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PubMed1986

The effects of antihypertensive drugs on serum lipids and lipoproteins. II. Non-diuretic drugs.

This review examines the effects of various antihypertensive drugs on blood lipids, lipoproteins, and apolipoproteins. A large number of studies have documented the elevation of total cholesterol, triglycerides, low density lipoprotein (LDL) cholesterol, and very-low density lipoprotein (VLDL) cholesterol with many thiazide-type diuretic drugs, albeit mainly in short term studies. When added to thiazide diuretics, both beta 1-selective and non-selective beta-blocking drugs elevate total triglycerides and VLDL triglycerides, lower high density lipoprotein (HDL) cholesterol and raise the ratio of total cholesterol to HDL cholesterol ratio. Most non-selective beta-blockers have similar effects when used as monotherapy, but the beta 1-selective agents appear not to affect HDL cholesterol in monotherapy. Prazosin appears free of adverse lipid effects and has improved lipid-lipoprotein concentrations in many studies. Preliminary data on several other drugs also suggest a favourable lipid profile and additional study is warranted - among these are guanabenz, clonidine, pindolol, labetalol, indapamide, and guanfacine. Elevations in serum triglycerides are often ignored on various counts, but triglycerides have been found to be a strong risk factor in European studies and in women over the age of 50 years in the Framingham study. Despite the unfavourable short term effects of diuretics, the theoretical risk of the lipid-lipoprotein changes remains unclear because HDL cholesterol and the total cholesterol to HDL cholesterol ratio are often unchanged. For this and other reasons, a long term trial comparing thiazide-type diuretics with drugs with the most favourable lipid-lipoprotein profile is needed. Until this is accomplished, in most settings diuretic-based regimens are still preferred initially since they are of proven, if limited, efficacy against the cardiovascular complications of hypertension.

Adrenergic alpha-Antagonists↗
PubMed1988

Serum lipoproteins during treatment with antihypertensive drugs.

Hypertension and certain alterations in serum lipoproteins such as a decrease in high density lipoprotein-cholesterol (HDL-C), an increase in low density lipoprotein-cholesterol (LDL-C) and perhaps also elevated triglycerides (Tg), are complementary coronary risk factors. Moreover, it has become evident that several of the drugs used for standard antihypertensive therapy may also interact with lipoprotein metabolism. The following has been observed after 1 to 12 months of treatment. Various diuretics can significantly increase LDL-C and/or very LDL-C and total C/HDL-C ratio, while HDL-C is often largely unchanged; Tg also are often elevated. LDL-C increased in diuretic-treated men and in chlorthalidone-treated postmenopausal women but not in chlorthalidone-treated premenopausal women. The latter may be protected from this side effect. Drug dosages were usually high in these studies. Indapamide, given at a dose of 2.5 mg/day, seems to exert no relevant effect on the lipoproteins. It is not established whether this difference is related to the nature of the drugs or the doses used. There is little doubt that the dose of chlorthalidone used was greater than that required for a full antihypertensive effect of this drug. Several beta-blockers given as monotherapy induce significant increases in Tg and a tendency for decreases in HDL-C. These changes are most prominent on non-selective beta 1+2-blockers without partial intrinsic sympathomimetic activity (ISA), less pronounced on highly selective beta 1-blockers without ISA, and even more discrete or absent on beta-blockers with distinct ISA. Other sympatholytics such as reserpine, methyldopa, debrisoquine, urapidil, clonidine, labetalol, or postsynaptic alpha-blockers (prazosin, trimazosin, doxazosin etc.) did not affect or, postsynaptic alpha-blockers in particular, sometimes even slightly decreased Tg or LDL-C and very LDL-C values. During combination therapy, diuretic-induced increases in LDL-C were at short term prevented or reversed by the concomitant administration of certain beta-blockers, but not by sympatholytics such as reserpine, methyldopa or clonidine. With combined diuretic-prazosin treatment, a tendency for slightly higher HDL-C was reported. Angiotensin converting enzyme inhibitors (captopril, enalapril) and calcium channel blockers (verapamil, nifedipine, nitrendipine, diltiazem) seem to be largely devoid of undesirable effects on serum lipoproteins. Monotherapy with the potent direct vasodilator carprazidil improved blood pressure and significantly increased HDL-C. Whether and to what extent the observed variations in lipoproteins may persist beyond 1 year of treatment is as yet unclear.(ABSTRACT TRUNCATED AT 400 WORDS)

Antihypertensive Agents↗
PubMed1990

Effects of drugs on glucose tolerance in non-insulin-dependent diabetics (Part I).

Non-insulin-dependent diabetes mellitus (NIDDM) is being increasingly diagnosed as its importance as a risk factor for the development of cardiovascular disease continues to be recognised. Good metabolic control remains a major goal of drug therapy as it decreases the severity and incidence of diabetic complications. Many drugs have been known to interfere with glucose control, either in a beneficial or, more commonly, in a deleterious fashion. Unfortunately in many instances drug-induced effects have not been looked at specifically in NIDDM. Thiazide diuretics have been shown to cause a deterioration in glucose control not only in the general population but especially in patients who have impaired glucose tolerance. While the effect appears less with potassium supplementation and the lower dosage employed nowadays, thiazide diuretics are best avoided in diabetic patients. Loop diuretics have been reported to reduce glucose control to a lesser extent than thiazides. Although indapamide would appear not to interfere with blood sugar control in NIDDM, higher doses that cause potassium loss may cause a deterioration. beta-Adrenoceptor antagonists have been reported to cause a rise in blood sugar and glycosylated haemoglobin in NIDDM. The effect may be more marked in patients on oral hypoglycaemic agents as opposed to diet alone and in those on concomitant thiazide diuretics. The greatest effect was seen with propranolol, and the least with cardioselective and the less lipophilic beta-blockers. It is of interest that alpha-blockade with prazosin seems to antagonise beta-adrenoceptor blocker-induced deterioration in glucose control. The calcium antagonists have differing effects which may be structure related. In some, but not all, studies use of the dihydropyridines such as nifedipine has been associated with a deterioration in glucose control in NIDDM. Long term studies are needed to assess definitively their effect on glucose control. Verapamil, on the other hand, has in 1 small study been found to have a beneficial effect on glucose control in NIDDM. Centrally acting alpha-agonists such as the antihypertensive drug clonidine have not been shown to result in a deterioration in glucose control when used in NIDDM, although there are isolated case reports. Long term therapy with the more specific agonist guanfacine was reported in 1 uncontrolled study to have a beneficial effect on glucose tolerance in NIDDM. Uncontrolled studies suggest that phenothiazines may aggravate diabetic control. The significance of a number of recent observations is not fully clear.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Low dose loop diuretics in essential hypertension. Experience with torasemide.

Diuretics belong to the class of antihypertensive drugs recommended for first-line therapy of essential hypertension. Although they are widely and effectively used for the treatment of hypertension, the question remains whether their possible negative influence on metabolic and electrolyte parameters could partly offset the benefit of blood pressure reduction with respect to reduction of coronary artery disease. Recently published data demonstrate that much lower doses of thiazides exert the same antihypertensive effect as the higher doses used in the past and even prescribed today. These lower doses produce relatively little change in biochemical parameters. Thus, the postulated risks can be avoided by using the lowest effective dose. Traditionally, loop diuretics of the furosemide (frusemide) type are rarely used as first-line antihypertensive agents. They seem to display less efficacy coupled with an intense diuresis when used in standard available doses. However, there is evidence that newly developed loop diuretics, in lower doses than used in congestive heart failure, are effective antihypertensive agents. For example, torasemide 2.5mg once daily, which does not exert a significant diuresis over 24 hours compared with placebo, lowers elevated blood pressure to a similar extent than thiazides or related compounds. This antihypertensive effect is accompanied by less, if any, changes in metabolic or electrolyte parameters compared with widely used standard diuretics such as hydrochlorothiazide, indapamide or chlorthalidone. The influence on serum potassium and magnesium is similar to or even less than fixed combinations of hydrochlorothiazide and triamterene or amiloride. Thus, low-dose torasemide constitutes an alternative to established thiazide antihypertensive therapy.

Diuretics↗
PubMed1991

Torasemide. A review of its pharmacological properties and therapeutic potential.

Torasemide (torsemide) is a high-ceiling loop diuretic which acts on the thick ascending limb of the loop of Henle to promote rapid and marked excretion of water, sodium and chloride. Like furosemide (frusemide), its major site of action is from the luminal side of the cell. Torasemide is at least twice as potent as furosemide on a weight-for-weight basis, produces equivalent diuresis and natriuresis at lower urinary concentrations and has a longer duration of action, allowing once-daily administration without the paradoxical antidiuresis seen with furosemide. Torasemide also appears to promote excretion of potassium and calcium to a lesser extent than furosemide. In trials of up to 48 weeks' duration in patients with mild to moderate essential hypertension, torasemide, administered as a single daily dose, has been shown to achieve adequate blood pressure control reaching steady-state within 8 to 12 weeks. Those patients not responding initially have generally responded to a doubling of the dose. Comparative trials of up to 6 months show torasemide is as effective as indapamide, hydrochlorothiazide or a combination of triamterene/hydrochlorothiazide in maintaining control of blood pressure. Torasemide has also been used successfully to treat oedematous states associated with chronic congestive heart failure, renal disease and hepatic cirrhosis. In short term trials control of blood pressure, bodyweight and residual oedema has been sustained. Torasemide appears to be a useful alternative to furosemide in these patients, providing potent and long-lasting diuresis while being relatively potassium and calcium sparing. In clinical trials to date torasemide has been well tolerated with adverse effects of a mild, transient nature reported by only small numbers of patients. Changes in biochemical parameters have been common, including decreases in plasma sodium and potassium levels and increases in plasma creatinine and uric acid levels. These changes are typical of loop diuretics. No changes were clinically significant nor were clinically relevant changes noted in glucose metabolism, cholesterol or triglyceride levels or in haematological values. Thus, torasemide is an interesting new loop diuretic with potential use in the treatment of mild to moderate essential hypertension and of oedematous states in which diuretic therapy is warranted. Preliminary studies suggest it to be as efficacious as other diuretics in common use and to have some advantage over furosemide in duration of action and in effects on potassium and calcium. However, further long term trials in larger groups of patients are needed to delineate the place of torasemide in therapy fully, both as a single agent and in combination with other currently accepted drug regimens.

Animals↗
PubMed2000

Diuretics as a basis of antihypertensive therapy. An overview.

Diuretics have been, except for during a few recent years, the most commonly used therapy for hypertension. Although use of these agents fell significantly in the early 1990s, since then it has begun to increase again. Their recent return to popularity reflects 3 major factors: (i) recognition of the effectiveness of much lower dosages than previously used, thereby providing good antihypertensive activity with fewer adverse effects; (ii) the excellent reductions in morbidity and mortality achieved by low dosage diuretic-based therapy in multiple randomised controlled trials in elderly patients with hypertension; and (iii) the increasing recognition that some diuretic-induced shrinkage of effective blood volume is essential for the adequate treatment of many, if not most, patients with hypertension. Therefore, diuretics will probably continue to be the basis for antihypertensive therapy, and the indapamide sustained release 1.5 mg formulation provides all the essential characteristics of diuretic therapy.

Antihypertensive Agents↗
PubMed1994

In vitro effect of nicotine on red blood cell deformability in untreated and treated essential hypertension.

The in vitro effect of nicotine (10(-7) mol l-1) on red blood cell (RBC) deformability in essential hypertension, efficacy of antihypertensive treatment (with the combination of enalapril, nifedipine and indapamid) on hypertension-induced decrease in RBC deformability and interaction between nicotine and efficacy of antihypertensive treatment were investigated in the blood samples obtained from 16 patients with untreated hypertension (UH) and 18 patients with treated hypertension (TH). Fourteen healthy subjects served as normotensive (NT) group. RBC deformability was assessed by using a gravity-driven microfiltration technique. In the UH group, the RBC deformability was found to be significantly lower than those in NT (0.623 +/- 0.06 versus 0.753 +/- 0.078, p < 0.001) and in TH (0.623 +/- 0.06 versus 0.732 +/- 0.055, p < 0.001) groups. The RBC deformability in the TH group was not significantly different than that in the NT group (0.753 +/- 0.078 versus 0.732 +/- 0.055, p > 0.05). Nicotine, in vitro, decreased deformability in the NT (0.668 +/- 0.067 versus 0.753 +/- 0.078, p > 0.0001), UH (0.509 +/- 0.052 versus 0.623 +/- 0.06, p < 0.0001) and TH (0.651 +/- 0.046 versus 0.732 +/- 0.055, p < 0.001) groups. The effect on the UH group was significantly greater than those in the NT (p < 0.0001) and TH (p < 0.0001) groups. These results suggest that nicotine and hypertension independently and cumulatively decrease the RBC deformability and nicotine inhibits the efficacy of antihypertensive treatment on RBC deformability.

Adult↗
PubMed1989

Pathogenetic and therapeutic relevance of cardiovascular pressor reactivity to norepinephrine in human hypertension.

In normotensive humans with a positive family history of essential hypertension, blood pressure (BP) is often dysregulated. Body sodium, blood volume, plasma angiotensin II (AngII), epinephrine and norepinephrine (NE), their responses to changes in sodium intake or posture, as well as baroreflex function, beta-receptor-mediated cardiac responsiveness, and the responsiveness of BP to AngII appear to be largely unaltered. However, the responsiveness of BP to NE is commonly exaggerated. An increase in potassium intake may improve the NE hyperreactivity and concomitantly lower BP within the "normotensive" range. Therefore, a selective vascular NE hyperreactivity relative to existing sympathetic activity seems to be a common familial abnormality predisposing for the development of essential hypertension. In borderline or established essential hypertension, an inappropriate vascular reactivity relative to sympathetic activity probably complements other mechanisms contributing to the maintenance of hypertension. Various antihypertensive treatments may lower BP at least in part by improving cardiovascular NE (hyper)reactivity without provoking an equivalent rise in sympathetic activity. These include dietary potassium supplementation, thiazide-type agents, indapamide, calcium channel blockers, postsynaptic alpha 1-blockers, and AngII converting enzyme inhibitors.

Animals↗
PubMed1999

Thermodynamic ionization constants of antihypertensive drugs.

The thermodynamic ionization constants (pKa) of indapamide, clonidine and methyldopa have been determined at 25 degrees C and 35 degrees C by pH titration technique. The pKa varies linearly with mole fraction of dioxane. The thermodynamic parameters have been calculated.

Algorithms↗
PubMed2000

Regression of left ventricular hypertrophy: do antihypertensive classes differ?

Left ventricular hypertrophy (LVH) is now recognized as a major risk factor for cardiac morbidity and mortality, a component of which is independent of associated coronary heart disease. The mechanisms that underlie this risk are increasingly understood and include disturbances in cardiac electrophysiology, coronary perfusion and myocardial contractile function. Recognition that regression of LVH confers prognostic benefit has focused attention on developing optimal treatments to achieve this. Early studies suggested that regression is achievable using a variety of antihypertensive classes. Many of these early studies were either poorly controlled or of inadequate size to provide reliable comparisons between different agents. Subsequently a number of meta-analyses, based on selections of these early studies, have been published. More recently, a number of well-designed prospective clinical trials have been published or are under way. In summary of these results: (1) the extent of regression seen in early studies appears to be greater than that reported in recent large, well-designed trials, possibly due to regression to the mean in small studies with high coefficients of variation for echocardiographically measured left ventricular (LV) mass index; (2) meta-analyses based on these early studies tend to suggest that angiotensin-converting enzyme (ACE) inhibitors may be most effective in regressing LVH; (3) recent larger trials [Treatment Of Mild Hypertension Study (TOMHS), the Veterans Administration (VA) study, and Left ventricular hypertrophy: Indapamide Versus Enalapril (LIVE)] indicate that angiotensin-converting enzyme inhibitors and diuretics maintain a strong place in achieving regression of LVH. Long-term studies currently under way should help clarify the prognostic benefit associated with regression of LVH using antihypertensive therapy. Future work will focus on whether regression of LV mass is associated with reversal of the underlying pathophysiology of hypertrophy and, ultimately, whether prevention of LVH should be the optimal goal.

Antihypertensive Agents↗
PubMed1999

The inhibitory effect of diuretics on carbonic anhydrases.

A classification of diuretics mainly comprises mercurials; carbonic anhydrase inhibitors, thiazide diuretics, loop diuretics, inhibitors of renal epithelial Na+ channels and antagonists of mineralocorticoid receptors. We studied in this paper the relationship between diuretics and carbonic anhydrase (CA). Our in vitro and in vivo results show that all diuretics inhibit carbonic anhydrase II and renal CA IV. Further, our data show that they also inhibit epithelial cell CA in the renal tubules. The changes in intracellular pH (pHi) induced by these diuretics through CA inhibition would influence: a) the coupling to their receptors affecting information transmission to the epithelial cells of renal tubules as well as diuretic response; b) the decrease of Na+ exchanger (thiazide), of Na+ - K+ - 2Cl- relation (loop diuretics), Na+ channel blocking in distal and collecting tubules (amiloride, triamterene), as well as the antagonism between spironolactone and aldosterone at the mineralocorticoid receptor level, suggest that this competition might also be produced on CA II and on renal CA IV, which, in turn, could be influenced by pH-induced changes, the binding of the diuretic to its membrane receptor as well as the activity of the brush membrane or cytosolic pump. Furosemide and indapamide, diuretics known to have vasodilating effects, induce the fall of blood pressure that parallels the decrease of CA I activity. These results show the involvement of CA in the mechanism of action of the diuretics and in their actions associated with vasodilating effects. pH changes resulting from the action of CA contribute to the action of diuretics. All diuretics inhibit CA isozymes.

Aged↗
PubMed2001

Vasoconstrictive drugs increase carbonic anhydrase I in vascular smooth muscle while vasodilating drugs reduce the activity of this isozyme by a direct mechanism of action.

Carbonic anhydrase (CA) is a zinc enzyme that catalyses the reversible hydration reaction of CO2 and plays a major role in the acid-base balance. We have previously shown that certain vasoconstrictive therapeutic agents increase CA I activity whereas vasodilating drugs reduce the activity of this isozyme by a direct mechanism of action. In this paper we studied the effect of other vasoconstrictive and vasodilating agents on CA I activity in order to elucidate the involvement of vascular smooth muscle CA I in vasoconstrictive and vasodilating processes. We studied the in vitro effects of noradrenaline, prostaglandin F2 alpha, thromboxane A2, leukotriene B4, angiotensin II, vasopressin, indomethacin, prazosin, hydralazine, clonidine, reserpine, prostaglandin I2, indapamide, furosemide, amlodipine, verapamil and irbesartan on purified human red blood cell CA I and vascular smooth muscle CA I isolated from rabbits. In vivo, we selected six groups of five rabbits each, which were administered the following substances in acute experiments: orciprenaline (group 1), desmopressin (group 2), verapamil (group 3), irbesartan (group 4), acetazolamide (group 5) and placebo (control group). Vascular smooth muscle CA I activity and systolic blood pressure were determined and compared with those of the control group. In vitro results showed that all the vasoconstrictive agents studied increased purified and human erythrocyte CA I activity as well as vascular smooth muscle CA I, while vasodilating substances reduced the activity of isozyme by a direct mechanism of action. The same results obtained in vivo showed that activation of vascular smooth muscle CA I increased blood pressure while its inhibition reduced blood pressure. The results of this study suggest that pHi changes, induced by activating or inhibiting CA I in vascular smooth muscle, might be responsible for changes in vascular tonus.

Animals↗
PubMed2001

Pharmacoutilization of antihypertensive drugs: a model of analysis.

OBJECTIVES: To identify clinical and economic indicators of pharmacoutilization of antihypertensive drugs. PATIENTS AND METHODS: 4614 subjects receiving a first prescription for amlodipine, atenolol, fosinopril, indapamide, or losartan were included in the study. All prescriptions filled during the study period from January 1, 1997 to December 31, 1998 were considered. A retrospective analysis was carried out on information recorded in the drug database. The percentage of patients continuing, discontinuing, and switching the initial treatment, duration of treatment, and doses used were calculated together with total costs. RESULTS: A large proportion of patients (65.1%) discontinued the treatment. From the analysis of the mean daily dose taken by patients who continued the treatment, it was found that many subjects took a drug dosage which was below the therapeutic dose range, whereas the administration of doses above the therapeutic range occurred only occasionally. Continuation of treatment accounted for 48.1% of total costs, switching accounted for 20.8%, and discontinuation represented 31.1% of total expenditures. CONCLUSIONS: With adequate markers, helpful data can be collected for monitoring the quality of antihypertensive drug prescriptions and the rational usage of resources in the general practice setting.

Antihypertensive Agents↗
PubMed2001

[Left ventricular hypertrophy: pathogenesis, diagnosis and therapy].

The life expectancy of hypertonic patients is basically determined by the complications of their disease. The increasing hypertension induces compensated processes in cardiovascular system, however, these alterations further worsen the mortality rates. It is evident that left ventricular hypertrophy (LVH) should be prevented. If it is the case, it has to be moderated among the possible circumstances. To regression of LVH produced by hypertony the decrease of hypertension is not enough, while the process is rather complex. Because the structural changes in the interstitial tissue followed by the alterations of heart myocytes hypertrophy, hyperplasy and apoptosis of myocytes, as well as the interstitial and perivascular fibrosis, coronary remodelling and necrosis in the consequence of insufficient blood circulation can be widely observed. The individual prognosis of LVH can be determined by echocardiography, while the concentric remodelling the development of excentric and concentric hypertrophy is strictly parallel with the increase in the mortality and morbidity rates. According to the evidences the treatment consists of life mode controlling and suitable drug therapy. First line medicines are the ACE-inhibitors and indapamides, later on these drugs can be further combined with calcium antagonists and beta-blockers, if necessary.

Antihypertensive Agents↗
PubMedDate not supplied

Global impact of stroke.

As the developing world becomes increasingly industrialized and urbanized, and its vast populations adopt more westernized diets and lifestyles, the burden of cardiovascular disease and disability is growing at an alarming rate. The results of prospective observational studies conducted in both western and eastern populations have established the strong association between the primary incidence of stroke and the level of blood pressure. Further, randomized clinical trials of antihypertensive therapy have demonstrated a reduction in primary stroke risk. Among persons with a history of cerebrovascular disease, data from the United Kingdom Transient Ischemic Attack Aspirin Trial (UKTIA) has demonstrated a similar relationship between blood pressure and secondary stroke risk. Trials of blood-pressure lowering in patients with a history of cerebrovascular disease also suggested a reduction in stroke risk. However, patients numbers in these trials were small, and the results were not conclusive. PROGRESS (Perindopril pROtection aGainst Recurrent Stroke Study) is a large, randomized, double-blind, controlled trial designed to provide a definitive answer to these questions. Its primary aim is to determine the effect of blood-pressure lowering on stroke incidence in patients with a history of a previous stroke or transient ischemic attack. A total of 6,105 patients were randomized to receive perindopril (plus indapamide) or placebo in seven regions of the world. The current mean follow-up period exceeds 30 months, and a total follow-up period of at least 4 years is planned. Secondary outcomes include the incidence of other major cardiovascular events, such as myocardial infarction, and of cognitive decline and dementia. Both the major event rate and the degree of adherence to randomized therapy exceed initial projections, which suggests that the study should have the power to achieve its main objectives by the planned completion date of 2001.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

A double-blind trial of perindopril and nitrendipine in incipient diabetic nephropathy.

UNLABELLED: We conducted a randomised, double-blind multicentre trial to compare the efficacy of the inhibitor of the angiotensin-converting enzyme (ACE) perindopril (P) with nitrendipine (N) in incipient diabetic nephropathy. METHODS: Forty-six patients with insulin-treated diabetes mellitus and mild-to-moderate hypertension and stable microalbuminuria were examined. P 4 or 8 mg once daily was compared to N 20 or 40 mg once daily; an optional open combination treatment with indapamide 2.5 mg once daily was given when needed. Main outcome measures were urinary albumin excretion rate, creatinine clearance and isotopic clearance measurements after 12 months. RESULTS: Baseline characteristics (blood pressure, HbA1, renal function) were highly comparable between groups. No serious adverse events occurred during the study period. Blood pressure was controlled (<140/90 mmHg) in all patients except for one in each group who dropped out. At the end of the study, albumin excretion rate was stabilized in both groups (P: 72% of baseline, N: 108%, NS). There were no significant differences found in radiometric clearance measurements. Creatinine clearance rose in patients treated with P by 10.0 ml/min on average, while it decreased by 9.8 m/min under N treatment (group effect: p<0.05). CONCLUSIONS: In this head-to-head comparison, P and N were effective in stabilising most parameters of renal function in incipient diabetic nephropathy.

Adolescent↗
PubMed2002

[The effect of aspirin on rheological properties of erythrocytes in essential hypertension].

Essential hypertension is one of the most important risk factors for cardiovascular diseases. Its pathophysiological mechanism is unknown. Recent data suggests that deformability and aggregation of red blood cells may play an important role in the regulation of blood rheology in hypertension. Simultaneously there are reports suggesting that antihypertensive effects of angiotensin converting enzyme inhibitors (ACEI) could be counteracted by high doses of aspirin. We postulate that these effects could be related to the changes in blood rheology. Accordingly we designed a study to evaluate the effect of low or high dose of aspirin on deformability and aggregability of red blood cells from patients with essential hypertension. Deformability and aggregability of red blood cells were measured by laser diffractometer (Rheodyn SSD, Myrenne GmbH) and computerized automatic aggregometer (MA1 Myrenne GmbH, Germany), respectively. The effects of aspirin on deformability and aggregation of red blood cells were studied ex vivo in whole blood from three groups of patients with essential hypertension (group I: 10 patients receiving placebo, group II: 23 patients receiving 75 mg/day p.o. aspirin for 3 days, and group III: 23 patients receiving 300 mg/day p.o. aspirin for 3 days). Subjects in all groups received the same combination of antihypertensive agents consisting of: one of ACEI (enalapril or perindopril), one of beta-antagonists (metoprolol or bisoprolol), and diuretic agent (indapamid). In patients receiving high dose of aspirin (300 mg/day) we observed that erythrocyte aggregability was 25% higher than in the placebo group (MEA = 25.8 +/- 6 SD, vs MEA = 20.6 +/- 3 SD, p < 0.05). Aspirin had no effects on deformability of erythrocytes or on arterial blood pressure. High doses of aspirin or possibly also other nonsteroidal anti-inflammatory drugs (NSAID) in patients receiving antihypertensive therapy can directly affect rheological properties of the blood due to the activation of red blood cell aggregation. Increased aggregation of red blood cells during antihypertensive therapy may be an important indicator of the worsening of organ perfusion.

Adrenergic beta-Antagonists↗
PubMed2002

[Hypertension and microcirculation].

The importance of the microcirculation (comprising the smallest arteries, arterioles, capillaries and venules) in hypertension and other cardiovascular diseases is well known. The small resistance arteries develop structural changes such as an increase in the wall/lumen ratio and the capillary networks of different vascular beds become rarefied in response to increased blood pressure. These changes not only contribute to hypertensive lesions of target organs but also maintain or amplify the increased blood pressure by increasing peripheral resistances, so creating a vicious circle. Microvascular changes in hypertension may also lead to an increased reflection of the pressure wave towards the heart from the peripheral reflecting sites. This reflected wave also increases systolic blood pressure without increasing the diastolic pressure, thereby increasing the pulse pressure. A high pulse pressure may induce lesions of the vessel walls and of the endothelium of the large arteries, and this is known to be a significant independent risk factor for cardiovascular mortality, especially in the elderly. Microvascular rarefaction could possibly be reversed by therapeutic angiogenesis with cytokines but this treatment is difficult to deliver to the myocardium and is not yet available in clinical practice. Some conventional antihypertensive therapies, including the association of a low dose angiotensin converting enzyme inhibitor, perindopril, and a diuretic, indapamide, may have a beneficial effect on the microcirculation. It has been demonstrated clinically that these drugs specifically reduce the pulse pressure, probably by decreasing the reflected pressure wave, and, therefore, additional benefits in terms of a reduction of cardiovascular risk can be expected.

Arterioles↗