Chronic Essential Hypertension Research Articles

Prognostic importance of vascular lesions in acute renal failure with microangiopathic hemolytic anemia (hemolytic-uremic syndrome): Clinicopathologic study in 20 adults

Renal biopsies obtained from 20 adult patients within 30 days after onset of acute renal failure with microangiopathic hemolytic anemia ("the hemolytic-uremic syndrome") were studied. Lesions were graded independently by two observers without knowledge of the clinical history. All patients who did not have refractory hypertension were treated with heparin. Ten of the patients died, and four developed end-stage renal failure requiring chronic dialysis. Six patients, however, had a relatively good outcome: two recovered completely and four developed mild-to-moderate chronic renal failure not requiring dialysis. The six patients with a good outcome had significantly less severe arterial intimal thickening on biopsy compared with the remaining patients with a poor outcome. The patients with a good outcome and those with a poor outcome did not differ in the severity of glomerular lesions. The clinical features did not allow a prediction of late outcome. These results suggest that early renal biopsies may be helpful in predicting prognosis in the "hemolytic-uremic syndrome." This clinical syndrome may occur either in apparently healthy people, or may complicate the course of a chronic essential hypertension.

A prospective study of angiotensin II pressor responsiveness in pregnancies complicated by chronic essential hypertension

The present study was designed to (1) outline, in a prospective manner, vascular responsiveness to angiotensin II (A-II) in gravidas with essential hypertension and (2) ascertain if increased sensitivity to infused A-II could be detected before worsening of hypertension developed in those women who were destined to develop superimposed pregnancy-induced hypertension (PIH). Sixty-three women with chronic essential hypertension were studied sequentially throughout pregnancy and two groups of patients were defined on the basis of clinical outcome and serial measurements of vascular reactivity to exogenenously administered A-II. The first group consisted of 29 gravidas with chronic hypertension alone and the second group was composed of 34 patients with chronic hypertension who were destined to develop superimposed PIH. Vascular resistance to infused A-II (more than 7 ng. per kilograms per minute required to increase diastolic blood pressure 20 mm. Hg) was observed from weeks 21 to 27 of gestation in both groups of patients. In the gravidas with essential hypertension alone, resistance to A-II persisted throughout the remainder of pregnancy. However, in those women destined to develop PIH, an increased sensitivity to A-II developed after week 27 of gestation and the differences in mean values between the two groups of patients became highly significant after week 30 of gestation (P < 0.025). Although individual determinations obtained in both groups of patients between weeks 28 and 32 of pregnancy suggested that pressor responsiveness to A-II might be used as a screening technique to identify those women destined to develop PIH, additional studies conducted between weeks 28 and 32 of gestation will be required before the efficacy of such a screening technique is clearly established.

Control of cardiac output in essential hypertension

Cardiac and renal hemodynamics and cardiopulmonary and total blood volume were determined in 202 men, 101 with normotension and 101 of the same age with chronic essential hypertension, normal renal function and balanced sodium intake and urinary output. Cardiac output was identical in the two groups, whereas blood pressure and total peripheral resistance were significantly different. The two groups exhibited strong differences in the correlation study: (1) Correlations of blood pressure with, respectively, heart rate, cardiopulmonary blood volume and total blood volume were significant in the normotensive group but not in the hypertensive group. (2) Correlations of cardiac output with, respectively, heart rate, cardiopulmonary blood volume and total blood volume were significant in both groups. (3) Correlations of renal blood flow with, respectively, cardiac output, blood pressure and total blood volume were significant in the hypertensive group but not in the normotensive group. This study provides evidence that: (1) the volume and neural control of blood pressure are disrupted in hypertension whereas control of cardiac output is maintained; and (2) adaptive mechanisms involving renal function are necessary to the maintenance of normal cardiac output in patients with essential hypertension.

Learned control of decreases in systolic blood pressure.

A NUMBER of studies have demonstrated that when humans are provided with exteroceptive feedback of specific aspects of cardiovascular performance, they rapidly learn to control responses of the system in question. Increases and decreases in heart rate1, decreases in heart rate variability2, and changes in vasomotor tone3 have all been demonstrated to be subject to control under conditions of augmented sensory feedback. The findings suggest that the use of augmented sensory feedback may be effective in the training of other aspects of cardiovascular behaviour. Such a technique would be particularly valuable in the training of blood pressure decreases in individuals exhibiting chronic essential hypertension. Recently Shapiro, Tursky, Gershon and Stern4 gave one group of subjects a brief signal whenever their systolic blood pressure exceeded a prescribed value and another group of subjects a brief signal whenever their blood pressures fell below a prescribed value. Using this procedure and making reinforcement depend on the appropriate response, these investigators were able to produce average increases and decreases in systolic blood pressure of about 1 and 5 mm Hg respectively in their two groups of subjects. If these general procedures could effect greater decreases in blood pressure, their potential therapeutic utility would be enhanced. Following the finding by Brener, Kleinman and Goesling5 that the degree of cardiovascular control is a direct function of the amount of augmented sensory feedback provided during training, we have attempted to maximize the amount of blood pressure information fed back to subjects within the constraints of the monitoring system used.

Pre-eclamptic toxaemia, essential hypertension, chronic essential hypertension+toxaemia, and chronic renal disease, (R.C.O.G. table 5)

Pre-eclamptic toxaemia, essential hypertension, chronic essential hypertension+toxaemia, and chronic renal disease, (R.C.O.G. table 5)

Pre-eclamptic toxaemia, essential hypertension, chronic essential hypertension + toxaemia, and chronic renal disease, (R.C.O.G. Table 5)

Pre-eclamptic toxaemia, essential hypertension, chronic essential hypertension + toxaemia, and chronic renal disease, (R.C.O.G. Table 5)

The role of the catecholamines in hypertension: A review ∗

T ODAY medullary adrenal tumors which contain varying increased amounts of epinephrine and norepinephrine are known to cause hypertension which is relieved when the tumors are removed surgically. The question now arises as to whether the catecholamines play a role in chronic essential hypertension of unknown etiology. The two catecholamines, epinephrine and norepinephrine, are produced in the chromafi tissue of the normal adrenal medulla or wherever chromaffin tissue is located in the sympathetic nervous system, the heart, and the brain. More recently, chromaffin tissue has been demonstrated around the nerves and blood vessels of the skin. In 1894, Oliver and SchZfer’ first demonstrated that intravenous administration of adrenal extracts to animals was followed by a pressor response, and the question arose as to the role of the adrenal gland in the pathogenesis of hypertension. In the following four years, Abel and Crawford,3 Aldrich3 and Takamine4 isolated crystalline epinephrine (adrenalin) from the adrenal gland. In 1904, Stolz5 synthesized both adrenalin and its amino homologue, noradrenalin. From 1905 to 1945 the work of various investigators including Elliott,6 Loewi,’ Cannon and Lisshk8 and Cannon and Uridilg led to the belief that adrenalin was the specific hormone of the adrenal gland as well as the neurohormonal transmitter of the adrenergic nerves. Because of some discrepancy between the effect of stimulation of the sympathetic nervous system and that of adrenalin, Cannon postulated the existence of two sympathins, E and I. In 1910, Barger and DalelO pointed out that there was a closer resemblance between the effects of stimulation of the sympathetic nervous system and those of noradrenalin, but this work was overlooked for many years, with only sporadic reports of similar observations. From 1945 to 1948, von Euler” and various other workers (Gaddum and Goodwin,12 Folkow and UvnW3) established that noradrenalin was the neurohormonal transmitter of the sympathetic nervous system and that both adrenalin and noradrenalin were the specific hormones of the adrenal medulla. Because of the possible role noradrenalin (norepinephrine) might play in the production of hypertension, and with the simultaneous introduction of new antihypertensive drugs, the biochemists, pharmacologists, physiologists and clinicians entered into the most extensive investigations to ascertain if possible the cause and the best treatment for hypertension. From 1925 to the late 1940’s, patients with hypertension were treated with a wide variety of operations on the sympathetic nervous system. Adson,l* in 1924, introduced the limited bilateral lumbar sympathetic ganglionectomy. During the ensuing period, the most widely used procedure was the thoracolumbar sympathectomy of Smithwick and Thompson,15 in which the ganglionectomy extended from Tb-9 to Ll-2. In 1939, Grimson”j carried out total sympathectomies. This latter method carried a high mortality and morbidity. However, sympathectomy demonstrated that it was possible to lower the blood pressure permanently in many cases of essential hypertension and to normal levels in some. This was accomplished by interfering with vasoconstrictor reflexes involved in certain homeostatic adjustments of the circulation, especially those which come into

Pre-eclamptic toxaemia, essential hypertension, chronic essential hypertension + toxaemia and chronic renal disease, (R.C.O.G. table 5)

Pre-eclamptic toxaemia, essential hypertension, chronic essential hypertension + toxaemia and chronic renal disease, (R.C.O.G. table 5)

Clinical evaluation of hypertensive patients: Indications for and utilization of the isotope renogram, separated renal function study and aorticorenal arteriogram ∗

Four cases of hypertension secondary to lesions of the renal arteries are presented with comments on the history, results of physical and laboratory examinations and surgical findings. Points emphasized are as follows: 1. 1. Hypertension of renal or renal arterial origin should be suspected in the presence of: (A) acute hypertension in young patients with angiospastic ocular changes; (B) rapidly progressive symptomatic hypertension of recent onset; (C) abrupt acceleration of chronic essential hypertension; (D) a history suggestive of a recent renal vascular accident; (E) a continuous bruit over the superolateral area of the abdomen and (F) a disparity in the size and function of the kidneys on excretory urography. 2. 2. In our experience the isotope renogram has served as an excellent screening procedure for the evaluation of renal function in hypertensive patients. 3. 3. Renal arteriography is a highly desirable procedure which aids in the more complete evaluation of hypertensive patients in whom abnormalities suggestive of renal arterial disease are found on physical or urographic examination or in the isotope renograms. This is especially true when surgical intervention is planned. The vagaries of translumbar aorticorenal arteriography are legion. Retrograde aortographic technics for renal arteriography are technically more satisfactory in our experience. 4. 4. Evaluation of function of each kidney alone may on occasions prove not only of diagnostic help, but more importantly, it may provide evidence of the adequacy of function of the individual kidneys, and thus may prove decisive regarding the feasibility of surgical intervention.

Table “A” summary of 391 cases of pre-eclamptic toxaemia, essential hypertension, chronic essential hypertension plus toxaemia, chronic renal disease

Table “A” summary of 391 cases of pre-eclamptic toxaemia, essential hypertension, chronic essential hypertension plus toxaemia, chronic renal disease

Effects of pressor and depressor agents on pulmonary and systemic pressures of normotensives and hypertensives.

Summary and ConclusionsThe pulmonary and brachial artery pressures and their responses to pressor and depressor agents have been studied in normotensive and hypertensive subjects. Pulmonary artery pressure is within the same range in both groups. The response of pulmonary artery pressure to pressor and depressor agents used is also the same in both groups. It is emphasized that the elevation of pulmonary artery pressure due to angiotonin, epinephrine, and nor-epinephrine is the same in hypertensive and normotensive subjects. It is concluded that none of these or any similarly acting substances plays a part in sustaining the blood pressure elevation in patients with chronic essential hypertension.