There was no significant difference in serum DBH activity between normal subjects and individuals with hypertension in any age group. tfurthermore, there was no significant correlation of mean blood pressure with serum DBH activity with or without correction of DBH for age differences; Highly significant correlations of serum DBH activity were found in sibling-sibling pairs and in mean parent-child pairs.
High blood pressure and elevated plasma renin activity have been normalized with a unilateral revascularization in the elder patient, and with the treatment of propranolol in the younger one.
Further investigation of a family with normaldosteronemic hyperpotassemia and low-reninhypertension showed seven members from three generations, who ranged in age from 4 to 56 years, to be affected.
Hypertension and hyperpotassemia that were accompanied by normal plasma aldosterone and low renin levels and were responsive to chlorothiazide administration were found in a 29-year-old patient and two decades later in his 21-year-old son.
An investigation was made of daytime plasma prolactin levels in three groups of women aged 50 to 64 years: (1) 139 women with a family history of breast cancer; (2) 50 women on Rauwolfia treatment for hypertension, and (3) 90 women of a control group.
Thus, subnormal kallikrein-kininogen-kinin concentrations could be the cause of reduced vasodilating influence leading to both clinical and experimental hypertension.
Calf muscle haemodynamics and the renin-angiotensin-aldosterone system in normotensive subjects with a familial predisposition to hypertension: changes during increased salt intake.
Blood pressure, plethysmographically determined muscle blood flow in the calf at rest and during maximal dilatation, plasma renin activity, angiotensin II and plasma and urinary aldosterone were determined in normotensive men with a positive family history of hypertension (n = 17) and in an age- and weight-matched control group (n = 15) during usual sodium intake and after four weeks of increased salt intake.
Comparison of the kidney function of normotensive subjects likely to develop hypertension with that of matched controls resistant to hypertension showed, in the former, a higher glomerular filtration rate (GFR), greater tubular reabsorption, larger 24-h urinary output, larger fraction of cardiac output to the kidney, and lower plasma renin activity.
The rate of sodium-lithium countertransport (SLC flux) across red cell membranes has been reported to be elevated in hypertensive persons and their relatives as compared to normotensive individuals without family histories of hypertension.
Changes in blood pressure, pulse rate, and plasma catecholamines, renin activity, cortisol, and calcium were studied in 16 normotensive subjects (eight with a family history of hypertension) for 5 hours following ingestion of alcohol-free and alcohol-loaded beer.
In subjects with a family history of hypertension, the renal vascular response to diltiazem was enhanced (p less than 0.01) despite similar values of plasma renin activity, angiotensin II concentration, and sodium excretion.
After changing to the high sodium diet, body weight, exchangeable sodium, and sodium clearance increased and renin decreased significantly (P less than 0.05) and to a similar extent in the two groups; systolic blood pressure increased only in subjects with a family history of hypertension.
Elastin synthesis was studied in blood vessels from newborn calves with severe pulmonary hypertension induced by alveolar hypoxia in order to investigate the cellular stimuli that elicit changes in pulmonary arterial connective tissue production.
In a preliminary report, a study of the TaqI polymorphism of the human renin gene did not reveal a significant difference between hypertensive patients with a family history of hypertension and normotensive controls.
Body sodium, the cardiovascular pressor reactivity to infused noradrenaline or angiotensin II, plasma levels of noradrenaline, adrenalin, renin, angiotensin II, aldosterone and atrial natriuretic peptide were measured on a low or high sodium diet in 10 normotensive young subjects without and 13 normotensive subjects with familial predisposition to hypertension.
This newly identified form of endocrine hypertension is strongly linked to excessive body weight but is associated with alterations in the renin-aldosterone and sympathetic nervous systems that are distinct from those encountered in obesity-related hypertension in the general population.
These results suggested that schoolchildren with a family history of hypertension might have an enhanced renin-aldosterone (R-A) system, resulting in elevation of blood pressure.
Body sodium, the cardiovascular pressor reactivity to infused noradrenaline or angiotensin II, plasma levels of noradrenaline, adrenalin, renin, angiotensin II, aldosterone and atrial natriuretic peptide were measured on a low or high sodium diet in 10 normotensive young subjects without and 13 normotensive subjects with familial predisposition to hypertension.
The effects of parental history of hypertension and menstrual phase on systolic and diastolic blood pressure (SBP, DBP) and heart rate (HR) responses to two frustrating cognitive tasks were examined in 47 normotensive, young adult women.
The family at increased risk for future coronary heart disease is the family with a member who has 1) had one or more myocardial infarctions before age 55 years; 2) has levels of LDL cholesterol greater than 75th percentile for age; 3) has excessively low levels of HDL2 cholesterol; 4) has hypertension or has had a stroke, or both; 5) has excessive weight at any age and excessive weight gain during adulthood, or 6) smokes in the household.
A higher frequency of the genotypes for high RBC Na in pedigrees when the proband was hypertensive than normotensive provided evidence that this major locus increases susceptibility to hypertension.
Although we found no genetic linkage in this set of study subjects, the characterization of the restriction fragment length polymorphisms for the renin gene may be useful in future studies of other selected pedigrees for the presence of one or more of these to be a genetic marker in hypertension.
Blood pressure values were lower in the former and, conversely, Counter "+" hypertensives showed a higher prevalence of moderate or severe hypertension (65.5% vs. 32.6%; P = 0.0059) and higher values of stimulated plasma renin activity (1.63 +/- 0.52 vs. 0.81 +/- 0.15; P = 0.0443).