or peripheral perfusion and can effectively improve LVH. Certain ACE inhibitors may even slightly ameliorate abnormal insulin sensitivity and plasma glucose levels. While alpha-blockers share most of these desirable properties, these agents are more prone to precipitate orthostatic hypotension in the diabetic patient. The non-thiazide diuretic indapamide and the serotonin2-antagonist ketanserin also combine antihypertensive efficacy with metabolic neutrality. The ultimate goal of therapy is to improve life prognosis. In essential hypertension, conventional drug treatment based on diuretics in high dosage satisfactorily reduced cerebrovascular but not coronary complications or sudden death. In diabetic patients, the influence of antihypertensive therapy on prognosis has not been assessed prospectively. Based on retrospective analyses, Warram et al reported a 3.8 times higher mortality in diabetics treated with diuretics alone, than in diabetics with untreated hypertension (Arch Intern Med. 1991;151:1350). H. H. Parving calculated that effective BP control in patients with diabetic nephropathy might reduce 10 year-mortality from about 65 to 20 percent (J Hypertension. 1990; 8[Suppl 7]:187).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antihypertensive therapy in diabetic patients. 128 10

Angiotensin converting enzyme inhibitors are utilized in the treatment of essential hypertension and of chronic cardiac failure. They are also employed in the treatment of the myocardial lesion of ischemia-reperfusion, which involves oxygen free radicals. In the present study we investigated the possibility of three angiotensin converting enzyme inhibitors (captopril, enalapril, lisinopril) to act as hydroxyl radical scavengers. The rate constants for reactions of those compounds with .OH were determined using the deoxyribose method. All there compounds proved to be good scavengers of .OH with rate constants of about 10(10)M-1s-1 and are iron chelators specially enalapril. The fact that captopril possesses a thiol group does not confer an higher antioxidative capacity. These results suggest that scavenging of oxygen free radicals may be a possible mechanism contributing to the therapeutic effect of angiotensin converting enzyme inhibitors.
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PMID:[Angiotensin-converting enzyme inhibitors as neutralizers of hydroxyl radical]. 132 14

The results from recent studies suggest that the endogenous opioid beta-endorphin (beta-E) is related to pain modulation. Therefore, plasma beta-E levels were studied in 23 patients with essential hypertension (EH) and in 7 patients with coronary artery disease (CAD) during asymptomatic ischemic events and in 5 patients with CAD during symptomatic ischemic events. Blood samples for beta-E were taken at the moment of silent ST depression, pointed with alarm by the real time ECG monitor "Q Med Monitor" (USA). Control blood samples were taken under the same conditions without ischemic events. Control plasma beta-E levels were significantly higher (p less than 0.01) in patients with EH as compared to that in both groups of patients with CAD (22.9 +/- 4.0 vs 7.0 +/- 1.9 and 4.5 +/- 1.6 pmol/l). At the time of silent ischemia, beta-E showed a significant increase in patients with EH (+10.1 +/- 2.1 pmol/l, p less than 0.01) and in patients with CAD (+10.7 +/- 1.3 pmol/l, p less than 0.05) as compared to the control levels. However, plasma beta-E showed no increase (+1.0 +/- 0.6 pmol/l, p greater than 0.1) during symptomatic ischemia as compared to the control levels. Thus, differences in the circulating levels of beta-E may be associated with the presence or absence of pain during myocardial ischemia.
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PMID:[Plasma beta-endorphin level in "silent" myocardial ischemia during Holter ECG monitoring]. 140 1

In untreated essential hypertension cardiovascular structural changes will develop after some time. In arteries and arterioles, thickening and reduced compliance of the vascular wall is noted and in the left ventricle, myocardial hypertrophy. Both types of changes will enhance the risk of ischemia and of developing cardiac complications, i.e. coronary heart disease, myocardial infarction and heart failure. Methods for measurement of vascular and cardiac hypertrophy are reviewed and the value of echo-cardiographic evaluation of the hypertensive patient is stressed.
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PMID:[Cardiovascular changes in arterial hypertension]. 146 23

To determine whether myocardial ischemia is accompanied by variation in heart rate and/or blood pressure, ST-segment analysis on Holter-ECG and ambulatory blood pressure monitoring was performed in 78 patients (64 males/14 females) with essential hypertension. Thirteen out of 55 patients (24%) with angiographically proven coronary artery disease (CAD) showed ST-segment depression (ST-D; group A pos). We observed 41 ST-D (1-11 ST-D; median: 2) lasting from 1 min to 70 min 15 s (median: 4 min 42 s) and an average depression of 185 +/- 48 mV. In comparison, in 6 of 23 patients (26%) with a normal angiogram 24 ST-D (1-10; median: 3; group B pos), which showed longer duration (1 min to 109 min 20 s; median: 11 min 10 s) and less depression (137 +/- 47 mV) have been found. 73.3% of all ST-D in group A pos and all in group B pos were preceded by an average increase in heart rate of 13 bpm. Exclusively, 12 episodes of ischemia (29.3%) in patients with CAD and 8 (33.3%) in patients without CAD were accompanied by an increase in blood pressure, which was more distinct in group A pos. Transient myocardial ischemia can be shown in hypertensive heart disease unrelated to CAD. A clear correlation between an increase in blood pressure and ST-D could not be proven.
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PMID:[Blood pressure variability and transient myocardial ischemia in patients with essential hypertension]. 151 10

To determine the role of the sympathetic nervous system in myocardial ischemia with essential hypertension, plasma norepinephrine, heart rate (HR), blood pressure (BP), and the HR.BP double product at the time of silent ischemia during pacing and exercise treadmill test (ETT) were compared with basal values in 20 patients with sustained essential hypertension and stable angina, 3 to 60 days (12.6 +/- 11.6) after discontinuation of all antihypertensive and coronary vasodilator therapy. Group I (N = 6) had silent ischemia with a higher HR.BP product at ETT than at pacing (ratio = 157 +/- 10.4% [+/- SD] v a value in group II [N = 5] of 102 +/- 18.8 [P less than .01]. Group III (N = 9) had no silent ischemia at ETT or pacing. Group I v group II plasma norepinephrine levels at rest and with pacing silent ischemia were 76 +/- 37 v 138 +/- 36 pg/mL, P less than .02, and 101 +/- 50 v 230 +/- 43 pg/mL, P less than .01, respectively. In groups I and II plasma norepinephrine levels were significantly lower than those of group III. Eleven of 20 patients had ischemia on pacing or ETT. Left ventricular myocardial mass were greater (224 +/- 49 v 180 +/- 28 g, p less than .05), HR (67 +/- 13 v 76 +/- 11 beats/min, P = NS) and plasma norepinephrine levels at rest (104 +/- 47 v 241 +/- 99 pg/mL, P less than .01), pacing (160 +/- 81 v 338 +/- 94 pg/mL, P less than .01), and ETT (758 +/- 268 v 1203 +/- 611 pg/mL, P less than .05), were lower in patients with ischemia (N = 11, group II) than in patients without ischemia (N = 9, group III) on pacing or ETT. Eight patients were on reserpine prestudy; reserpine prestudy was associated with lower basal HR (63 +/- 9 v 76 +/- 12 beats/min, P less than .05) and plasma norepinephrine (106 +/- 48 v 169 +/- pg/mL, P less than .07) and greater ratio of HR.BP double product on ETT/pacing, (141 +/- 33 v 111 +/- 19, P less than .02). The sympathetic nervous tone of group I was low at baseline but there may have been raised alpha/beta-receptor responsiveness to laboratory stresses with concomitant micro/macrovascular constriction at higher oxygen demand.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Altered sympathetic tone in hypertensives with angina and lowered threshold for pacing ischemia. 163 36


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