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Biomedical subjects

W Riesen

Publications and source records attributed to W Riesen.

At least 19 recordsLinked to original sources

Insulin sensitivity in normotensive subjects during angiotensin converting enzyme inhibition with fosinopril.

The effect of the new ACE-inhibitor, fosinopril, on insulin sensitivity (SI), glucose homoeostasis and lipid profile has been examined in 24 young, healthy, normotensive men. SI, fasting plasma glucose and insulin, serum total triglycerides (Tg) and lipoprotein cholesterol (C) fractions, and ACE activity were assessed after subjects had taken placebo for 1 week and after 3 further weeks either on placebo (12 subjects) or fosinopril 20 mg daily (12 subjects), administered in a double-blind, randomized order. Measurements were made after 3 days on a standard diet (2500 kcal/d, 45% carbohydrates, 40% fat and 15% proteins) and after an overnight fast. Compared with control values at the end of the run-in placebo phase, fosinopril reduced plasma ACE activity (from 106 to 24 nmol.ml-1.min-1), Significantly increased plasma potassium and lowered upright systolic blood pressure. It also improved the k-value of the glucose disappearance rate after glucose load (from -1.70 to -1.88%.min-1) and tended to increase SI slightly although not significantly (from 10.2 to 12.0.10(-4).min-1.microU-1.ml-1). Fasting plasma glucose, insulin, serum total, high-, low-, and very-low density lipoprotein cholesterol fractions and total triglycerides were unchanged following fosinopril and placebo. The findings indicate that in healthy lean humans, ACE inhibition with fosinopril is neutral with regard to lipoprotein and carbohydrate metabolism, and that it may slightly enhance cellular glucose disposal. This calls for further evaluation in individuals at high risk of developing insulin resistance and in patients with impaired insulin sensitivity related to hypertension, obesity, decreased glucose tolerance and diabetes mellitus.

Adult

Plasma insulin during physiological and pathophysiological changes in atrial natriuretic factor.

Changes in plasma insulin in response to a physiological or pathophysiological elevation in circulating atrial natriuretic factor (ANF) have been investigated. Plasma insulin, glucose, immunoreactive (ir) ANF, effective renal plasma flow (ERPF), glomerular filtration rate (GFR), absolute and fractional excretion of sodium (FENa), have been measured in 14 volunteers before and during infusion of low doses of ANF or vehicle (V). Each subject received single-blind in a randomized sequence at 2 week-intervals: V alone, or ANF 4, 8 and 16 ng.kg-1.min-1, induced over 90 min. Plasma irANF was increased 2.5- to 11-fold during the ANF infusion as compared to the test with the vehicle. Plasma insulin did not change during V administration (baseline vs V: 22 vs 21 microU.ml-1) and was unchanged during ANF at 4, 8 and 16 ng.kg-1.min-1 (19, 19, 21 microU.ml-1, respectively). Blood pressure, ERPF and GFR were not affected, and diuresis, FENa and urinary Na excretion were increased significantly and dose-dependently during ANF, but not V infusion. Compared to baseline, ANF 4, 8 and 16 ng.kg-1.min-1 increased urinary Na excretion by 147,241 and 446 mumol.min-1, respectively. The findings indicate that, in normal humans, an acute increase in irANF within or slightly above the physiological range, which modified natriuresis and diuresis, did not alter circulating plasma insulin.

Atrial Natriuretic Factor

[Comparison of a calorie-defined diet with the conventional exchange diet in Type 2 diabetes mellitus].

Meal planning using food exchange lists is problematic for many elderly type 2 diabetic subjects because the system is too complicated and too rigid regarding the daily meals. In addition, exchange lists are calorically imprecise. 12 non-insulin-dependent diabetic subjects agreed to participate in the present study (6 male, 6 female; age 40-82 years, weight 80 +/- 6 kg; HbA1c 7.3 +/- 0.3%); they received sequentially in randomized order either a diet using exchange lists, or a diet defined by total amount of allowed daily calories ("calorie diet"), both containing approx. 25 calories/kg ideal body weight/day, each for 8 weeks. The "exchange lists" mainly contained foods which were defined according to their content in carbohydrates (including bread exchanges, fruit exchanges, milk exchanges, vegetable exchanges). With the "calorie diet" the patients were relatively free during the day, the only rule being that they were allowed to consume a certain amount of calories per day, using a "calorie ruler". The results demonstrated that body weight decreased similarly during both diet periods (2.0 +/- 0.8 kg during the exchange list diet; 2.5 +/- 0.9 kg during the "calorie diet"). Fasting blood glucose concentration decreased during the "calorie diet" by 7% (p less than 0.05; fasting blood glucose at the end of the "calorie diet" was lower than after the exchange list diet (p less than 0.016). Serum lipoproteins were similar after both diet periods. 10/12 patients preferred the "calorie diet" because of its simplicity and flexibility. It allowed consumption of instant food which was calorically defined but difficult to convert into the exchange system.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged

Unaltered insulin sensitivity during calcium channel blockade with amlodipine.

The sensitivity of peripheral tissues to insulin is of pathophysiological, therapeutic and possibly also of prognostic relevance. Calcium channel blockers are widely used in the treatment of cardiovascular disorders that are commonly associated with decreased insulin sensitivity (SI). To evaluate the effects of calcium channel blokkade on SI, glucose homoeostasis and lipid profiles, studies were made of SI (determined by the Minimal Model Method of Bergman), basal glucose and insulin levels, serum total triglyceride (Tg) and lipoprotein cholesterol (C) fractions and certain other variables in 38 healthy young men (24 y) during placebo and after 3 weeks of calcium channel blockade with amlodipine 5 mg once daily. Measurements were made after 3 days on a standard diet (2200 kcal.day-1, 45% carbohydrates, 40% fat and 15% proteins) and after an overnight fast. Compared to placebo, amlodipine decreased supine systolic blood pressure (P less than 0.01). Heart rate, body weight and 24 h urinary sodium excretion were unaltered, and so were fasting plasma glucose (placebo vs amlodipine: 4.86 vs 4.83 mmol.l-1, respectively) and insulin levels (7.7 vs 7.9 microU.ml-1), SI (10.5 vs 9.6.10(-4) x min-1 pro microU.ml-1), serum total Tg, C and lipoprotein C fractions. The findings demonstrate unchanged insulin sensitivity and secretion, as well as lipoprotein regulation, during maintenance administration of 5 mg amlodipine daily to healthy young men.

Adult

Reproducibility of insulin sensitivity measured by the minimal model method.

Insulin resistance is a critical component underlying the altered glucose homeostasis in a variety of metabolic and non-metabolic disorders. Aging, body fat distribution, obesity, diabetes mellitus or hypertension are well recognized conditions associated with an impaired tissue sensitivity to insulin action. Apart from such constant factors, insulin sensitivity can be acutely modified by independent variables such as physical exercise, dietary factors, alcohol intake or harmless drugs. To evaluate the day-to-day intra-individual variation in insulin sensitivity, glucose homeostasis and lipid profiles, we investigated the insulin sensitivity index (S1) (determined by the minimal model method of Bergman), basal and post-glucose-load insulin and glucose levels, serum total triglyceride and lipoprotein cholesterol fractions in 15 healthy young men (24 +/- 1 year, mean +/- SEM), on two different occasions at an interval of 3 weeks (days 1 and 21), after 3 days of a standard dietary regimen and after an overnight fast. Blood pressure, heart rate, body weight and 24 h urinary sodium excretion were almost identical in the two phases. S1(day 1) varied from 4.2 to 15.8 x 10(-4).min-1 pro microU/ml (mean: 10.2 +/- 0.9) and correlated with S1(day 21) (11.2 +/- 1.2 x 10(-4).min-1 pro microU/ml, r = 0.78, p less than 0.0007). The slope of the relationship did not differ from 1 (1.01, p greater than 0.90), the intercept was close to the origin (0.8, p greater than 0.73) and the coefficient of variation was 14.4%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Altered insulin sensitivity, hyperinsulinemia, and dyslipidemia in individuals with a hypertensive parent.

PURPOSE: Essential hypertension is, in some patients, complicated by impairment of insulin-mediated glucose disposal and hyperinsulinemia. Whether this metabolic disturbance is a consequence of the hypertensive process or whether it may precede, and thus possibly promote, the development of hypertension has been unknown. SUBJECTS AND METHODS: Searching for hereditary or familial defects in hypertension-prone humans, we prospectively investigated insulin sensitivity, plasma insulin and glucose, and serum lipoproteins in normotensive offspring of essential hypertensive as compared with age- and body habitus-matched offspring of normotensive families. RESULTS: Compared with 78 control subjects, 70 offspring of essential hypertensive parents had similar age (mean +/- SEM: 24 +/- 1 versus 24 +/- 1 years, respectively) and body mass index (22.3 +/- 0.2 versus 22.4 +/- 0.2 kg/m2), a blood pressure of 127/77 +/- 1/1 versus 123/76 +/- 1/1 mm Hg (p less than 0.05 for systolic), and significantly elevated (p less than 0.01 to 0.001) fasting plasma insulin levels (9.9 +/- 0.3 versus 8.6 +/- 0.3 microU/mL), serum total triglycerides (1.03 +/- 0.06 versus 0.83 +/- 0.03 mmol/L), total cholesterol (4.37 +/- 0.08 versus 3.93 +/- 0.07 mmol/L), low-density lipoprotein cholesterol (2.45 +/- 0.08 versus 2.14 +/- 0.07 mmol/L), and total/high-density lipoprotein cholesterol ratio (4.3 +/- 0.1 versus 3.7 +/- 0.1). Insulin sensitivity was lower (9.4 +/- 0.7 versus 13.2 +/- 1.1 x 10(-4) x minute-1/microU/mL, p less than 0.001), while post-glucose-load plasma insulin levels were higher (p less than 0.05) in the 41 offspring of essential hypertensive parents than in the 38 offspring of normotensive parents so investigated. CONCLUSION: These findings demonstrate that young normotensive humans in apparently excellent health but with one essential hypertensive parent tend to have an impairment of insulin-mediated glucose disposal, hyperinsulinemia, and dyslipidemia. It follows that a familial trait for essential hypertension seems to coexist commonly with defects in carbohydrate and lipoprotein metabolism that can be detected before or at least at a very early stage of the development of high blood pressure as judged by resting blood pressure measurements.

Adolescent

Postsynaptic alpha 1-blockade with terazosin does not modify insulin sensitivity in nonobese normotensive subjects.

Plasma insulin levels and the sensitivity of peripheral tissue to insulin (SI) have pathophysiological, therapeutic, and possibly also prognostic relevance. To investigate the effects of short-term selective alpha 1-adrenergic receptor blockade in nonobese normotensive humans on glucose and lipoprotein homeostasis, we assessed SI (determined by the minimal model method of Bergman), before and after glucose load plasma, glucose, and insulin levels, serum total triglycerides and lipoprotein cholesterol fractions, and some other variables in 20 healthy young men (26 +/- 1 years old, mean +/- SEM) during placebo and after 5 weeks of terazosin administration at a dose up to 10 mg once daily. Measurements were made after 3 days of standard diet (2,500 kcal/day, 45% carbohydrates, 40% fat, and 15% proteins) and after an overnight fast. Compared to placebo, terazosin decreased the upright systolic blood pressure (placebo vs. terazosin: 125 +/- 2 vs. 117 +/- 2 mm Hg, p less than 0.05) and increased supine (63 +/- 2 vs. 70 +/- 1 beats/min, p less than 0.05) and upright (77 +/- 2 vs. 88 +/- 2 beats/min, p less than 0.01) heart rates, while the body weight was unaltered. Terazosin did not significantly modify fasting plasma glucose (5.08 +/- 0.09 vs. 5.23 +/- 0.08 mmol/L, respectively), or insulin (8.9 +/- 0.5 vs. 8.6 +/- 0.6 microU/ml), SI (14.3 +/- 1.8 vs 11.8 +/- 1.5 x 10(-4)/min/microU/ml), the areas under the insulin or glucose curves, serum total triglycerides, and cholesterol or lipoprotein cholesterol fractions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists

Association between sympathetic activity and the atherogenic serum cholesterol fraction.

A possible modulating influence of noradrenergic activity on serum lipoproteins was assessed under placebo conditions and following 4 weeks of sympathetic neurone blockade with debrisoquine in 9 normal subjects, 11 patients with mild essential hypertension, 9 normotensive, and 9 hypertensive hemodialysis patients. Plasma norepinephrine (NE) did not differ significantly among groups on placebo and was consistently reduced (P less than 0.05-0.001) by sympathetic blockade. The latter also decreased (P less than 0.05-0.001) plasma total cholesterol (C) as well as low and very low density lipoprotein cholesterol (LDL + VLDL-C) in the three patient groups. In the two dialysis groups, basal levels of plasma triglycerides (Tg) were increased and high density lipoprotein cholesterol (HDL-C) was diminished (P less than 0.01-0.001); sympathetic blockade lowered Tg and raised HDL-C (P less than 0.01-0.001). In normal subjects, sympathetic blockade did not significantly modify plasma lipoproteins. In the three patient groups, significant correlations (r = 0.62 - 0.88; P less than 0.05 - less than 0.001) existed between (a) basal plasma NE and total C or LDL + VLDL-C and (b) debrisoquine-induced changes in NE and changes in total LDL + VLDL-C. These findings suggest that in essential hypertension as well as in hemodialysis patients, the atherogenic C fraction, represented by LDL + VLDL-C, may be modulated by the noradrenergic activity.

Adult

[Methods of cholesterol determination: conventional procedure or "dry chemistry"?].

The search for the cardiovascular risk factor cholesterol should essentially be done in the physicians' laboratory. The majority of such analyses is performed by 'dry' chemistry tests. This review compares this technique with conventional methods for the determination of cholesterol. The reagents and the reaction mechanisms are principally the same for both techniques, i.e. fully enzymatic methods are used. In 'dry' chemistry the reagents are fixed on a solid carrier. The reactive state is provided by the liquid of the specimen. Two principles are employed: the technique of strips which is already utilised in urinary analysis and the system of multiple film layers as it is common in color-film technique. Three already introduced systems are discussed: the Seralyzer (Ames), the Ektachem (Kodak), and the Reflotron (Boehringer, Mannheim), and one system which is still in evaluation (the Clinistat, Ames). All the systems give a good agreement provided that they are operated by well-trained operators. Problems arise with quality control, since matrix effects are particularly important. The exactitude of the results depends on the calibration. Both, the Reflotron and the Clinistat are calibrated by the manufactories himself, the employer has no influence and is entirely dependent on the reliability of the producer. Although clinical chemistry analyses are facilitated by 'dry' chemistry it is by no means devoid of risks because the errors are more difficult to recognize.

Blood Chemical Analysis

Antihypertensive and hypouricaemic effects of nitrendipine in chronic renal failure.

To evaluate the potential therapeutic value of calcium antagonists in hypertension associated with impaired renal function, blood pressure (BP), certain regulatory factors, and metabolic correlates of cardiovascular risk have been assessed in 15 patients with mild to marked chronic renal failure before and after 6 weeks of therapy with nitrendipine. Compared to placebo, nitrendipine (mean final dose 55 mg/day) decreased supine BP from 173/102 to 146/81 mm Hg and upright BP from 170/105 to 145/86 mm Hg. Heart rate, body weight (+0.8 kg) and exchangeable sodium (+176 mmol, not significant) were minimally increased, and plasma and whole blood volume, plasma angiotensin II and creatinine concentrations, and urinary electrolyte and creatinine excretion were not significantly changed. Nitrendipine increased uric acid excretion and lowered plasma uric acid by 24%; glucose, insulin, serum total lipids, and lipoprotein fractions were unchanged.

Adult

Changes in lipoproteins induced by the remnant kidney tissue or binephrectomy in chronic uremic patients treated by hemodialysis.

The role of the remmant kidney tissue in uremic patients undergoing hemodialysis treatment has rarely been considered to influence the changes in lipoprotein and lipid metabolism. Twenty hemodialyzed patients with remnant kidneys and 11 anephric patients were studied to examine whether the presence or the absence of remnant kidney leads to qualitative or quantitative changes of the lipids and lipoproteins. Anephric patients showed a significantly higher triglyceride level, 3.66 +/- 0.49 (SEM) mmol/L v 2.34 +/- 0.09 mmol/L in patients with remnant kidneys (P less than .01), higher very-low-density lipoprotein (VLDL) triglycerides, 1.24 +/- 0.30 mmol/L v 0.69 +/- 0.09 (P less than .04), and higher HDL-triglycerides, 1.22 +/- 0.29 mmol/L v 0.66 +/- 0.09 mmol/L (P less than .04). APO-AI was significantly decreased in anephric patients, 95.2 +/- 13.3 mg/dL v 129.7 +/- 6.02 mg/dL in patients with remnant kidneys (P less than .01). APO-B was similar in both groups. All APO-C and APO-E were significantly lower in anephric patients, APO-CI 6.13 +/- 0.87 mg/dL v 8.47 +/- 0.42 mg/dL in patients with remnant kidneys (P less than .01), APO CII 1.00 +/- 0.01 mg/dL v 10.0 +/- 0.01 mg/dL (P less than .0001), APO-CIII 10.12 +/- 1.43 mg/dL v 26.0 +/- 2.86 mg/dL (P less than .0005), and APO-E 8.0 +/- 0.02 mg/dL v 12.0 +/- 0.01 mg/dL (P less than .03). These results point out important differences between women and men. In women binephrectomy promotes a decreased concentration of all APO-C but has no influence on APO-AI concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoprotein A-I

Stimulus-response coupling in marine sponge cell aggregation: lipid metabolism and the function of exogenously added arachidonic and docosahexaenoic acids.

Cells of the marine sponge, Microciona prolifera, the most ancient of the animal cells which clump on recognition, resemble neutrophils and platelets in undergoing stimulus-response coupling when exposed to Ca2+ ionophores and phorbol esters. We have studied lipid content and remodelling in sponge cells by thin-layer, gas-liquid, and high-performance liquid chromatography (HPLC) analyses supplemented by ultraviolet and mass spectroscopy. Phosphatidylcholine (PC) (35.6%), phosphatidylethanolamine (PE) (27.4%) and phosphatidylserine (PS) (21.4%) constituted the bulk of phospholipids detected. The major fatty acids were all polyenoic; 22:6 (22%), 26:2 (17%) and 26:3 (15%). Arachidonic acid (20:4), present as 2.7% of total phospholipid, and docosahexanoic acid (22:6) were found to elicit aggregation of sponge cells when added (10 microM) in synergy with ionomycin (1 microM), resembling in their effects those of phorbol esters (but not phorbol) and 1-oleyl-2-acetylglycerol (OAG). Moreover, 20:4 and 22:6, as well as phorbol ester and OAG, overcame the block to aggregation imposed by colchicine and vinblastine. Kinetic studies of lipid remodelling showed that aggregating cells diverted [14C]22:6 or [14C]20:4 from triacylglycerol into diacylglycerol and phospholipids; appearance of label in phosphatidic acid and phosphatidylinositol (PI) anteceded labeling of phosphatidylcholine. In unstimulated cells, [14C]22:6 was rapidly incorporated into phosphatidylcholine with little accumulation in phosphatidate. Although 22:6 and 20:4 resembled OAG and phorbol esters in overcoming the effects of colchicine and vinblastine (which had no effects on overall lipid metabolism), they did not reverse the block to aggregation of nordihydroguaiaretic acid (NDGA) (which inhibited lipid metabolism). Under none of these circumstances was 22:6 or 20:4 converted to cyclooxygenase or lipoxygenase products in the course of aggregation: all labeled acyl groups remained present as unmodified fatty acids on alkaline hydrolysis. These data not only extend the observations of Muller et al. (J. Biol. Chem. 262 (1987) 9850-9858) on the role of phosphoinositides and C kinase in marine sponge cell aggregation, but also demonstrate that sponges form diacylglycerols in the process. We suggest that exogenous 22:6 and 20:4 (like phorbol esters or OAG) can substitute for endogenous diacylglycerol in the activation of protein kinase C.

Animals

Metabolic changes in healthy men using fat-modified diets. I. Disposition of serum cholesterol.

The effect of typical fat-modified diets on serum lipids, lipoproteins and apolipoproteins, on the intravenous fat-tolerance test and on fecal sterol excretion were observed in a group of men living at home and compared to that of their normal diets. Two 4-week-long diet periods alternated with four periods of 6 weeks' duration during which the men followed their normal dietary habits and accustomed life-styles. According to a randomized cross-over design sunflower oil and corn oil were used as the main fat sources for the fat-modified diets. Both diets lowered total cholesterol considerably acting mainly on LDL cholesterol, without affecting plasma triglycerides significantly. Apolipoprotein A-I and A-II concentrations in serum remained constant, and clearance of triglyceride-rich lipoproteins, as measured by an intravenous fat-tolerance test (Intralipid test), was not significantly affected. While changes of all measured parameters pointed in the same direction, serum total and LDL cholesterol levels were significantly lower with corn oil than with the sunflower oil. Excretion of endogenous sterols (fecal sterol balance) was higher with the fat-modified than with the normal diet. This increase in sterol excretion closely corresponded to the extent of serum cholesterol lowering.

Adult

Antihypertensive and metabolic effects of ketanserin in diabetic patients with mild hypertension.

Ketanserin is a serotonin S2 receptor antagonist with antihypertensive activity. Its effects on blood pressure, glucose metabolism and serum lipids were assessed in 24 patients with diabetes mellitus and mild arterial hypertension in a double blind, placebo-controlled trial. Ketanserin in doses up to 80 mg daily caused a slight decrease of supine BP (from 159/97 +/- 19/11 to 153/90 +/- 20/9 mm Hg; NS/P less than 0.01) and upright BP (from 160/102 +/- 18/13 to 151/93 +/- 12/12 mm Hg; P less than 0.05/NS). However, these pressures did not differ significantly from the levels observed in the placebo group. Supine and upright heart rate, body weight, plasma sodium and potassium, serum creatinine, glucose, C-peptide, glycosylated haemoglobin, serum cholesterol and triglycerides, their lipoprotein fractions, apolipoprotein A1, A2 and B concentrations and the responses of serum glucose and insulin to a standard oral glucose loading test did not change. These findings indicate that the selective S2 receptor antagonist ketanserin did not unfavourably influence glucose and lipid metabolism in diabetic patients with arterial hypertension.

Adult

Comparative effects of doxazosin and hydrochlorothiazide on serum lipids and blood pressure in essential hypertension.

The efficacy and safety of doxazosin (mean dosage 6.9 mg, range 1 to 16) in the treatment of essential hypertension were compared in a double-blind study with those of hydrochlorothiazide (HCTZ) (mean dosage, 84.6 mg, range 25 to 100) in 104 hypertensive patients treated once daily for 6 months. Thirty-five patients were also assessed for comparative effects of the 2 agents on serum lipid parameters. Doxazosin produced potentially favorable changes from baseline in the concentrations of serum lipid fractions (total triglycerides, total cholesterol, high density lipoprotein [HDL] cholesterol and the derived HDL/total cholesterol ratio) compared with HCTZ. The decreases in total triglyceride and total cholesterol concentrations and an increase in the HDL/total cholesterol ratio were significantly different (p less than 0.006) from the opposite changes observed with HCTZ. Clinically relevant decreases from baseline in supine and standing blood pressures at 24 hours after administration did not significantly differ between the 2 agents. The incidence and severity of side effects were similar for both drugs. Three patients receiving doxazosin and 6 receiving HCTZ were withdrawn due to drug-related clinical side effects including 2 patients receiving HCTZ who were withdrawn because of laboratory test abnormalities. Eight HCTZ- and 1 doxazosin-treated patients developed hypokalemia and 6 HCTZ-treated patients developed hyperuricemia. These findings indicate that doxazosin and HCTZ provide comparable antihypertensive efficacy after 6 months of treatment using a once-daily regimen, but doxazosin produces a beneficial effect on the serum lipid profile as well as fewer biochemical aberrations.

Adrenergic alpha-Antagonists

Cardiovascular effects of verapamil in essential hypertension.

Calcium antagonists may affect the regulation of body sodium and adrenergic-dependent mechanisms. Exchangeable sodium, blood volume, plasma norepinephrine, renin, aldosterone, pressor responsiveness to norepinephrine, heart rate responses to isoproterenol, and lipid metabolism were studied in 15 patients with essential hypertension after 8 weeks of treatment with verapamil (348 +/- 68 (SD) mg/day). Supine blood pressure decreased from 153/103 +/- 19/12 mm Hg to 140/95 +/- 14/12 mm Hg (P less than 0.01). Exchangeable sodium, blood volume, plasma norepinephrine, renin and aldosterone, serum total cholesterol, the lipoprotein fractions, and apoprotein levels were unchanged. The norepinephrine pressor and the isoproterenol chronotropic doses tended to increase, whereas the dose-response curve of blood pressure related to plasma norepinephrine was significantly displaced to the right (F = 5.34; P less than 0.05). The antihypertensive effect of verapamil is associated with a decreased cardiovascular pressor responsiveness to norepinephrine without changes in endogenous noradrenergic activity. Moreover, verapamil does not modify the sodium/fluid volume state, the activity of the renin-angiotensin aldosterone axis, or lipid metabolism.

Adult