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Exogenous obesity is characterized hemodynamically by expanded intravascular (plasma) volume associated with an increased cardiopulmonary volume and cardiac output. In contrast, essential hypertension is related to an increased total peripheral resistance that is more or less uniformly distributed throughout the component organ circulations associated with a contracted plasma volume in proportion to the height of arterial pressure. Thus, both cardiac output and total peripheral resistance are elevated in obesity hypertension, and both impose a load on the left ventricle, resulting in both a volume and a pressure overload left ventricular hypertrophy. Although renal vascular resistance is not as increased as it is in lean hypertensive patients, these patients are subjected to hyperfiltration and proteinuria. Additionally, these hemodynamic alterations coexist with carbohydrate intolerance, hyperinsulinemia, hyperlipidemia, and hyperuricemia. With weight reduction and associated pressure reduction, the hemodynamic and metabolic changes reverse toward normal. However, should this not be achievable, the angiotensin converting enzyme inhibitors and calcium antagonists provide rational physiological approaches to drug therapy. With these agents pressure reduction is achieved through a fall in vascular resistance without intravascular volume expansion, and this is associated with reduced left ventricular mass and preserved cardiac and renal function, and without exacerbation of preexisting metabolic perturbations. Hence, these two classes of antihypertensive agents may provide a rational and physiological means for reversing the pathophysiological alterations of hypertensive disease in those obese patients in whom weight control is not possible.
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PMID:Obesity hypertension. Converting enzyme inhibitors and calcium antagonists. 173 Apr 48

The effect of lacidipine, a dihydropyridine calcium antagonist on lipid metabolism, has been followed in 8 patients with uncomplicated mild to moderate essential hypertension treated for up to 14 months. There were significant reductions in the systolic and diastolic pressures, from 167/102 to 146/91 mm Hg at 2 months, and to 137/85 mm Hg at the end of the study. Blood lipid concentrations did not change during the observation period (cholesterol 5.1 vs 5.3 mmol.l-1, triglycerides 1.1 vs 1.0 mmol.l-1, HDL-cholesterol 1.1 vs 1.2 mmol.l-1). The results show that lacidipine did not affect lipid metabolism and suggest that calcium antagonists may be safely prescribed for a prolonged period to patients with combined hypertension and hyperlipidaemia.
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PMID:Effect of lacidipine, a long-acting calcium antagonist, on hypertension and lipids: a 1 year follow-up. 174 41

In practice, some of the major problems for the physician who treats hypertension are patients who are resistant to treatment or who have other complicating risk syndromes. Therefore the overall efficacy of an antihypertensive agent must include an assessment of effect in patients with serious ancillary problems. In this article, doxazosin is reviewed for its efficacy in the treatment of severe essential hypertension and specific complications or conditions of mild or moderate essential hypertension, namely, left ventricular hypertrophy, hyperlipidemia, noninsulin-dependent diabetes mellitus, renal insufficiency, pheochromocytoma, chronic obstructive pulmonary disease, peripheral vascular disease, and smoking. Doxazosin is particularly efficacious in many specific subgroups of patients with hypertension, and the results of relevant studies are discussed.
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PMID:Efficacy of doxazosin in specific hypertensive patient groups. 182 52

Current research is being directed toward the identification of markers of cardiac risk in hypertension, according to demographic, clinical, genetic, challenge-response and laboratory predictors. Much interest has centered around cationic transporters as laboratory markers, not only because they might make good predictors of cardiac risk, but also because of their potential for explaining the pathophysiology of that disorder. To date, there is no cationic transporter that clearly discriminates between subjects with low and with high cardiac risk, although the sodium-lithium (Na(+)-Li+) countertransport in red blood cells has come the closest. High rates of Na(+)-Li+ countertransport have been found to be associated not just with essential hypertension but more specifically with subgroups of patients suffering from essential hypertension who have a higher frequency of severe hypertension and increased risk of cardiac disease. Here, we examine different lines of clinical evidence suggesting that increased Na(+)-Li+ countertransport activity may identify patients with essential hypertension who are at an increased risk of cardiac disease because they also present other cardiac risk factors, namely hyperlipidemia and/or left ventricular hypertrophy. In addition, the pathophysiological basis for the association of hypertension and the above cardiac risk factors with increased Na(+)-Li+ countertransport are discussed.
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PMID:Is the erythrocyte sodium-lithium countertransport a molecular marker of cardiac risk in hypertension? 183 76

Erythrocyte sodium-lithium countertransport (SLC) was measured in 17 patients with either combined hyperlipidaemia or hypercholesterolaemia before and after lipid lowering therapy. Before treatment SLC related to the serum triglyceride level and was increased in combined hyperlipidaemia. After treatment the SLC had returned to normal and the change in SLC was related to the change in serum triglyceride levels. Raised SLC is associated with essential hypertension but is not related to blood pressure. Therefore, the association of raised SLC with hyperlipidaemia and essential hypertension appears to have different underlying mechanisms.
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PMID:Lipid lowering therapy leads to a reduction in sodium-lithium countertransport activity. 185 57

Hypertension is often associated to other risk factors, such as abnormal lipid and carbohydrate metabolism, which should be considered for the choice of antihypertensive drug treatment. Doxazosin is a postsynaptic alpha-1 adrenoceptor blocker suitable for once a day treatment regime. It seems to induce fewer side effects than older drugs of the same class and it may improve lipid and carbohydrate profile, thereby reducing the risk of coronary artery disease. To verify its effects on blood pressure, serum lipids and glucose tolerance, doxazosin (1-8 mg od) was given for 8 weeks to 32 patients suffering from essential hypertension, of whom 16 had fasting serum cholesterol higher than 6 mmol/l and/or fasting serum triglycerides higher than 1.9 mmol/l. Sitting and standing blood pressure were significantly reduced (from 163 +/- 18/101 +/- 6 mmHg to 147 +/- 19/94 +/- 8, p less than 0.001 and from 162 +/- 18/107 +/- 9 to 145 +/- 18/95 +/- 8, p less than 0.001, respectively) at a mean daily dose of 5 mg. Normotension or a good hypotensive response was achieved in 60% of the patients. The daily dose which turned out to be effective in 50% of the patients was 7 mg. The drug treatment was well tolerated and orthostatic hypotension was never observed either on starting treatment or on increasing dosage. Blood lipids and glucose tolerance were not significantly affected. Doxazosin is therefore an effective antihypertensive agent suitable for use in patients with essential hypertension alone or combined with hyperlipidemia.
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PMID:[Doxazosin for the treatment of arterial hypertension]. 215 71

The study objective was to determine the effects of monotherapy with clonidine and atenolol versus placebo on serum lipids, apolipoproteins, and blood pressure in patients with mild primary hypertension. The protocol comprised a double blind, randomized, placebo-controlled 5-month prospective study carried out in an outpatient general internal medicine clinic in a university medical center. There were 92 patients ages 18 to 70, with mild primary hypertension (sitting diastolic blood pressure of greater than 90 mm Hg and less than 105 mm Hg) without significant cardiac, renal, cerebrovascular, hepatic, neoplastic, or hematologic disorders. Patients with severe hyperlipidemia or peripheral vascular disease were also excluded. All factors known to effect serum lipids were held constant throughout the study (i.e., diet, weight, exercise, caffeine, tobacco). Atenolol and clonidine significantly reduced blood pressure when compared with placebo. Atenolol caused significant increases in serum triglycerides and apolipoprotein B (p less than 0.05) and significant reductions in high-density lipoprotein-cholesterol, apolipoproteins A-I and A-II (p less than 0.05). Atenolol also induced a significant adverse effect on all lipid ratios, increasing total cholesterol/high density lipoprotein-cholesterol, low density lipoprotein-cholesterol/high density lipoprotein-cholesterol, apolipoprotein B/apolipoprotein A-I and apolipoprotein B/apolipoprotein A-II ratios and decreasing low density lipoprotein-cholesterol/apolipoprotein-B ratio (p less than 0.05). Clonidine caused significant reductions in high-density lipoprotein-cholesterol, apolipoproteins AI and AII (p less than 0.05 but was neutral on all other lipids, lipid subfractions, and apolipoproteins. Clonidine did not significantly alter any of the lipid ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of clonidine hydrochloride versus atenolol monotherapy on serum lipids, lipid subfractions, and apolipoproteins in mild hypertension. 219 93

Early antihypertensive intervention in diabetes often means intervention in a cluster of cardiovascular risk factors including glucose intolerance per se, hyperlipidemia, obesity and hypertension, which are not just coexistent but may be causally linked together by the resistance of peripheral tissues to the action of insulin. Blood pressure lowering treatment should therefore be metabolically neutral in order to avoid aggravation of this risk factor syndrome. Clinical studies applying CE-inhibitors in type II diabetes are critically reviewed under this aspect. The majority of the available studies in type II diabetes report a reduction of insulin resistance and a marginal improvement of metabolic control. The order of magnitude in HbA1 reduction is nearly 10% of the glycosylated haemoglobin, reduction of fasting and postprandial blood glucose approximates 1 mmol/l. From a more extended view, considering essential hypertension as insulin resistant and thus possibly "prediabetic" state, this marginal metabolic effect gets further support from recent studies in essential hypertension consistently reporting an improvement of metabolic parameters of similar magnitude. This might become a central argument in the discussion about individualized and metabolically neutral antihypertensive treatment in essential hypertension.
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PMID:Clinical studies with CE-inhibitors in diabetes. 220 31

Hypertension and diabetes mellitus are chronic medical conditions that frequently coexist. In the United States, it is estimated that 10 million persons suffer from diabetes mellitus, 60 million from hypertension, and 3 million from the combination of the two. There may be a causal relationship between hypertension and diabetes. Obesity may be a precipitating factor for both hypertension and non-insulin-dependent diabetes mellitus. Those with insulin-dependent diabetes mellitus generally become hypertensive only with the onset of nephropathy. Glucose tolerance, insulin resistance, and hyperinsulinemia frequently occur with essential hypertension and may be aggravated by hypertension therapy, especially with diuretics and beta-blockers. Hyperinsulinemia may be an important common factor promoting sodium retention, sympathetic nervous system stimulation, and inhibition of the sodium pump. The Working Group on Hypertension in Diabetes has outlined a flexible modified version of the stepped-care approach to the treatment of hypertension in diabetes. Management is complex because diabetes is associated with autonomic neuropathy, sexual dysfunction, hyperlipidemia, and fluid and electrolyte disorders. All these problems can be exacerbated by antihypertensive treatment. Nonpharmacologic measures, which address weight reduction and sodium restriction, are logical, but aggressive antihypertensive medication is invariably necessary. Diuretics and/or beta-blockers were the mainstay of treatment until the introduction of angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers. These newer agents have no deleterious effects on carbohydrate metabolism and are generally better tolerated. Antihypertensive therapy may slow the rate of deterioration in diabetic nephropathy. This was first shown with diuretics, beta-blockers, and hydralazine and more recently with ACE inhibitors, which provide effective blood pressure control and a significant drop in albuminuria without affecting the glomerular filtration rate adversely. ACE inhibition may also lead to increased insulin sensitivity and glucose disposal rate. Long-term trials are needed to assess the effects of these new agents on the treatment of hypertension in the diabetic population.
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PMID:Diabetes mellitus and hypertension. 222 Jul 97

The drug treatment of mild hypertension has been shown to afford protection against fatal and nonfatal strokes, congestive heart failure, progression to more severe levels of hypertension, and all-cause mortality, but not against the complications of coronary artery disease. The lack of benefit against coronary artery disease may result from failure to reduce other risk factors or because the drugs employed increased coronary risk. It can be taken as axiomatic that effective preventive antihypertensive therapy is more likely with drugs with mechanisms and sites of action that are focused on the underlying pathophysiology than with drugs that lower blood pressure by means unrelated to the hypertensive process. Adrenergic predominance plays a major role in the initiation and maintenance of essential hypertension and, consequently, the alpha-adrenergic receptor inhibitors were among the first substances to receive serious consideration as antihypertensive agents. However, since these drugs are nonselective, feedback control of transmitter norepinephrine was lost and, consequently, the clinical expectations of the early alpha-adrenergic receptor inhibitors in the treatment of high blood pressure were not fulfilled. The discovery of selective postjunctional alpha 1-adrenergic-receptor inhibitors, such as prazosin and doxazosin, which preserve feedback control of transmitter norepinephrine release, was the crucially important step in the development of specific drugs to combat the hyperactivity of adrenergic vasoconstrictor nerves in hypertension. These drugs have been shown to normalize hemodynamics in hypertensive patients. They lower blood pressure through a reduction in peripheral resistance at rest and during exercise, independent of changes in heart rate and blood pressure, with minimal reflex activation or tolerance development. Alpha 1-adrenergic-receptor inhibitors, such as prazosin and doxazosin, represent an attractive choice for initial therapy in all grades of hypertension and are especially appropriate in hypertensive patients with congestive heart failure, asthma and chronic obstructive airways disease, renal impairment, diabetes mellitus, hyperlipidemia, benign prostatic hyperplasia, or gout, and in those involved in vigorous work, sports, or exercise. There are no known contraindications to these drugs, except in patients who are sensitive to quinazolines.
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PMID:Pharmacologic basis for the use of doxazosin in the treatment of essential hypertension. 256 23


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