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Biomedical subjects

J H Laragh

Publications and source records attributed to J H Laragh.

At least 145 records · Page 8Linked to original sources
PubMed1989

Assessment of the effects of alpha- and beta-blockade in hypertensive patients who smoke cigarettes.

A 24-week, crossover, comparison study was conducted to observe the effects of alpha-blockade with prazosin and beta-blockade with propranolol on blood pressure and plasma lipoprotein levels in 15 hypertensive cigarette smokers. Before treatment, mean sitting blood pressure was 140/100 mm Hg and rose to 147/105 mm Hg after the patients smoked two cigarettes. Treatment with prazosin and propranolol lowered sitting blood pressure to 127/89 mm Hg and 129/91 mm Hg, respectively (not significant), and did not alter the pressor response to smoking. The total cholesterol level at baseline was 207.3 +/- 11.0 mg/dl. This increased to 210.5 +/- 10.2 mg/dl with propranolol treatment and decreased to 201.0 +/- 11.1 mg/dl with prazosin treatment. The low-density lipoprotein cholesterol level was 132.5 +/- 8.1 mg/dl at baseline, 136.9 +/- 8.3 mg/dl with propranolol treatment, and 129.4 +/- 9.0 mg/dl with prazosin treatment (0.05 less than p less than 0.10 between-group comparison). The data indicated that whereas prazosin and propranolol are equally effective in controlling blood pressure in hypertensive cigarette smokers, effects on plasma lipoproteins also may need to be considered when selecting a first-step antihypertensive agent in this coronary-prone population.

Adult↗
PubMed1989

Relationship of atrial natriuretic factor to left ventricular volume and mass.

Although atrial natriuretic factor is primarily of atrial origin, recent observations indicate that the hormone is also synthesized by hypertrophied left ventricular myocardium. To assess the separate influences of left ventricular and left atrial dilatation and left ventricular hypertrophy on human atrial natriuretic factor levels, left atrial dimension and volume and left ventricular dimension and mass were compared in 49 normal subjects, in 33 patients with chronic aortic regurgitation, and in 15 patients with chronic mitral regurgitation. When compared with normal subjects, patients with chronic aortic and mitral regurgitation had similarly dilated and hypertrophied left ventricles (p less than 0.0005), while only mitral regurgitation patients had significantly enlarged (p less than 0.0005) mean left atrial dimension and volume. Likewise, plasma atrial natriuretic factor was elevated among patients with mitral regurgitation (60.3 +/- 47.0 fmol/ml) but was normal in patients with aortic regurgitation (19.0 +/- 11.0 fmol/ml versus 12.4 +/- 5.2 fmol/ml in normals; both p less than 0.0005 versus mitral regurgitation). Among all 97 subjects, atrial natriuretic factor levels correlated more closely with left atrial dimension and volume (r = 0.62 and 0.64, p less than 0.0005) than with left ventricular dimension (r = 0.44, p less than 0.0005) or mass (r = 0.40, p less than 0.0005). In addition, multivariate analysis indicated that left atrial volume bore a stronger independent relationship to plasma atrial natriuretic factor levels than either age or left ventricular variables.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Insufficiency↗
PubMed1989

Atrial natriuretic factor in normal and hypertensive pregnancy.

Atrial natriuretic factor may play a role in the regulation of blood pressure, renal function, and volume homeostasis in normal and pathologic states. Atrial natriuretic factor and plasma renin activity were measured by radioimmunoassay in pregnant women with normal blood pressure (n = 29), chronic hypertension (n = 17), and preeclampsia (n = 18) during the first, second, and third trimesters and in the postpartum period. Serial data were obtained in 11 patients. Nonpregnant age-matched women were used as controls (n = 14). In normal gestation and in chronic hypertension, atrial natriuretic factor levels were in the same range as that in the control group. Mean atrial natriuretic factor was significantly higher in the antepartum and postpartum periods in severe preeclampsia. There was an inverse relationship between atrial natriuretic factor and plasma renin activity in pregnancies complicated by chronic hypertension or preeclampsia. Although fluctuations in atrial natriuretic factor levels did not predict preeclampsia, atrial natriuretic factor did correlate with the severity of the disease.

Atrial Natriuretic Factor↗
PubMed1989

Plasma atrial natriuretic factor in essential hypertension: relation to cardiac size, function and systemic hemodynamics.

To evaluate determinants of elevated plasma atrial natriuretic factor levels in patients with hypertension, immunoreactive plasma atrial natriuretic factor in 54 normal subjects and 40 untreated hypertensive patients was compared with echocardiographic measurements of cardiac size, function and systemic hemodynamics. In normal subjects, plasma atrial natriuretic factor was related to age, systolic blood pressure and left atrial and ventricular chamber sizes, but only age and ventricular size were independent predictors. In untreated hypertensive patients, atrial natriuretic factor was directly related to age, atrial size, systolic pressure, peripheral resistance and ventricular systolic performance; age, atrial size and peripheral resistance were independent predictors. Eight patients with elevated atrial natriuretic factor values (greater than 25 fmol/ml) were significantly (p less than 0.01) older and had greater atrial and ventricular size and higher systolic pressure and function than normal subjects or patients with normal natriuretic factor levels. Plasma atrial natriuretic factor was inversely related to peak diastolic filling rate in normal subjects (r = -0.59; p less than 0.001), whereas it was positively related to the proportional contribution of atrial systole to left ventricular filling in hypertensive patients (r = 0.77; p less than 0.001). These findings suggest that in normal subjects, impairment of ventricular relaxation with age may contribute to atrial natriuretic factor secretion by increasing left atrial afterload; the correlation with left ventricular size may reflect physiologic fluctuations in plasma volume. In patients with uncomplicated hypertension, left atrial enlargement and consequent stronger atrial contraction contributed to increased atrial natriuretic factor release, whereas no independent relation existed with left ventricular hypertrophy or systolic function. Because ventricular relaxation was normal and ventricular size and systolic performance were increased in hypertensive patients with high atrial natriuretic factor levels, the observed increase in left atrial size and atrial contribution to ventricular filling might reflect a primary increase in venous return in this subset of hypertensive patients.

Adult↗
PubMed1989

Increased plasma atrial natriuretic factor and reduced plasma renin in patients with poorly controlled diabetes mellitus.

1. To investigate atrial natriuretic factor (ANF) and its relationship to the renin system in diabetes, we measured plasma immunoreactive ANF and plasma renin activity (PRA) in 27 non-ketotic diabetic patients without evidence of cardiac or overt renal disease, and compared them with 26 age- and sex-matched normal subjects. 2. Diabetic patients were divided prospectively into poor (PGC, n = 14) or moderate (MGC, n = 13) glycaemic control depending on their concurrent plasma glycohaemoglobin (HbA1) levels (greater than 9% or less than 9%, respectively). Plasma ANF was elevated in PGC diabetic patients (15.7 +/- 1.8 fmol/ml, mean +/- SEM) compared with MGC diabetics (9.9 +/- 0.8 fmol/ml, P less than 0.001) and normal subjects (10.1 +/- 1.3 fmol/ml, P less than 0.05). 3. In contrast, PRA was lower in the PGC diabetic patients (1.3 +/- 0.3 pmol of angiotensin 1 h-1 ml-1) compared with the other groups (2.5 +/- 0.5 and 2.1 +/- 0.2 pmol of angiotensin I h-1 ml-1, P less than 0.05). Diabetic groups had proportionally more patients with high prorenin values (over 30 ng h-1 ml-1) than the normal group, but there was no difference between the diabetic groups. 4. Among the diabetic patients, ANF was directly related to HbA1 (r = 0.49, P less than 0.005) and urinary albumin excretion (r = 0.40, P less than 0.02), and was inversely related to PRA (r = 0.36, P less than 0.04) and plasma creatinine (r = -0.42, P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1989

The effects of calcium channel blockade on blood pressure and calcium metabolism.

To study the relation of calcium channel blockade to calcium metabolism, we measured serum ionized calcium (Ca++i0), magnesium (Mg), calcitonin (CT), and 1,25-dihydroxyvitamin D (1,25-D) before and after short-term therapy with verapamil 120 mg three times daily in essential hypertensive subjects on low (10 mEq) and high (200 mEq) dietary sodium intakes. Salt-sensitive compared with salt-insensitive subjects on high v low dietary salt intake had lower Ca++i0 (P less than .05), higher 1,25-D (P less than .02), and a greater hypertensive responsive to verapamil (% delta DBP = 17.7 v -8.2, P less than .05). The % delta DBP was related to the initial CT (r = 0.68, P less than .05), initial 1,25-D (R = -0.89, P less than .01), and to the drug-induced % delta 1,25 D (R = .60, P less than .05). Thus, lower initial calcium and calcitonin levels, higher initial levels of 1,25-D, and a greater drug-induced suppression of 1,25-D were associated with an enhanced hypotensive response to verapamil. Verapamil elevated Ca++i0 (2.46 +/- 0.04 to 2.53 +/- 0.04 2.00 mEq/L, P less than .05), and suppressed Mg (2.00 +/- 0.03 to 1.84 +/- 0.03 mEq/L, P less than .01) and 1,25-D levels (66.7 +/- 8.1 to 51.6 +/- 5.7 pg/mL, P less than .05). These results suggest interactive effects of sodium and calcium metabolism in essential hypertension, especially among salt-sensitive individuals. We conclude that alterations of calcium metabolism may underlie the sensitivity to verapamil therapy and may contribute to its hypotensive effects.

Blood Pressure↗
PubMed1989

Effects of calcitonin, calcitonin analogues, and calcitonin gene-related peptide on basal in vitro renin secretion.

We investigated the relation of calcitonin as a calcium-active hormone to its more recently described effects on peripheral vascular tone. Basal renal renin secretion in vitro in rat kidney slices was studied in the presence of salmon calcitonin (SCT, 4400 U/mg), amino acid substituted analogues of SCT, 16-alanine SCT (6200 U/mg) and 12,16,19 tri-alanine SCT (350 U/mg), and of rat calcitonin gene-related peptide (rCGRP). All calcitonin species at the same hypocalcemic activity (1 U/mL) modestly but significantly suppressed renin secretion from control levels (9.79 +/- 0.44 to 7.51 +/- 0.53, 7.70 +/- 0.72, and 7.78 +/- 0.90 Goldblatt units/g/h for SCT, 16-ala SCT, and tri-ala SCT, P less than .05 for all calcitonins v control), whereas rCGRP had no effect. Thus, on a molar basis, the renin suppressing effects of the various calcitonin species paralleled their bioassay-defined calcium sequestering activity, 16-ala SCT greater than SCT much greater than tri-ala SCT. Lower concentrations of SCT (10(-2) U/mL and 10(-4) U/mL, approximately 6 X 10(-10) and 6 X 10(-12) mol/L, respectively) had virtually identical effects. Moreover, verapamil (5 X 10(-6) mol/L) blocked the SCT-induced suppression of renin secretion (9.79 +/- 0.44 v 9.36 +/- 1.05 GU/g/h, P = NS). We conclude that the juxtaglomerular apparatus is a calcitonin-responsive system, in which calcitonin and its analogues act to suppress basal renin secretion in vitro. This effect seems to depend on and may be mediated by modulating cellular calcium uptake, and suggests a wider, calcium-related role for calcitonin than had previously been suspected.

Animals↗
PubMed1989

Hemodynamic responses to converting enzyme inhibition in patients with renal disease.

We studied the effects of lisinopril on mean arterial blood pressure (MAP), plasma renin activity (PRA), and renal hemodynamics in nine patients with chronic renal disease and hypertension, before, and after three months of therapy. Lisinopril normalized blood pressure in five of nine patients (responders) and did not in the remaining four (nonresponders). PRA rose after lisinopril (4.8 +/- 2.6 ng/mL/h to 25 +/- 15 ng/mL/h, P less than 0.05) in responders, but not in nonresponders (2.0 +/- 1.4 ng/mL/h to 3.4 +/- 2.9 ng/mL/h). Glomerular filtration rate remained stable in both groups (responders: 43 +/- 11 mL/min to 43 +/- 22 mL/min; nonresponders: 39 +/- 25 mL/min to 32 +/- 21 mL/min). In the responders renal hemodynamics remained stable after lisinopril (renal plasma flow: 223 +/- 80 mL/min to 216 +/- 91 mL/min; filtration fraction: .20 +/- .04 to .20 +/- .05; renal vascular resistance: 386 +/- 179 to 326 +/- 209 units). In the nonresponders, renal plasma flow decreased (228 +/- 141 mL/min to 162 +/- 117 mL/min, P less than 0.005), filtration fraction increased (.19 +/- .08 to .24 +/- .12, P less than 0.05), and renal vascular resistance increased (695 +/- 747 to 1265 +/- 1574 units, P less than 0.05) after chronic lisinopril therapy. We conclude (1) there is a heterogeneous response to lisinopril in patients with chronic renal disease and hypertension, (2) lisinopril monotherapy may result in effective blood pressure control without renal hemodynamic compromise, and (3) an increase in PRA following converting enzyme inhibition may identify those in whom the circulating renin angiotensin system is participating in systemic hypertension and intrarenal hemodynamic changes.

Adult↗
PubMed1989

Parity and perceived job stress elevate blood pressure in young normotensive working women.

This study examined the effect of physiological, behavioral, and psychosocial stressors on blood pressure measured in the work environment, home environment, and during sleep in a sample of 50 normotensive working women (average age = 30.2 +/- 7.4 years; average education = 4.3 years college). The results of separate stepwise regression analyses performed on the pressures measured in each environment showed that perceived job stress (P less than .05) and body fat or mass (P less than .05) significantly elevated systolic pressure in all situations, whereas home stress (P less than .05) and number of children (P less than .05) had the most marked effect on diastolic pressure variation over the day. These results suggest that the daily variation of systolic pressure in working women is related to stress on the job, and that diastolic pressure variation is associated with home stress, which may include stress arising from child care.

Adult↗
PubMed1989

Issues, goals, and guidelines in selecting first-line drug therapy for hypertension.

Modern antihypertensive therapy is enriched by an explosion in drug development that makes available increasingly specific agents whose effects have advanced our understanding of pressor mechanisms. This and other research into hypertensive mechanisms has defined the clinical, pharmacological, and endocrinologic heterogeneity of human hypertension. The sum of these developments is a greatly enhanced ability to identify curable and definable causes of hypertension and to pathophysiologically stratify the remaining cases of essential hypertension. Modern treatment can be much more specific than before. When long-term drug therapy is indicated, the regimen is more likely to achieve a primary goal for each patient, that is, the fewest possible drugs in the smallest amount and in lowest frequency. Two clinically quantifiable mechanisms for long-term arteriolar vasoconstriction can be identified within the spectrum of human hypertension. The first, renin-mediated vasoconstriction, is directly related to the plasma renin level. The second, sodium-volume-related vasoconstriction, is marked by a reciprocally subnormal renin level and involves abnormal sodium retention and calcium transport. A baseline renin-sodium profile can identify the pressure of one of these two forms of vasoconstriction and therefore is the key for the diagnosis of the two curable disorders that fully express one of the two pressor mechanisms--renovascular hypertension and primary aldosteronism. Renovascular hypertension, more common than once thought, is often cured by angioplasty. It is important to diagnose these curable forms before beginning long-term drug therapy. The renin-sodium profile, used in conjunction with serum potassium and creatinine measurements, is valuable not only in screening patients for curable forms, but also for stratifying the remainder according to the pathophysiological vasoconstrictor mechanism that underlies the hypertension. Converting enzyme inhibitors or beta-blockers are, by themselves, often effective in correcting the hypertension of high- or medium-renin patients, whereas calcium antagonists, diuretic agents, or alpha-blockers alone are most effective against the low-renin form of vasoconstriction. In the large midzone of renin values, if monotherapy fails, a rational basis for combined antirenin-antisodium volume therapies can be developed.

Antihypertensive Agents↗
PubMed1989

Tissue levels of active and total renin, angiotensinogen, human chorionic gonadotropin, estradiol, and progesterone in human placentas from different methods of delivery.

The components of the renin system are present in placental tissue, but their function in this tissue is not known. We investigated the relative distribution of the various components throughout the placenta to determine whether the distribution is consistent with a role for them in parturition or in stimulation or inhibition of placental hormone biosynthesis. Thus, active and total renin were measured in fetal membranes (chorion laeve and amnion) and in discoid placenta (chorion frondosum and chorion plate) of women who were delivered vaginally (n = 12) or by cesarean section with (n = 6) or without labor (n = 9). The interrelationships between active and total renin and angiotensinogen, progesterone, hCG, and estradiol concentrations were investigated. Labor had no significant effect on the concentration of active or total renin, angiotensinogen, hCG, or estradiol in any part of the placenta. Tissue progesterone concentrations were higher in placentas from women who underwent vaginal deliveries than in those who had cesarean sections with or without labor (P less than 0.02). The chorion laeve had 20 times more total renin per g than the discoid placenta and 3 times more than the amnion. In contrast the discoid placenta had 5 times more hCG per g and 3 times more progesterone per g than the fetal membranes. The concentration of estradiol was lower in amnion, while that of angiotensinogen was lower in the chorion frondosum than in all other regions. The tissue concentrations of active renin, prorenin, or total renin were not related to those of any of the other hormones. Altogether these data do not provide evidence of a role for the placental renin system in parturition or placental hormone biosynthesis.

Angiotensinogen↗
PubMed1989

Hydrochlorothiazide is not additive to verapamil in treating essential hypertension.

Calcium channel blockers, a newer class of antihypertensive medications, have gained considerable acceptance as monotherapeutic agents, particularly in low renin hypertension where diuretics are also most effective. To study whether thiazide diuretics exert an additional antihypertensive effect in the setting of calcium channel blockade, we gave verapamil hydrochloride (360 mg/d) or hydrochlorothiazide (25 mg/d) alone and in combination in an open study to 13 hypertensive patients with mild to moderate essential hypertension. Both verapamil and hydrochlorothiazide lowered blood pressure (170 +/- 17/109 +/- 6 mm Hg pretreatment to 150 +/- 25/95 +/- 8 mm Hg with verapamil; 170 +/- 5/109 +/- 2 mm Hg pretreatment to 164 +/- 25/103 +/- 10 mm Hg with hydrochlorothiazide), but addition of hydrochlorothiazide to verapamil resulted in no added benefit (150 +/- 25/95 +/- 8 mm Hg vs 150 +/- 20/95 +/- 6 mm Hg). Furthermore, while hydrochlorothiazide lowered serum potassium values (4.2 +/- 0.25 mmol/L to 3.7 +/- 0.35 mmol/L) and stimulated plasma renin activity (1.5 +/- 1.3 ng/mL/h) pretreatment to 3.3 +/- 2.7 ng/mL/h with verapamil), verapamil only modestly elevated renin activity (1.5 +/- 1.3 ng/mL/h pretreatment to 2.7 +/- 2.5 ng/mL/h with verapamil) and did not lower potassium values. Altogether, the data suggest that in essential hypertension, at least for verapamil, concurrent diuretic therapy may not be helpful or warranted.

Blood Pressure↗
PubMed1988

Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation.

11 patients with atheromatous renovascular hypertension had a history of multiple episodes of pulmonary oedema. 7 had stenosis of both renal arteries, 2 had stenosis of the artery to a solitary kidney, and 2 had unilateral stenosis with an intact contralateral kidney. Successful revascularisation (by angioplasty in 8, and surgery in 3) improved blood pressure and renal function, and virtually eliminated pulmonary oedema. In a second series of 55 consecutive patients with azotaemia and renovascular hypertension, pulmonary oedema occurred in 13 (23%). Blood pressure and renal function were not significant predictors of pulmonary oedema, but coronary heart disease and bilateral (vs unilateral) renal artery stenosis were. Bilateral renal artery stenosis may be a specific and treatable predisposing factor to pulmonary oedema in azotaemic hypertensive patients.

Acute Disease↗
PubMed1988

Relation of concentric left ventricular hypertrophy and extracardiac target organ damage to supranormal left ventricular performance in established essential hypertension.

Increased cardiac performance has been documented in patients with early systemic hypertension, but its prevalence and determinants in patients with uncomplicated sustained essential hypertension have not been characterized. Radionuclide cineangiography in 116 patients with uncomplicated essential hypertension showed that 12 of 116 (10%) had supranormal resting left ventricular (LV) ejection fraction (greater than 70%, above the highest value in normal subjects), while 104 patients had a normal resting ejection fraction (45 to 70%). Patients with a high resting ejection fraction had higher systolic and diastolic blood pressure compared with patients with normal resting ejection fraction (182 mm Hg vs 169, p less than 0.01, and 110 vs 103, p less than 0.05, respectively), markedly greater echocardiographic LV mass (136 vs 94 g/m2, p less than 0.01), smaller ventricular dimensions in systole (2.5 vs 3.1, p less than 0.01) and diastole (4.4 vs 4.9, p less than 0.05), and higher relative wall thickness (0.61 +/- 0.20 vs 0.39 +/- 0.98, p less than 0.001). Patients with supranormal resting ventricular performance had lower end-systolic wall stress than normal volunteers or patients with normal resting LV function (48 vs 64 vs 74 X 10(3) dynes/cm2, respectively). Patients with an elevated LV ejection fraction also had significantly more abnormal funduscopic examinations and greater proteinuria. Thus, a subset of essential hypertensive patients with moderately to severely elevated blood pressure developed marked concentric LV hypertrophy associated with subnormal end-systolic stress and supranormal LV performance.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗