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Biomedical subjects

S Julius

Publications and source records attributed to S Julius.

At least 127 records · Page 7Linked to original sources
PubMed1990

The Tecumseh Blood Pressure Study. Normative data on blood pressure self-determination.

In Tecumseh, Mich, we obtained blood pressure (BP) self-determination data in 608 healthy adults (327 men, 281 women; average age, 32.6 +/- 3.5 years) representing a wide range of educational backgrounds. The average (+/- SD) home BP (average 12.7 readings over 1 week) was 120.7/74.8 +/- 10.4/8.6 mm Hg for men and 110.9/69.9 +/- 10.1/7.7 for women. One hundred thirty-three subjects remeasured their home BP 1 year later and a strong correlation between the two readings was obtained (r = .70). Large-scale BP self-determination is feasible. Based on the BP distribution in Tecumseh, the upper limit of normalcy for home BP (2 SDs above the mean) is 142/92 mm Hg for men and 131/85 mm Hg for women.

Adult↗
PubMed1989

Increased beta-adrenergic tone enhances arterial compliance in hyperkinetic borderline hypertension.

Arterial compliance, assessed by the stroke volume-pulse pressure relationship, was measured in 32 patients with a high cardiac output together with borderline hypertension and 26 control subjects with normokinetic borderline hypertension. Measurements were obtained in the supine position both before and after 0.2 mg/kg intravenous propranolol. Baseline arterial compliance was significantly greater in the hyperkinetic group (P less than 0.01). The inter-group difference was no longer significant after the administration of propranolol, since compliance tended to increase in the normokinetic group and decrease in the hyperkinetic group. Therefore, disparities in vascular beta-adrenergic tone between hyperkinetic and normokinetic borderline hypertensive patients probably contribute to group differences in arterial compliance.

Arteries↗
PubMed1989

Behaviour and hypertension: a pathophysiological puzzle.

Patients with borderline hypertension typically show enhanced sympathetic and decreased parasympathetic tone, characteristic personality traits (submissiveness, hostility) and hyperreactivity to mental stress. It has been proposed that the hypertensive personality results in a persistent 'defence reaction', enhancing sympathetic outflow from the central nervous system and reactivity to stress. But evidence from pharmacological intervention trials suggests that blood pressure reactivity is controlled independently of average baseline blood pressure. A study comparing the effects of the centrally-acting alpha 2-agonist, clonidine, and the selective beta 1-blocker, atenolol, demonstrated that both drugs had a comparable antihypertensive action on baseline blood pressure. However, neither agent affected stress responses to mental arithmetic, submaximal isometric handgrip exercise or cold pressor testing. We conclude that studies of stress reactivity, while of interest to students of circulatory control, are unlikely to yield insights into the causes of human hypertension.

Arousal↗
PubMed1989

Neurogenic pressor episodes fail to cause hypertension, but do induce cardiac hypertrophy.

Repeated neurogenic pressor episodes by hindquarter compression were elicited in nine experimental dogs. Conscious dogs underwent 6 hours of compression every day over a period of 9 weeks. The average mean blood pressure increase during the compression periods was 25 mm Hg, but after decompression the blood pressure promptly returned to baseline values. This blood pressure response was constant and did not change over the 9-week period. The blood pressure increase was associated with a significant increase of plasma norepinephrine values. After validity of the model was established, echocardiographic measurements were performed at baseline and after 3, 6, and 9 weeks of compression in six experimental and six time-control dogs. Concentric left ventricular hypertrophy was already detectable at 3 weeks, and at the ninth week, the left ventricular mass was 28% above the baseline value. The left ventricular mass in time-control dogs remained unchanged over the same period of time. The time-left ventricular mass curves in experimental dogs were significantly different (by profile analysis), had different means (p less than 0.005), were not parallel (p less than 0.0006), and the overall group difference was highly significant (p less than 0.00001). Since left ventricular hypertrophy, a poor prognostic sign in clinical situations, can evolve before established hypertension, present therapeutic recommendations based on permanently elevated blood pressure values may not be entirely justified.

Animals↗
PubMed1989

Brain and the regulation of blood pressure: a hemodynamic perspective.

The central nervous system subserves the homeostasis of the circulation and is organized as a negative feedback system. The following properties of such a feedback system are of interest: a) the setting; b) the range of the regulation; and c) the nature of the feedback (regulated) variable. In this review we show that in hypertension blood pressure is set at a higher level, but regulation of blood pressure in hypertension is normal. The central nervous system is involved in maintaining a higher set point in early human hypertension as well as in many forms of experimental hypertension. Results from trials of antihypertensive drugs suggest that setting of the baseline level of blood pressure and regulation of blood pressure variability are independent properties and are probably regulated by different areas of the central nervous system. It is, therefore, unlikely that research on blood pressure "reactivity" will elucidate the pathophysiology of the central resetting of baseline blood pressure level in hypertension. We present evidence that in subserving the circulation, the central nervous system regulates and senses blood pressure and not flow. Pathophysiologic implications of this concept are discussed particularly in regards to the apparent decrease of sympathetic tone during the evolution of hypertension.

Animals↗
PubMed1989

Practical utility of blood pressure readings obtained by self-determination.

We have found self-determination of blood pressure to be a valuable technique in the evaluation and management of our patients. It is sensitive and the patients can detect minor changes in their blood pressures. The method has yielded reproducible results, with identical readings being obtained 6 weeks apart. Recently, we extended the application of self-determination to a larger group of young adults (n = 534) representing a wide range of employment and educational backgrounds. The average time spent teaching them was 20 min. A reading within 5 mmHg of the observer's was achieved in three to 10 attempts (mean 3.7 +/- 1.1) and there was a good correlation between the observer and the subject for both systolic (r = 0.988) and diastolic (r = 0.976) pressures. The average home blood pressure was 120.7 +/- 9.1/75.7 +/- 7 mmHg for men and 111.6 +/- 11/70.1 +/- 8 mmHg for women. We conclude that blood pressure self-determination is sensitive, reproducible and easy to learn.

Adult↗
PubMed1989

Angiotensin converting enzyme inhibitors and the progress of antihypertensive therapy.

Drug treatment of hypertension reduces morbidity and mortality most effectively in moderate to severe cases. However, most patients have only mild hypertension, for which traditional drug treatment is not consistently successful. Angiotensin converting enzyme (ACE) inhibitors provide superior control of mild hypertension. They have a haemodynamically favourable mechanism of action, are well tolerated and can produce a predictable response within a narrow and convenient dose range. Further, ACE inhibitors are lipidneutral, and they positively affect some of the mechanisms conducive to the development of atherosclerosis. Further research in this area is warranted. The ACE inhibitors may also help prevent end-organ damage in hypertensive patients who also have diabetes, kidney disease, left ventricular hypertrophy or a combination of these disorders. The case for renoprotection in diabetic hypertensives is strong enough to recommend preferential use of ACE inhibitors for these patients. The positive effects shown in left ventricular hypertrophy may also be produced by other modern antihypertensive agents, while the advantages of ACE inhibitors in essential hypertension with renal damage remain largely conjectural. There have been encouraging clinical results, but ongoing larger trials may provide a more definitive answer.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Quality of life during antihypertensive treatment. Refining its measurement to individualize drug selection.

Three questions relating to assessment of quality of life during antihypertensive therapy are discussed here. 1. Can the quality of life be measured? The two approaches thus far explored have used external parameters, such as counting days of work lost or changes in sexual function, and subjective assessment by patients, through completion of a questionnaire. The latter presents problems of reliability and sensitivity of the instrument as well as comparability of results across various studies. 2. Should quality of life be measured? If morbidity due to hypertension is reduced but quality of life is also reduced without an associated improvement in longevity, it is important to know exactly how and to what extent quality of life is impaired. Also, measurement of quality of life should make possible improved compliance with antihypertensive therapy. 3. How can quality of life be measured? Results of the studies evaluating quality of life associated with antihypertensive therapy leave much to be desired. A study protocol is proposed that would use the voluntary drop-out rate as the point of comparison. Research would then unravel the behavioral factors specifically affected by a given treatment. Through such studies, the effects of drugs on quality of life could become a criterion in individualization of treatment.

Antihypertensive Agents↗
PubMed1988

Transition from high cardiac output to elevated vascular resistance in hypertension.

The early phase of hypertension (borderline hypertension) is characterized by a hyperkinetic circulation caused by excessive sympathetic drive and decreased parasympathetic inhibition to the heart. In later phases the cardiac output becomes normal, but the hypertension is still neurogenic, as demonstrated by the fact that continued pharmacologic parasympathetic, beta- and alpha-adrenergic inhibition normalizes the blood pressure. In both of these phases of the process, plasma norepinephrine values are elevated. These patients also show characteristic behavioral patterns; they are outward oriented, submissive, but experience unexpressed anger and frequently harbor hostile feelings. In late phases of hypertension the cardiac output is normal and the total peripheral resistance is elevated. This hemodynamic transition can be explained by a secondary response to elevated blood pressure. The heart becomes less responsive as a result of altered receptor responsiveness and decreased cardiac compliance, whereas the responsiveness of arterioles increases because of vascular hypertrophy, which leads to changes in the wall-to-lumen ratio. However, one observation eludes explanation: the absence of plasma norepinephrine elevation in later phases of hypertension. We propose a new conceptual framework to explain the disappearance of elevated plasma norepinephrine in the course of hypertension. The concept is based on a wide range of observations with the use of various receptor-blocking agents during neurogenic pressor responses. Invariably, the blood pressure response is preserved, but the hemodynamic pattern can be altered from a high cardiac output to high total peripheral resistance or vice versa.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1988

Interaction between renin and the autonomic nervous system in hypertension.

The abnormal distribution of plasma renin values described in established essential hypertension are also found in patients with very early, borderline hypertension. In established hypertension, renin values have been used to draw inferences about the pathophysiology of blood pressure elevation. Within this concept, the low-renin state is considered a volume-dependent (volume expanded) form of hypertension. The high-renin state is viewed as high-resistance hypertension caused by a renin-dependent vasoconstriction. However, the pathophysiology of high- and low-renin borderline hypertension does not follow the prediction from the volume-vasoconstriction theory. The high-renin state is often associated with an increase in cardiac output and normal values of vascular resistance. Even when the cardiac output is normal and the total peripheral resistance is elevated in high renin, the vasoconstriction is not renin-angiotensin dependent. The high-renin borderline and mild hypertension is a state of generalized, increased, sympathetic drive to the heart, blood vessels, and kidneys. After the influence of the autonomic nervous system is removed by pharmacologic blockade, blood pressure in patients with high-renin values becomes normal. To the contrary, pharmacologic antagonization of angiotensin II with a converting enzyme inhibitor does not lead to normal blood pressure values in patients with high-renin. Patients with borderline hypertension with low renin have normal plasma and blood volume values. However, because of decreased compliance of the peripheral capacitance space, the blood volume is shifted from the peripheral to the central (cardiopulmonary) portion of the circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

University of California, Davis, conference: Mild hypertension.

Prevalence of "higher than normal" blood pressures in a community is inversely related to the magnitude of the elevation; the milder grades of elevation are far more prevalent. A multifactorially inherited tendency to develop hypertension is modulated by multiple environmental influences. Autonomic nervous and behavioral factors plausibly appear to contribute to the initiating mechanisms of hypertension; the associated hemodynamic changes and the resulting cardiovascular structural changes interact to perpetuate the process. The complex interaction of hypertension and atherosclerosis is further complicated by direct as well as secondary effects of antihypertensive drugs on atherogenesis. Attributable cardiovascular risk is generally proportional to the degree of hypertension across the entire range of elevated blood pressure; this kind of relationship holds also for normal versus subnormal blood pressure values. Pharmacologic lowering of blood pressure, however, does not confer proportional benefit. Thus, such lowering of blood pressure to normotensive levels does not reduce the risk level to that in the normotensive population. Therapeutic outcome is influenced by the interaction of blood pressure lowering, type of antihypertensive agents used, existing risk factors, and target organ damage. Benefits of lowering blood pressure in established mild hypertension (diastolic blood pressure greater than 95 mm Hg) are confirmed. Drug treatment of patients with lower diastolic blood pressure or with isolated elevations of systolic blood pressures continues to be controversial as does the choice of initial therapeutic agent(s). The large-scale experience of clinical trials encompassing the long-term risks and benefits of the drug treatment of mild hypertension is limited to the use of diuretics and adrenergic beta blockers. A variety of new and promising therapeutic agents for use as alternate choices for initial therapy needs to undergo comparative evaluation.

Adolescent↗
PubMed1988

Effects of ketanserin on blood pressure and platelet aggregation in elderly men with mild hypertension.

Thirteen men, age 60 +/- 2 years (mean +/- SEM) with mild hypertension, 151 +/- 4/95 +/- 3 mm Hg, completed a randomized, double-blind, placebo-controlled crossover trial of ketanserin therapy. In comparison to placebo, ketanserin treatment at 40 mg bid for 6 weeks lowered systolic and diastolic blood pressure, 148 +/- 4/92 +/- 3 vs. 140 +/- 6/86 +/- 3 mm Hg, P = 0.19/0.02. The rate of platelet aggregation in response to ADP and epinephrine was unchanged while the response to serotonin was greatly diminished. Neither the systemic pressor response nor the pupillary mydriatic response to phenylephrine was significantly altered. Plasma norepinephrine concentration declined significantly. Ketanserin reduced blood pressure, particularly the diastolic component, in elderly men with mild hypertension. While antagonism of serotonin's effects on platelet aggregation was evident, blockade of alpha 1-receptor-mediated events was not apparent. The results suggest that during chronic therapy the antihypertensive effects of ketanserin were mediated by serotonergic blockade and a possible lytic effect on sympathetic drive. The dual effects of ketanserin on blood pressure and platelet aggregation may be beneficial in reducing cardiovascular complications in hypertensive patients.

Adult↗
PubMed1988

The therapeutic dilemma of hypertension in the elderly.

There are good reasons to treat hypertension in the elderly. Elevated blood pressure at any age increases morbidity and mortality from cardiovascular disease. Treatment trials suggest that antihypertensive treatment in the elderly decreases strokes, may improve the cardiovascular morbidity, but does not prolong life. Consequently, elevated blood pressure in people over 65 years of age should be treated, but there is no justification for an overly aggressive approach. Knowledge of side effects of various drugs and appreciation of a patient's specific features permit individual 'tailoring' of the treatment and optimise the outcome. No present-day antihypertensive drugs are specific for the elderly. The drive to combat cardiovascular morbidity and mortality in the elderly continues. New drugs are under development and promise to further improve results.

Aged↗
PubMed1988

Sympathetic hyperactivity in early stages of hypertension: the Ann Arbor data set.

Patients with borderline hypertension frequently have a hyperkinetic circulation that is neurogenic and can be normalized with autonomic blockade of the heart. The abnormality is of central nervous system origin and due to increased sympathetic stimulation and decreased vagal inhibition of the heart. A subset of patients characterized by high plasma renin and norepinephrine values clearly has a neurogenic hypertension since their blood pressure becomes normal after cardiac blockade and vascular alpha-adrenergic blockade. Since many patients with borderline hypertension have a high cardiac output, and the majority of patients with more advanced hypertension have increased vascular resistance, two questions arise. Is the "hyperkinetic state" a special condition unrelated to established hypertension or is there, in the course of hypertension, a transition from "high output" to "high resistance" state? The literature strongly suggests that patients with hyperkinetic borderline hypertension later proceed to develop the established high resistance form of hypertension. The most likely mechanism for this transition is a change in cardiac and vascular responsiveness due to prolonged excess sympathetic stimulation combined with structural pressure-induced changes in these organs. This analysis of the events in the course of hypertension is of necessity based on an arbitrary definition of the hyperkinetic state usually set at a cardiac index at least two standard deviations above the normal mean. A bivariate analysis of our data (268 normotensive and 186 patients with borderline hypertension) suggests that there indeed are two different populations in this data set. Based on this commingling analysis, the occurrence of a hyperkinetic state was five-fold as frequent in patients with borderline hypertension than in the normotensive population.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1988

Amlodipine in hypertension: an overview of the clinical dossier.

The database on amlodipine, a calcium antagonist of the 1,4-dihydropyridine class, was obtained from clinical trials in the United States, Canada, and Europe. The clinical dossier describing the efficacy and safety of once-daily amlodipine in the treatment of hypertension is extensive, well organized, and logically designed. It shows that amlodipine is an effective antihypertensive drug, providing smooth 24-h blood pressure control without orthostatic hypotension, and that it is well tolerated as monotherapy and in combination with other antihypertensive drugs. A total of 18 clinical studies were reviewed; 1,091 patients received amlodipine whereas 805 received either placebo or another drug for comparison. The common entry criteria include a supine and standing diastolic blood pressure in the range 95-114 mg Hg. Blood pressure measurements were made 24 h after the last dose of amlodipine in all studies. Amlodipine is clearly superior to placebo and induces a clinically significant reduction in blood pressure (mean reductions 23/13 mm Hg supine, 24/12 upright in one representative study) with similar heart rates in the supine and standing positions. Blood pressure control shows a smooth profile over 24 h with once-daily dosing, and there is no tolerance with long-term administration of the drug. The useful clinical dose is in the range of 5-10 mg, which is well tolerated in comparison with clinical doses of atenolol, hydrochlorothiazide, or verapamil. Amlodipine can be used as monotherapy in a large proportion of patients but may also be combined with a beta-blocker, diuretic, or angiotensin converting enzyme inhibitor. Based on these observations, amlodipine may prove to be an attractive addition to our antihypertensive armamentarium.

Amlodipine↗
PubMed1987

Role of cardiopulmonary mechanoreceptors in the postural regulation of renin.

To change the stretch on cardiopulmonary mechanoreceptors, large shifts of blood in the capacity space were elicited by tilting and by exerting positive lower body pressure in the tilted position. Twelve volunteers underwent invasive hemodynamic studies and in 10 other subjects cardiac size was determined by radionuclide cardiography. In all 22 subjects tilting caused the expected increase of renin, which was abolished by lower body compression. Decompression caused renin to increase again. Right atrial pressure in invasive studies and end-systolic and end-diastolic counts in noninvasive studies showed a significant and strong negative correlation with renin and norepinephrine levels. Thus, the degree of stretch of the cardiopulmonary mechanoreceptors is a major determinant of reflex regulation of renin release in humans.

Adolescent↗