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The relation between hypertension and diabetic nephropathy is complex. Nephropathy is probably involved in the elevated blood pressure found in diabetic patients. In maturity onset diabetes, patients may also have hypertension which is associated with obesity or essential hypertension. It has been suggested that in both types of diabetes, hypertension enhances the development of diabetic nephropathy. Moreover, an aggressive antihypertensive treatment seems able to reduce rate of decline in kidney function in insulin-dependent diabetic patients with patent nephropathy. In this work, creatinine clearance and microalbuminuria in 20 diabetic patients (mostly with maturity-onset-diabetes) with known moderate and effectively treated hypertension were therefore measured and the results were compared with those for 18 normotensive diabetic patients and 22 controls. Duration of diabetes was from one to 26 years (mean: 11 years) and duration of hypertension was from one to 35 years (mean: 10 years). Patients and controls had normal serum creatinine and proteinuria below 0.1 g/l. Microalbuminuria was measured by immunonephelometric assay using specific antiserum (sensitivity = 1.5 mg/l; intra and interassay coefficients: 6.5% and 8% respectively). The highest value was observed in hypertensive diabetic patients with retinopathy (group 1). But hypertensive patients without retinopathy (group 2) and normotensive patients also had significantly increased microalbuminuria. In group 1, microalbuminuria was significantly higher than in group 2. The creatinine clearance was reduced in groups 1 and 2 versus normotensive diabetics, but hypertensive patients were older.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Microalbuminuria in diabetics with moderate hypertension]. 309 93

From a genetic standpoint, humans living today are Stone Age hunter-gatherers displaced through time to a world that differs from that for which our genetic constitution was selected. Unlike evolutionary maladaptation, our current discordance has little effect on reproductive success; rather it acts as a potent promoter of chronic illnesses: atherosclerosis, essential hypertension, many cancers, diabetes mellitus, and obesity among others. These diseases are the results of interaction between genetically controlled biochemical processes and a myriad of biocultural influences--lifestyle factors--that include nutrition, exercise, and exposure to noxious substances. Although our genes have hardly changed, our culture has been transformed almost beyond recognition during the past 10,000 years, especially since the Industrial Revolution. There is increasing evidence that the resulting mismatch fosters "diseases of civilization" that together cause 75 percent of all deaths in Western nations, but that are rare among persons whose lifeways reflect those of our preagricultural ancestors.
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PMID:Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective. 313 45

The personality trait of alexithymia was assessed in 95 patients (35 male, 60 female) with affective illnesses, receiving lithium prophylactically, by means of Schalling-Sifneos Personality Scale (SSPS). The mean SSPS score was similar to that of the healthy population: only 8 patients had a score below 50 points. No relationship was observed between alexithymia score and age, diagnostic category (bipolar I, bipolar II, unipolar) and the duration of lithium therapy. Lower SSPS scores (i.e. high alexithymia) were found in subgroups of male patients with essential hypertension and female patients with lithium-induced obesity. The results suggest that alexithymic traits have no relationship to the pathogenesis of affective illness but may play some role in somatic symptoms emerging in affective patients on lithium prophylaxis.
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PMID:Alexithymia and somatic conditions in patients with affective illnesses during lithium prophylaxis. 314 60

Body mass index, alcohol and salt consumption, and parental history of hypertension were examined as possible predictors of the development of essential hypertension in 1,031 persons, ages 30-49 years at entry, with documented normotension followed by documented hypertension after a mean interval of 6 years. In a comparison with 1,031 matched persistently normotensive persons initial body mass index and percentage increase in body mass index were each predictive of hypertension. Consumption of three or more alcoholic drinks a day at baseline was also predictive, more so if this level of intake persisted than if it diminished. Heavy salt intake as crudely estimated at baseline by one question was also associated with the development of hypertension. Parental history of hypertension was also predictive, more so for hypertension in the mother than for hypertension in the father, and the association was apparent only in female subjects. These characteristics at baseline showed independent associations with subsequent hypertension in multivariate analysis. When follow-up data were included in the multivariate analysis, alcohol consumption at the hypertensive examination was much more strongly related than at the baseline examination, suggesting a short-term effect, and heavy salt consumption was no longer predictive, possibly because of a marked loss of subjects due to missing follow-up data. This large study confirms longitudinally the importance of obesity, weight gain during adulthood, alcohol, family history, and, to some extent, salt as predictive and possibly causal factors for essential hypertension.
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PMID:Precursors of essential hypertension: body weight, alcohol and salt use, and parental history of hypertension. 321 72

Body constituents (cellular and extracellular mass, fat, extracellular fluid) were examined by means of K-40 whole-body radiometry in male essential hypertension patients with normal body weight and alimentary obesity. Second-stage essential hypertension was associated with a reduction of body cell mass, its relative parameters in particular. This fall was even more pronounced in patients with alimentary obesity. Apparently, increased proportion of fat in relation to body cell mass, which is more active metabolically, alters water-salt balance and, consequently, arterial blood pressure.
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PMID:[Body constitution of patients of different somatotypes with hypertension]. 324 60

Reasons are given why calcium, obesity and genetics cannot be considered primary factors in the etiology of essential hypertension. This leaves the major protagonists as salt and neuroendocrine responses to the emotions aroused by the social environment. Most essential hypertension is renin dependent and associated with the physiological changes induced by arousal of the defence response. The psychosocial stimulation associated with this arousal induces an increase in salt appetite. This makes the salt consumption of society a measure of the social stress to which it is exposed. Primitive people whose blood pressure remains normal throughout their lives may lack modern societies' physically protective achievements but their religiously prescribed social solidarity may protect them from psychosocial stress. Our chronic suppression of awareness of emotional arousal together with loss of the ritualized support of affiliative behavior may result in repressed emotional responses which find somatic expression in diseases such as essential hypertension. Hypertensiologist George Pickering proposed that the primitive's ritual and taboo (the equivalent in our society might be the Alcoholic's Anonymous belief in a 'Higher Power') protect them from much anger and despair. He gave this precedence over salt as the primary factor in essential hypertension. New evidence supports this. Despite a high salt diet the blood pressure of socially adjusted rodents remains normal throughout their lifespan. On the other hand, the hypertension that develops when they are psychosocially stimulated is not abated by a low salt diet. In humans, the blood pressure of cloistered, secluded Italian nuns on a high salt diet has remained normal for 20 years while that of nearby village women has risen at a startling 2 mmHg/annum during the same period. On the other hand, in rapidly changing Malawi mature adult, rural and urban blood pressures are rising fast despite a low salt intake. Thus the evidence today argues that the most important factor in the etiology of essential hypertension is not salt but psychosocial stimulation.
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PMID:Stress, salt and hypertension. 327 18

In order to estimate the neuroendocrine function of the central nervous system eventually leading to growth hormone (GH) secretion in essential hypertension, 17 patients with mild arterial hypertension (7 obese and 10 with normal body weight) were examined. The control group consisted of 16 normotensive volunteers (7 obese and 9 with normal body weight). The GH secretion was determined by radioimmunoassay during nocturnal sleep. In all the subjects, the serum GH was also measured after placebo and after the centrally acting alpha 2-adrenergic agonist-clonidine administered i.v. in a dose of 0.15 mg. The fasting serum insulin concentration was also measured in all the subjects. Clonidine decreased the mean arterial pressure in all the subjects investigated. However, in response to clonidine an increase in GH secretion in all hypertensive and normotensive cases with normal body weight was demonstrated, whereas in all obese hypertensive and normotensive patients no significant GH rise was found. It indicates that inhibition of GH secretion in patients with essential hypertension is related to coexistent obesity rather than with that of arterial hypertension. A strong (r = 0.76) and significant (p less than 0.0005) correlation demonstrated between the maximal GH concentration during the nocturnal sleep and after clonidine suggests that the mechanism of GH inhibition in response to both these stimuli is similar and it probably is related to the inhibition of neurohormonal secretion of the growth hormone releasing factor (GRF). However, the negative correlation between the fasting insulin concentration and GH response to clonidine shown in obese subjects only, points to a more complex mechanism of GH inhibition in obesity.
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PMID:Growth hormone (GH) secretion during nocturnal sleep and after clonidine in patients with essential hypertension. 328 64

High blood pressure is prevalent in obesity and in diabetes, both conditions with insulin resistance. To test whether hypertension is associated with insulin resistance independently of obesity and glucose intolerance, we measured insulin sensitivity (using the euglycemic insulin-clamp technique), glucose turnover (using [3H]glucose isotope dilution), and whole-body glucose oxidation (using indirect calorimetry) in 13 young subjects (38 +/- 2 years [+/- SEM]) with untreated essential hypertension (165 +/- 6/112 +/- 3 mm Hg), normal body weight, and normal glucose tolerance. In the postabsorptive state, all measures of glucose metabolism were normal. During steady-state euglycemic hyperinsulinemia (about 60 microU per milliliter), hepatic glucose production and lipolysis were effectively suppressed, and glucose oxidation and potassium disposal were normally stimulated. However, total insulin-induced glucose uptake was markedly impaired (3.80 +/- 0.32 vs. 6.31 +/- 0.42 mg per minute per kilogram of body weight in 11 age- and weight-matched controls, P less than 0.001). Thus, reduced nonoxidative glucose disposal (glycogen synthesis and glycolysis) accounted for virtually all the defect in overall glucose uptake (1.19 +/- 0.24 vs. 3.34 +/- 0.44 mg per minute per kilogram, P less than 0.001). Total glucose uptake was inversely related to systolic or mean blood pressure (r = 0.76 for both, P less than 0.001). These results provide preliminary evidence that essential hypertension is an insulin-resistant state. We conclude that this insulin resistance involves glucose but not lipid or potassium metabolism, is located in peripheral tissues but not the liver, is limited to nonoxidative pathways of intracellular glucose disposal, and is directly correlated with the severity of hypertension.
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PMID:Insulin resistance in essential hypertension. 329 96

An association between alcohol consumption, blood pressure levels and the prevalence of hypertension has been described in close to twenty population studies. The relationship is independent of ethnic group, gender, type of alcohol, cigarette smoking and obesity, but additive to effects of obesity and oral contraceptive use. Several studies show a progressive rise in blood pressure throughout the entire range of alcohol consumption. Reports indicating a threshold for the effect at around 30 g ethanol per day (three standard drinks) may be artefactual due to underreporting of drinking levels. Drinkers consuming an average of 3 or more glasses per day have three to four times the prevalence of "hypertension" compared with teetotallers. A randomized, controlled trial of moderating alcohol consumption in normotensives has confirmed a direct pressor action of alcohol and is supported by studies in hypertensives. These observations have important implications for the prevention and management of essential hypertension in most communities.
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PMID:Epidemiology of alcohol and hypertension. 331 May 50

In the Vermont study of experimental obesity, heterogeneity of the response to overfeeding was a striking finding in normal subjects. There is also poorly defined heterogeneity within the areas of obesity, noninsulin-dependent diabetes, hyperlipidemias, and so-called essential hypertension. These disorders may occur in the same individual and have important mechanisms in common. Thus it is logical to strive for an integrated approach to nutritional and medical management rather than an approach fragmented between medical specialties. The rapidly developing computer programs now adapted to microcomputers hold promise of facilitating an integrated approach both in the clinical and in the investigative field.
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PMID:1987 Herman award lecture. A plea for an integrated approach to characterization and management of obesity, type II diabetes, hyperlipidemias, and hypertension: a role for the personal computer? 331 67


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