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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the cellular basis for the clinical and epidemiologic linkage of hypertension, left ventricular hypertrophy (LVH), obesity, and non-insulin-dependent diabetes mellitus (NIDDM) and have studied cytosolic free calcium and free magnesium levels in these syndromes. Specifically, intracellular free calcium is elevated and free magnesium is deficient in hypertension, and both are related (directly and inversely, respectively) to the ambient level of blood pressure, to LV mass index (and thus to the degree of cardiac hypertrophy), and to the hyperinsulinemia and insulin resistance of essential hypertension. Dynamically, the ability of dietary salt loading to elevate blood pressure corresponds to its ability to elevate cytosolic free calcium and reciprocally to suppress free magnesium levels. Conversely, the ability of calcium channel blockade to reverse salt-induced hypertension is related to its ability to prevent these transmembrane ionic effects. Higher steady-state free calcium or lower free magnesium, or both, are also observed in clinical states linked to hypertension, such as obesity and NIDDM. Oral glucose loading in normal subjects itself elevates free calcium and suppresses free magnesium levels, as does hyperglycemia in vitro. These data suggest an ionic hypothesis of cardiovascular and metabolic disease, in which a generalized defect in cell ion handling is present in all tissues, resulting in higher steady-state free calcium and lower free magnesium levels. In pancreatic beta cells, this would produce hyperinsulinemia; in fat and skeletal muscle, cause peripheral insulin resistance; and in renal tissue, increase proximal sodium resorption and increase urinary calcium excretion--all features of essential hypertension. In vascular smooth muscle, high cytosolic free calcium would increase smooth muscle tone and cause vasoconstriction, and in heart muscle, independent of blood pressure, would increase contractility and predispose to LVH. Therefore, what may appear clinically to be the separate syndromes of hypertension, obesity, and NIDDM may pathophysiologically be different manifestations of the same underlying cellular defect, thus explaining their frequent clinical coexistence. Therapeutically, reversal of this excess free calcium accumulation and/or free magnesium deficit with ion-specific agents, such as calcium channel blocking drugs, may thus ameliorate not only the elevated blood pressure of hypertension but also the concurrent excess morbidity and mortality of the concurrent cardiac, vascular, and metabolic aspects of the hypertensive state.
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PMID:Cellular calcium and magnesium metabolism in the pathophysiology and treatment of hypertension and related metabolic disorders. 138 62

The records of 150 consecutive patients undergoing thoracoabdominal aortic replacement from 1980 to 1991 were retrospectively reviewed. There were 89 men and 61 women; mean age was 67.8 years (range: 33 to 88 years). Since June 1989, a multimodality prospective perioperative protocol was used to reduce the risk of spinal cord dysfunction. Ischemia is minimized by complete intercostal reimplantation whenever possible, cerebrospinal fluid drainage, and maintenance of proximal hypertension during cross-clamping. Spinal cord metabolism is reduced by moderate hypothermia, high-dose barbiturates, and avoidance of hyperglycemia. Reperfusion injury is minimized by the use of mannitol, steroids, and calcium channel blockers. Ninety-seven percent of patients survived long enough for evaluation of their neurologic function. Spinal cord dysfunction was reduced from 6 of 108 (6%) in the preprotocol group to 0 of 42 in the protocol group (0%) (p less than 0.01). The overall 30-day operative mortality was not significantly different between the groups (9% versus 12%, p = NS). A multimodality protocol appears to be effective in reducing the risk of spinal cord injury during thoracoabdominal aortic replacement.
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PMID:Risk of spinal cord dysfunction in patients undergoing thoracoabdominal aortic replacement. 141 16

To determine whether calcium alters central cardiovascular regulation, cardiovascular responses to intracerebroventricular (ICV) injection of calcium were recorded in conscious Wistar rats. Calcium injection consistently produced dose-dependent decreases in mean parterial pressure and heart rate. Pretreatment with a calcium channel blocker, diltiazem, attenuated cardiovascular responses to calcium. Decreases in plasma norepinephrine indicated the contribution of sympatho-inhibition to vasodepression by calcium. Preceding calcium injection reduced pressor responses to ICV-injected angiotensin II. These findings suggest that there is a pharmacological interaction between calcium and angiotensin II in the central nervous system. In spontaneously hypertensive rats (SHR), cardiovascular responses to calcium was larger than Wistar Kyoto rats (WKY). By contrast, calcium reduced pressor responses to angiotensin II only in WKY but not in SHR. Because the central interaction between calcium and angiotensin II has been different in SHR, our results imply that this difference may be related to the maintenance of high blood pressure in SHR.
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PMID:Calcium suppresses central angiotensin II pressor response less in SHR. 142 16

The purpose of our review is to delineate the pathogenic steps linking arterial hypertension in diabetes to diabetic nephropathy. The results of recent studies suggest that arterial hypertension in diabetes might lay a decisive pathogenetic role in the evolution of diabetic nephropathy: the existence of a higher ratio of erythrocytic Na/Li counter-transport in nephropathic diabetics as well as higher pressure values in the parents of diabetics who develop nephropathy indicates that hypertension may be casually related to renal complications. Diabetes-associated hypertension involves the modification of two important pressure- regulation factors: 1. an alteration in extracellular volume and increased renal absorption of sodium which leads to an expanded pool; 2. increased cardiovascular reactivity to norepinephrine and angiotensin II, an effect which might be related to increased intracellular calcium. Hyperfiltration seems to be present at the onset of diabetes, and arterial hypertension increases the transglomerular pressure gradient which is thought to play an important role in the pathogenesis of kidney damage. Antihypertensive drugs such as ACE-inhibitors and calcium channel blockers tend to protect the regulation of renal function. This could be explained by the fact that ACE-inhibitors suppress the trophic effects of angiotensin II on the nephron, while calcium channel blockers might interfere with intracellular processes involved in cell hypertrophy that require the interaction of calcium ions. In the management of diabetes prevention of diabetic nephropathy requires early and careful correction of diabetes-associated hypertension. We discuss the major groups of antihypertensive drugs, their metabolic side-effects and intrarenal induced hemodynamic changes.
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PMID:[Diabetic nephropathy and arterial hypertension: the physiopathological aspects and antihypertensive treatment]. 145 55

Orthotopic heart transplant recipients treated with immunosuppressive regimens based on cyclosporine have a high incidence of hypertension. Cyclosporine-induced nephrotoxicity characterized by afferent glomerular arteriolar vasoconstriction also develops in these patients. Calcium channel antagonists produce afferent glomerular arteriolar vasodilation. Angiotensin-converting enzyme inhibitors (ACEI) dilate the efferent arteriole and have been suggested to decrease glomerular filtration rate in subjects taking cyclosporine. To test the hypothesis that calcium channel antagonists would improve glomerular filtration rate in heart transplant patients receiving ACEI treatment, we reviewed the charts of our patients whose treatment for hypertension had been changed from an ACEI to a calcium channel antagonist. A change in renal function was assessed by the average of serum creatinine level, blood urea nitrogen, and creatinine clearance within 3 months before and after the change from ACEI to calcium channel antagonist. Blood pressure was assessed on two different occasions before and after conversion to calcium channel antagonist. The data were analyzed by a paired Student t test. Serum blood urea nitrogen and creatinine levels decreased significantly when patients were treated with calcium channel antagonists (p < 0.05). Creatinine clearance increased in all patients when the treatment was converted to a calcium channel antagonist (CCA) (ACEI = 56.4 +/- 19.3 ml/min versus CCA = 71.06 +/- 23.77, N = 9; p < 0.005). A 5-mm Hg decrease occurred in mean arterial pressure when treatment was changed from ACEI to calcium channel antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of calcium channel antagonists on renal function in hypertensive heart transplant recipients. 145 46

Nitrendipine (NIT), a new potent calcium channel blocking agent, was administered to a patient with essential severe (191/119 mm Hg), refractory, and resistant hypertension (HT) to conventional triple drug regime. Three previous pregnancies had been unsuccessful in the past 4 years because of uncontrollable HT and repeated hypertensive crises. NIT (20 mg tablets) was given PO as a single morning dose and 15 months after BP control, she became pregnant again. With a 20 mg/day dose of NIT throughout pregnancy, a healthy 2400 g, 47 cm male boy was delivered by a non-emergency cesarean section at 37 weeks' pregnancy. Both mother and son remain normal months after birth. The results suggest NIT may be considered as an alternative for this type of patients and should be studied in clinical trials.
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PMID:Successful pregnancy in a severe hypertensive patient treated with nitrendipine. Case report. 145 33

The treatment of hypertension in pregnancy is justified by the need to reduce blood pressure in order to avoid the onset of preeclampsia, eclampsia, retarded intrauterine growth and even neonatal, perinatal and maternal death. The value of using drugs to treat slight-moderate hypertension in pregnancy is, however, not clearly defined in the literature. In fact, from an etiopathogenetic point of view, the significance of increased blood pressure in pregnancy has not yet been satisfactorily explained, and above all the positive significance of increased blood pressure not be forgotten since, up to diastolic levels of 90 mmHg, it is accompanied by an increase in birth weight. The aim of the present study was to verify the efficacy of pharmacological treatment in cases of slight-moderate hypertension during pregnancy in a population of 121 pregnant women attending the Obstetrics-Gynecological Clinic of the "Istituto per l'Infanzia" in Trieste during the period from 14-11-1984 to 24-4-1991. Data for this retrospective study were extrapolated from an analysis of medical records and then memorized in a data-base file. The degree of hypertension was classified as slight, moderate and severe according to blood pressure levels measured on hospitalisation. Clinical signs taken into account included: edema, proteinuria and hypoprotidemia. Anti-hypertensive therapy was selected between one or more associated drugs belonging to the following classes: central action and peripheral action anti-adrenergic drugs, beta-blockers, calcium channel blockers, vasodilators, diuretics, ACE-inhibitors and sedatives. Moreover, patients also received non-pharmacological treatment in the form of low sodium diets and bed-rest.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Moderate arterial hypertension in pregnancy: therapeutic aspects]. 148 Mar 1

The purpose of the study was to interpret the acute improvement in left ventricular (LV) filling induced by a new calcium channel blocker (SR 33 557) using Doppler echocardiography. Thirteen patients, 29 to 68 years old (mean 52) with mild to moderate hypertension were examined by Doppler echocardiography before and 4 hours after treatment (SR 33 557: 300 mg). The LV filling parameters, E, A, A/E, VTIM, VTIA, VTIA/VTIM, pressure half time (PHT) and isovolumic relaxation time (IRT) were measured. An index of left atrial pressure was obtained by measuring the mean pulmonary arterial pressure (PAP). The following hemodynamic parameters were also obtained: systolic blood pressure (SBP), heart rate (HR), PR interval (PR), stroke volume (SV) at aortic origin, total systemic resistances (TSR), pulse wave velocity (PWV) at thoracic descending aorta, LV end systolic stress (ESS), LV geometry (thickness/radius: th/r) and systolic function indices: mean VCF and contractility (mean VCF-ESS relationship). Following acute treatment, E and VTIM increased, A, VTIA and PHT did not change, and A/E, VTIA/VTIM ans IRT decreased, both significantly (p < 0.05). PAP did not change, HR, SBP, TSR, PWV, ESS decreased and PR increased both significantly (p < 0.05). LV geometry and systolic function did not change. No significant relationship was found between LV filling changes and changes in hemodynamic parameters. In conclusion, the acute increase in early LV filling induced by the calcium blocker treatment may be interpreted as the consequence of the improvement in LV relaxation in the absence of any change in left atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Apropos of acute changes in left ventricular filling induced by antihypertensive treatment]. 148 37

Clentiazem, 8-chloro diltiazem, is a calcium channel blocker currently undergoing evaluation for the treatment of stable angina and hypertension. As patients with ischaemic disorders often present some degree of heart failure, the aim of this study was to investigate the effect of congestive heart failure on clentiazem (200 micrograms kg-1, i.v. bolus) pharmacokinetics in a canine model. Congestive heart failure was induced in six dogs by rapid ventricular pacing (240 beats min-1) for 3-5 weeks. Clentiazem pharmacokinetics was studied in each dog under the control condition and after the development of clinical signs of heart failure (ascites, dyspnea, fatigue). Blood samples were collected up to 480 min post-dose. Clentiazem plasma concentrations were determined by high performance liquid chromatography. The area under the plasma concentration versus time curves (AUC0-infinity) was significantly increased in congestive heart failure dogs (8.8 +/- 1.6 vs 21.8 +/- 1.4 micrograms min ml-1) (mean +/- SEM). These changes were related to a reduction of the volume of distribution of the central compartment (0.9 +/- 0.1 vs 0.2 +/- 0.11 kg-1) and total body clearance (1.9 +/- 0.4 vs 0.7 +/- 0.21 h-1 kg-1). It is concluded that, in our model, congestive heart failure significantly modifies clentiazem disposition. These results suggest that caution should be exercised when clentiazem is given to patients with a low ejection fraction and a compromised cardiac function. Reduced loading and maintenance doses might be recommended in patients with severe congestive heart failure.
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PMID:Effect of congestive heart failure on clentiazem pharmacokinetics in a dog model. 148 42

Hypertension is a constellation of abnormalities, including metabolic disorders. The current approach to treatment of hypertension should not be dictated solely by measures to lower blood pressure. It must also take into consideration the effect of antihypertensive drug treatment on the development of atherosclerosis and many other important factors. Evidence from rabbit models and cell cultures indicates that calcium channel blockers are antiatherogenic through a variety of mechanisms. In addition to preserving endothelial function, these agents inhibit the following: Platelet aggregation Migration of monocytes and smooth-muscle cells into the intima Incorporation of low-density lipoprotein cholesterol into these cells Matrix formation Calcium overload in atherosclerotic lesions However, additional studies are needed to delineate the antiatherogenic effects of these and other antihypertensive agents.
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PMID:Antiatherosclerotic effects of calcium channel blockers. 149 83


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