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Biomedical subjects

D H Streeten

Publications and source records attributed to D H Streeten.

At least 19 recordsLinked to original sources
PubMed1992

Secondary hypertension. An overview of its causes and management.

Primarily hypervolaemic, high output forms of hypertension, with features indicating or strongly suggesting fluid overload as the cause of elevated cardiac output, resulting from renal disease with reduced glomerular filtration rate causing sodium retention, renal tubular causes of sodium retention, greatly excessive sodium intake and low renin hypertension, can be treated by reduction of sodium intake and potentiation of its excretion by diuretic therapy, removal of the cause (e.g. aldosteronoma), and calcium antagonists. Excessive vasoconstriction resulting from noradrenaline (norepinephrine) in neurogenic hypertension, phaeochromocytoma, orthostatic hypertension and alpha-adrenergic drug administration; angiotensin excess due to renal ischaemia brought about by aortic coarctation, renal arterial and arteriolar stenosis, intraluminal obstruction, external renal compression, renin-producing tumours, intrinsic kidney diseases and excessive renin substrate; and vascular structural disorders such as atherosclerosis, arteriolitides and fibrosis with or without calcification of major arteries may also induce hypertension. Secondary hypertension of uncertain mechanism may occur in hyperparathyroidism, hyper-or hypothyroidism, or acromegaly. All are best treated by appropriate correction of the endocrine excess or deficiency. It may also occur in pregnancy, where the mechanism may involve prostaglandin-thromboxane imbalance or calcium deficiency; calcium deficiency with some evidence of benefit from calcium supplements; and the recumbent hypertension paradoxically associated with autonomic failure. Excellent responses to specific correction of the underlying cause or pathogenetic mechanism is usual in young individuals but less frequent in older patients.

Cardiac Output, High↗
PubMed1992

Persistent hypotension associated with hypermedullipinemia: a new syndrome.

A new syndrome is described in a patient with advanced renal insufficiency. This consists of severe and persistent hypotension causing weakness but associated with a clear mental status. Also present is evidence for decreased vascular reactivity. The hypotension was not orthostatic. The hypotension was associated with a circulating vasodepressor substance having the characteristics of medullipin 1. The medullipin appears to have been derived from the remaining right kidney. Hypotension existed despite the presence of major prohypertensive mechanisms, including an endstage kidney, hyperreninemia and hyperaldosteronemia. It is likely that hypotension due to hypermedullipinemia is an entity occurring in the human being.

Adult↗
PubMed1992

Delayed orthostatic intolerance.

In seven patients who presented with lightheadedness, fatigue, "weakness," and sometimes syncope, blood pressure was found not to fall after standing for 3 to 4 minutes but to fall severely, frequently with syncope or presyncopal symptoms, after 13 to 30 minutes when measured every minute with an automatic device. This delayed orthostatic hypotension could be corrected with inflation of a pressure suit to 45 mm Hg. Its mechanism was further investigated with measurements of plasma catecholamines, plasma cortisol and aldosterone responses to corticotropin, and the effects of norepinephrine infusions on blood pressure and venous contractility. There was normal or excessive orthostatic norepinephrine release in all patients, evidence of impaired venous innervation in the legs in some, and various disorders in the other patients. Since therapeutic improvement in the orthostatic hypotension greatly reduced the symptoms, we concluded that orthostatic hypotension occurring after more than 10 minutes of standing is a potentially debilitating and often correctable disorder.

Adrenal Cortex Function Tests↗
PubMed1991

Atrial natriuretic hormone. Predictive of the hypokalemic response to thiazide therapy in essential hypertension.

Thiazide diuretics cause hypokalemia in some, but not all patients. Adding a second diuretic with a different mechanism of action greatly increases the chance of inducing hypokalemia. Suggestive causative factors include hyperaldosteronism, acid-base status, and the degree of natriuresis. Atrial natriuretic hormone (ANH), a circulating peptide secreted primarily by the heart in response to changes in intravascular volume, induces a natriuresis by a mechanism distinct from the thiazides. It was previously shown that furosemide and thiazide diuretics can increase plasma ANH levels in some patients, but reduce ANH levels in others. This phenomenon was investigated in 26 patients with uncomplicated essential hypertension to observe the relationships between ANH and changes in serum potassium (K+) in response to chronic hydrochlorothiazide therapy (HCTZ, 50 mg/day for 1 month). Regression analysis demonstrated significant correlations between K+ level after HCTZ and initial ANH (r = 0.68, P less than .001), change in K+ level and initial ANH (r = 0.40, P less than .05), K+ level after HCTZ and change in ANH (r = -0.64, P less than .001), and change in K+ levels and change in ANH levels (r = -0.38, P less than .05). By multivariate analysis, initial ANH level, but not the plasma aldosterone level, was significantly (P less than .05) related to the change in K+ after HCTZ. These results suggest that initial plasma ANH levels are a marker predictive for diuretic-induced hypokalemia.

Adult↗
PubMed1990

Effect of age on response of secondary hypertension to specific treatment.

There is substantial evidence to show that correction of the causes of secondary forms of hypertension usually but certainly not always restores blood pressure to normal. We have analyzed the effect of age on the response of the blood pressure to the removal of the cause of hypertension in groups of patients with primary aldosteronism, renovascular hypertension, Cushing's syndrome and hypothyroid hypertension. In the patients studied, surgical or medical elimination of the mechanism responsible for the hypertension when the patients were below the age of 40 reduced diastolic blood pressure 1 to 2 years later to below 90 mm Hg in 24 of 25 patients. In the patients who were treated when they were over 40 years of age, blood pressure remained above 90 mm Hg after corrective treatment in 23 of 61 individuals (38%). In the 4 groups studied there was a significant correlation between age and post-treatment systolic and/or diastolic blood pressure. The findings indicate the importance of correcting secondary hypertension at an early age.

Adult↗
PubMed1990

Pathogenesis of hyperadrenergic orthostatic hypotension. Evidence of disordered venous innervation exclusively in the lower limbs.

The pathogenesis of hyperadrenergic orthostatic hypotension was studied in eight patients. Correction of the abnormal orthostatic changes by an inflated pressure suit (MAST) confirmed previous evidence of excessive gravitational pooling of blood in the leg veins. Intravenous L-norepinephrine infusion raised diastolic blood pressure in the same relationship to the infusion-induced increments in plasma norepinephrine concentrations as in normal subjects, indicating normal arteriolar responses. Contractile responses of the veins to infused L-norepinephrine were measured with a linear variable differential transformer (LVDT). The venous responses of hand veins in the patients fell within the 95% confidence limits of the responses of normal hand veins, as did the responses of foot veins in the seven normal subjects. However, foot veins of the patients with hyperadrenergic orthostatic hypotension, and both hand and foot veins of patients with "diffuse" autonomic failure, were supersensitive to norepinephrine, as reflected by a steeper slope of the regression of log (norepinephrine infusion rate) on percentage reduction in venous distensibility, and a significantly lower ED50 (i.e., norepinephrine infusion rate that induced 50% reduction in venous distensibility). The findings suggest anatomical or functional postganglionic denervation of lower limb veins causing excessive gravitational blood pooling with consequent orthostatic hypotension in these patients.

Adult↗
PubMed1990

Effect of posture on plasma atrial natriuretic hormone and renal function during salt loading in patients with and without postural (idiopathic) edema.

The effect of posture on plasma atrial natriuretic hormone (ANH) and renal function was studied in subjects with idiopathic edema. Sixty-five subjects with edema but with no clinical evidence for cardiac, renal, or pulmonary diseases were studied after they had been off all medication for 1 week or more. They had nothing by mouth after midnight and were admitted to the Clinical Research Center at 0800 h. They voided, were weighed, and had their blood pressure and pulse measured in the recumbent and upright positions. A needle was inserted, and subjects were recumbent for 0.5 h, after which blood was drawn for measurement of plasma ANH, serum sodium, potassium, and (in 35 subjects) creatinine. They were then given 150 mL 0.14% sodium chloride solution to drink every 0.5 h for the next 6 h. Urine was collected every 0.5 h for measurement of sodium, potassium, and creatinine. After 4 h of recumbency repeat blood samples were drawn, subjects ambulated for 2 h, after which final repeat blood samples were drawn. Subjects were considered to have postural edema if their upright urinary sodium/previous 2-h urinary sodium was less than 33%, and to have a normal response if it was 33% or more. The clinical characteristics of the 34 patients with postural edema and 31 patients with a normal response were similar. Plasma ANH levels (initial, after oral saline, and after standing) were similar in the two groups, and there was no relationship between changes in ANH and urinary sodium with standing. In conclusion, under conditions of mild oral sodium chloride loading, changes in plasma ANH do not cause the abnormal sodium retention found in patients with postural edema.

Adult↗
PubMed1990

Vascular responsiveness to norepinephrine in sympathicotonic orthostatic intolerance.

Sympathicotonic orthostatic intolerance (hypotension, tachycardia, or both) is associated with normal or excessive orthostatic increases in plasma norepinephrine concentration and is reversible by the inflation of a military anti-shock trouser suit enveloping the lower limbs and abdomen. These facts suggest that one possible mechanism of the disorder might be a defect in alpha-adrenergic receptor or postreceptor responsiveness of the veins or arterioles. We have investigated in 11 patients and 15 healthy controls the blood pressure and heart rate responses to increasing rates of intravenous norepinephrine infusion (1 to 16 micrograms/min), the dorsal hand vein contractile responses to increasing rates of norepinephrine infusion (1 to 256 ng/min) with a linear variable differential transformer, and the platelet alpha 2-adrenergic receptor densities and dissociation constants. No statistically significant difference in any of these parameters was found between the normal subjects and nine of the 11 patients with orthostatic intolerance. The venous contractile response to norepinephrine was excessive in one patient and was virtually absent in another. Because supersensitivity of the hand veins to norepinephrine suggests up-regulation of alpha 2-receptors resulting from postganglionic autonomic insufficiency, this finding in one patient with sympathicotonic orthostatic hypotension might have been caused by venous denervation. The venous unresponsiveness to norepinephrine in the other patient presumably resulted from a defect in the venous receptors or smooth muscle function. It is evident that norepinephrine responsiveness and the innervation of the arterioles and hand veins was normal in the other nine patients, in whom the defect must have been mediated by some other mechanism.

Adolescent↗
PubMed1990

Primary hyperepinephrinemia in patients without pheochromocytoma.

Clinical features of epinephrine release led to the finding of spontaneously elevated plasma epinephrine concentrations in five patients, in four of whom plasma norepinephrine concentrations were normal. Adrenal medullary hyperplasia was suspected in one patient, whose first cousin had multiple endocrine neoplasia type IIa, and in two others, all of whom have experienced relief from symptoms during propranolol or atenolol administration. The other two patients had unilateral adrenal cysts, with negative metaiodobenzylguanidine scans and no histological evidence of pheochromocytoma, but complete relief of symptoms by excision of the cysts. In one patient, Cushing's syndrome and associated hypertension, diabetes, and ischemic finger-tip ulceration all disappeared after surgery. It is concluded that spontaneous hyperepinephrinemic manifestations can be received by beta-blockers or, when an adrenal mass is present, by unilateral adrenalectomy even when the metalodobenzylguanidine test result is negative.

Adrenal Gland Diseases↗
PubMed1989

A longitudinal study of the performance of hypertensive and normotensive subjects on the Wechsler Adult Intelligence Scale.

Performance on the Wechsler Adult Intelligence Scale was followed over two 5- to 6-year intervals for essential hypertensive Ss (EH; n = 22) free from medical complications and for normotensive Ss (N; n = 20). EH were treated with adrenergic beta-blocking drugs, diuretics, or both. Mean age was 46 years (SD = 12.6 years), initially (Time 1). Results were unaltered by adjustment for initial age. N improved modestly on the Verbal scale, from Time 1 to Time 2 only. EH neither improved nor declined on the Verbal scale. Scores remained unchanged for both EH and N Ss for the Performance scale. Overall, and at Times 2 and 3, Verbal scores were lower for the EH group. It was concluded that neither decline nor improvement in cognitive function over time are necessary outcomes of modest, carefully treated, uncomplicated hypertension in the middle years.

Female↗
PubMed1988

Prediction of renovascular hypertension. Comparison of clinical diagnostic indices.

One hundred and six patients were determined to have renovascular hypertension (RVH) out of 3520 patients with hypertension referred by their physicians for a 1-day blood pressure study (1-day BP study) to evaluate the presence of secondary forms of hypertension. The clinical indices (including serum potassium and creatinine concentrations) most likely to predict RVH were analyzed. Patients unlikely to have RVH were those with a diastolic blood pressure (DBP) less than or equal to 90 mm Hg (with or without BP medication) with a serum potassium concentration less than 3.4 mEq/L. A two- to threefold increased prevalence of RVH was associated with DBP greater than 110 mm Hg, an age of onset of hypertension of 51-69 years, or age of onset greater than 60 years with a DBP less than or equal to 100 mm Hg. A four- to sixfold increase came with an age of onset greater than 60 years, serum potassium (with or without BP medication) 2.9-3.3 mEq/L, or serum potassium less than 3.4 mEq/L with DBP greater than 90 mm Hg. A seven- to ninefold increase came with age of onset greater than 60 years with DBP greater than 110 mm Hg or serum potassium (with or without BP medication) of 2.3-2.8 mEq/L.

Adult↗
PubMed1988

Effects of thyroid function on blood pressure. Recognition of hypothyroid hypertension.

Hypothyroidism has been known to be associated, at times, with diastolic hypertension. We have found in 40 thyrotoxic patients that the induction of hypothyroidism by radioiodine therapy significantly increased diastolic blood pressure, raising it above 90 mm Hg in 16 (40%) of the patients. Restoration of euthyroidism with thyroxine administration significantly reduced the systolic and diastolic blood pressures in these patients, with a fall in diastolic pressure below 90 mm Hg in nine of 16 patients. The prevalence of hypothyroidism was determined by measurements of serum thyroxine and thyrotropin concentrations in 688 consecutive hypertensive patients, referred for evaluation and therapy of their hypertension. Hypothyroidism was found in 25 (3.6%) of the patients. Restoration of normal serum thyroxine and thyrotropin levels with thyroid hormone replacement therapy lowered diastolic blood pressure to levels below 90 mm Hg in 32% of these patients who could be followed up after withdrawal of all antihypertensive drug therapy when euthyroidism had been restored (i.e., 1.2% of the 688 patients). It is concluded that diastolic hypertension resulting from hypothyroidism is a relatively common disorder, present in 1.2% of our referred hypertensive patients, that should be sought and treated.

Adult↗
PubMed1988

Abnormal orthostatic changes in blood pressure and heart rate in subjects with intact sympathetic nervous function: evidence for excessive venous pooling.

The normal ranges of orthostatic changes in blood pressure and heart rate have been defined in 92 individuals aged 18 to 64 years. In 34 individuals whose symptoms (especially orthostatic light-headedness) suggested cerebral ischemia, but in whom none of the known causes of orthostatic hypotension could be identified, we have found one or more of five theoretically possible orthostatic circulatory derangements: systolic hypotension, diastolic hypotension, diastolic hypertension, excessive narrowing of the pulse pressure, and tachycardia after standing for at least 3 minutes. The orthostatic disorders of blood pressure and heart rate identified in the 34 patients were significantly reduced, almost always into the normal range, by external pressure of 45 to 50 mm Hg applied through an inflatable pressure suit. After labeling with sodium pertechnetate Tc 99m and reinjecting the erythrocytes contained in 3 to 6 ml blood, external gamma counting over a fixed site in the calf, both in the recumbent and in the standing posture, showed excessive gravitational pooling of blood in the legs of five patients with orthostatic diastolic hypertension, of four with orthostatic narrowing of the pulse pressure, and of 10 with orthostatic tachycardia alone. Plasma norepinephrine concentrations were usually normal in recumbency and elevated above normal limits during standing for 15 to 30 minutes in the 18 patients so observed. Red cell mass, plasma volume, and circulating blood volume were subnormal in more than half the seven patients in whom these measurements were made. We conclude that most of the patients with idiopathic sympathicotonic abnormalities of orthostatic blood pressure control have a venous pooling syndrome often aggravated by hypovolemia, the cause(s) of which remains to be determined.

Adolescent↗
PubMed1987

Prevalence, natural history and surgical treatment of exophthalmos.

The 95% confidence limits of exophthalmometer measurements have been defined by a single observer in 105 individuals who had no known thyroid disease, and found to be 10.5-18.8 mm. Measurements in 308 patients with thyrotoxicosis have shown that exophthalmos (greater than 19 mm) of one or both eyes was present in 21.3% of the patients. Among the 122 thyrotoxic patients whose exophthalmometer measurements could be performed annually for 3-19 years after correction of the thyrotoxicosis (usually with 131I), exophthalmos remained stable in 78.7%, worsened in 15.6% and became less severe in 5.7% of the patients. Transantral decompression of the orbits was performed in 15 patients with rapid subjective improvement in all and reduction in exophthalmometer measurements of 3.6 +/- 0.5 (mean +/- SEM) mm, and no serious side-effects. In view of these findings, transantral decompression should be considered more frequently in the treatment of severe or cosmetically damaging exophthalmos.

Adolescent↗
PubMed1987

Effect of sodium balance and calcium channel blocking drugs on blood pressure responses.

To study the role of calcium movements in mediating the effects of sodium chloride on the response of blood pressure to angiotensin II (ANG II), we infused ANG II before and after giving calcium channel blocking drugs (nifedipine and diltiazem) and calcium infusions to normal subjects during high and low sodium intakes. ANG II was also in nine patients with essential hypertension eating a low sodium diet. In preliminary studies, the effects of nifedipine, 20 mg p.o., on blood pressure and plasma renin activity were determined. Sensitivity to infused ANG II was calculated as the slope of the linear regression of the increase in diastolic blood pressure (DBP) expressed as a function of the ANG II infusion rate (mm Hg/ng ANG II/kg/min). During intake of a high sodium diet (Na, 200 mEq/day) both drugs significantly (p less than 0.05) reduced ANG II sensitivity, while on a low sodium diet (10 mEq Na), neither drug reduced ANG II sensitivity. There was a significant (p less than 0.001) inverse correlation between the initial ANG II-DBP sensitivity and the change in sensitivity induced by the calcium channel blocking drugs in normal subjects (r = -0.78) and in hypertensive patients (r = -0.70). Five hypertensive patients had greater than normal ANG II-DBP sensitivity that was significantly (p less than 0.05) reduced by nifedipine. Calcium infusion did not affect the ANG II-DBP sensitivity on either diet. The results suggest that in normal subjects increased DBP responses to ANG II, induced by an increase in sodium intake, are partially mediated by increased extracellular to intracellular calcium movements, since they are blocked by the structurally different calcium channel blocking drugs nifedipine and diltiazem. In hypertensive patients on a low sodium diet, increased DBP responses to ANG II infusion were blocked by nifedipine, indicating they are at least partly mediated by increased extracellular to intracellular calcium flux.

Adult↗
PubMed1987

Clinical significance of cognitive performance by hypertensive patients.

Fifty-four subjects with uncomplicated essential hypertension and 54 normotensive subjects were compared with regard to a widely employed clinical index of cognitive dysfunction (the Average Impairment Rating) calculated from neuropsychological tests that discriminate between brain-damaged and neurologically normal persons. Hypertensive subjects exhibited lower mean scores on this index when education was ignored, but results were not the same for highly educated and less well educated groups. There were no differences between exceptionally well educated hypertensive and normotensive subjects, but in the less well educated group, hypertensive subjects performed more poorly than normotensive subjects. The percentages of hypertensive and normotensive subjects scoring in a cognitively impaired range on the Average Impairment Rating were low and did not differ for either education group. These data indicate the important role of subtle differences in education level with respect to positive or negative findings for studies comparing hypertensive and normotensive subjects and illustrate the important role of clinical neuropsychological indices of cognitive dysfunction when one wishes to make meaningful inferences regarding cerebral cortical function in hypertensive subjects.

Adult↗