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At least 19 recordsLinked to original sources
PubMed2026

Hypertensive disorders of pregnancy and the risk for hypertension and cardiovascular and kidney disease. International Society of Hypertension position paper, endorsed by the World Hypertension League and European Society of Hypertension.

Hypertensive disorders of pregnancy (HDP) remain a leading cause of maternal and perinatal morbidity and mortality worldwide, especially in low- and middle-income countries. Moreover, HDP are directly linked to an increased risk of long-term cardiometabolic and kidney disease in mothers and offspring. Since prevention, diagnosis, and treatment of HDP remain suboptimal globally, enhanced understanding and implementation of current guidelines on HDP present a substantial opportunity to significantly reduce maternal and fetal morbidity and mortality. This position paper by the International Society of Hypertension reviews current knowledge in the field, identifies knowledge gaps and provides recommendations on the care of women with HDP and lifelong care, thereafter.

AT1R-Aas↗
PubMed1978

Hypertension induced by adrenocortical dysfunction--hypertension in 17 alpha-hydroxylase deficiency and metopirone-induced hypertension.

Hypertension in 17 alpha-hydroxylase deficiency was studied by comparing it with hypertension in Cushing syndrome or that in primary aldosteronism. Furthermore, the role of endogenous increases of ACTH, deoxycorticosterone, and 18 alpha-hydroxy-deoxycorticosterone upon blood pressure was studied in rats by administerating metopirone. Hypertension in 17 alpha-hydroxylase deficiency was considered to be more similar to that in primary aldosteronism from the studies on renin components, pressor responses to angiotensin II and norepinephrine, and renin responses to stimulations. Plasma catecholamines were slightly decreased in 17 alpha-hydroxylase deficiency. The hypertension was alleviated by the administeration of dexamethasone in 2 of 3 patients with 17 alpha-hydroxylase deficiency. However, in the remaining one who had an accelerated hypertension and normal renin, the hypertension was not alleviated by dexamethasone. In the animal studies, hypertension induced by metopirone was accelerated by salt loading of uni-lateral nephrectomy plus salt loading. In those rats, plasma ACTH, and deoxycorticosterone were markedly increased.

Adrenal Hyperplasia, Congenital↗
PubMed1976

The mechanism of low-renin hypertension: aldosterone response to sodium restriction and upright posture, angiotensin II, ACTH and potassium in patients with hypertension.

Plasma renin activity and aldosterone were measured simultaneously in 67 out-patients with essential hypertension. High aldosterone was more often in patients with high renin, and low levels of aldosterone were usual in those with low and normal renin. In order to study the mechanism by which aldosterone and renin acitvity are suppressed in low-renin hypertension, 25 patients (13 normal-renin hypertensives, 10 low-renin patients including 4 non-responders and two DOC excess hypertensives) were investigated as inpatients. Plasma renin activity, aldosterone and cortisol were determined by the following stimualtions with 3 days of sodium restriction and 2 hours of upright posture, angiotensin II infusion (at a dose which increased 20mmHg of diastolic blood pressure), ACTH administration (rapid i.m. injection of 0.25 mg of alpha 1-24 preparation) and potassium infusion (30 meq of potassium i.v.). Responses of aldosterone in normal-renin hypertensives to all stimulations were 3-5 fold increases from bases line values. Low-renin hypertensives except two of four non-responders showed the responses similar to those in normal-renin patients. The responses of two of the non-responders were similar to those in DOC excess hypertensives who showed reduced responses of aldosterone to some of these stimulations. Thus, it seems that low-renin hypertension is a clinical entity caused by a variety of mechanisms, and the mechanism by which low-renin hypertension is induced is not explained by one factor such as an unknown mineralocorticoid.

Adrenocorticotropic Hormone↗
PubMed1977

Hypertensive changes in experimental nephritis combined with experimental hypertension.

The role of hypertension in chronic glomerulonephritis was studied in rats with experimental hypertension and nephrotoxic serum nephritis. Nephrotoxic serum nephritis accelerated the hypertensive course of Godblatt's type of experimental hypertension both in the acute and chronic phases. Malignant hypertension was found to be caused in some rats by the nephrotoxic serum injection in the chronic phase of experimental hypertension. Nephrotoxic serum nephritis was more protracted in SHR than in control rats. These results suggest that hypertensive changes might aggravate glomerulitis, and that nephritic processes also facilitate the hypertensive changes.

Animals↗
PubMed1979

Pulmonary hypertension complicating portal hypertension.

We report 9 patients with pulmonary hypertension complicating portal hypertension. The cause of portal hypertension was cirrhosis in 7 patients, nodular regenerative hyperplasia of the liver in 1, and portal vein obstruction in 1. Six patients had been treated by portal-systemic shunting before the clinical onset of pulmonary hypertension. The interval between the first manifestation of portal hypertension and the recognition of pulmonary hypertension ranged from 2 to 15 years. Histologic examination in 1 of these patients revealed medial hypertrophy, concentric intimal proliferation, and plexiform lesions affecting the small pulmonary arteries. Pulmonary hypertension might result from the effect of a vasoconstrictive agent on the small pulmonary arteries or of a substance toxic to the walls of these vessels that is produced in the splanchnic territory, destroyed by the liver in normal subjects, and reaches the pulmonary arteries through portal-systemic shunts in these patients.

Adult↗
PubMed1976

Na-K-adenosine triphosphatase in the kidney of rats with renal hypertension and spontaneously hypertensive rats.

The rats with chronic renal hypertension caused by constricting one renal artery, exhibit a decrease in the activity of Na-K-ATPase in the outer medulla of the "untouched" kidney, as compared to this activity in the kidneys of intact normotensive rats and in the "untouched" kidney of the rats where renal artery constriction did not result in hypertension. There were no differences between the control normotensive Wistar rats and the spontaneously hypertensive rats (SHR) in the prehypertensive and early hypertensive stages (at the age of 6-8 weeks) as far as the activities of Na-K-ATPase and oxidoreductases (SDH and LDH) in the renal cortex, the outer and inner medulla are concerned. The spontaneously hypertensive rats with chronic hypertension had at the age of 16-20 and 27-29 weeks lower activity of Na-K-ATPase, SDH, and LDH in the outer renal medulla than the control normotensive Wistar rats. The experimental results indicate that in chronic arterial hypertension there is a decrease in the activity of Na-K-ATPase, in the outer renal medulla, which suggests a reduction in the resorpo sodium and water.

Adenosine Triphosphatases↗
PubMed1976

The use of spontaneously hypertensive rats for the study of anti-hypertensive agents.

Hypertension studies using laboratory animals have been conducted since 1930. These were not completely satisfactory because either surgery or pharmacologic induction were required to produce hypertensive animals. Many attempts have been made to breed spontaneously hypertensive rats, mainly from the Okamoto strain. The cause of hypertension in the rat, with specific reference to genetic aspects and pathogenicity, were reviewed. The hypertensive rat is an acceptable model for hypertension studies because of the stability of the hypertensive state and the reproducibility of experimental effects. It is a particularly useful model for screening antihypertensive agents. Development of mutant Okamato stran rats which have brain softening, cerebral hemorrhages, and myocardial infarctions would permit the screening of specific therapeutic agents with fewer side-effects. Mutants which develop obesity, hyperlipidism, and early atherosclerosis have been reported in Okamoto strain X Sprague-Dawley rat crosses.

Animals↗
PubMed1977

[The renin-angiotensin-aldosterone system in hypertensive subjects. III- The use of beta-blockers in reno-vascular hypertension (author's transl)].

Six patients with permanent hypertension with renal artery stenosis were treated by conservative reparative surgery appart from one of them (unilateral nephrectomy) and were all seen again at the 8th month at the earliest in the absence of any anti-hypertensive therapy. Study of the renin-angiotensin system carried out on a normal sodium diet, after stopping all anti-hypertensive treatment for at least 15 days, was combined with the anti-hypertensive response under the influence of a beta-blocker. There were two types of response pre-operatively: firstly, with beta-blockers alone a normal blood pressure which remained normal postoperatively; the second group of patients remained hypertensive, requiring the addition of diuretics, and remained hypertensive after surgery. This response, although non-specific, would appear to represent an important element in assessing the curability of reno-vascular hypertension.

Adrenergic beta-Antagonists↗
PubMed1978

Studies on the prevalence of renal disease and hypertension in relation to schistosomiasis. IV. Systemic blood pressure hypertension and related features.

Two comparable rural communities but with varying endemicity of urinary schistosomiasis in environs of Ibadan, Nigeria, have been studied by a total cross-sectional population survey. It has been found that:- (i) schistosomiasis does not predispose to raised blood pressure (ii) both diastolic and systolic blood pressure increase with age. (iii) prevalence of systemic hypertension is higher in females than males (iv) body weight and height are related to hypertension in both males and females (v) parity would seem to be related to hypertension in the females (vi) except in the younger female group (1--19 years) where polyuria, frontal headache, palpitations appear related to systolic hypertension, raised blood pressure would appear to have no symptoms. In particular headache in any part of the head bears no clear relationship. (vii) The majority of hypertensives would appear to belong to the primary variety but proteinuria among females has been found to be significantly related to hypertension.

Adolescent↗
PubMed1975

The hypertensive diseases. Evidence that systemic hypertension is a greater risk factor to the development of other cardiovascular diseases than previously suspected.

This report summarizes the clinical frequencies of systemic hypertension and necropsy evidence of cardiomegaly in various cardiovascular conditions (Table I), termed "the hypertensive diseases" because of their frequent association with systemic hypertension. Although long recognized as a major risk factor, systemic hypertension appears to be an even greater risk factor to the development of various cardiovascular conditions than previously appreciated. Hypertension by itself appears to be the sole underlying factor in most cases of nontraumatic cerebral arterial or aortic (dissection = partial rupture) rupture. In association with hyperlipidemia, hypertension clearly accelerates atherosclerosis and its devastating consequences.

Angina Pectoris↗
PubMed2024

Multi-organ gene expression analysis and network modeling reveal regulatory control cascades during the development of hypertension in female spontaneously hypertensive rat.

Hypertension is a multifactorial disease with stage-specific gene expression changes occurring in multiple organs over time. The temporal sequence and the extent of gene regulatory network changes occurring across organs during the development of hypertension remain unresolved. In this study, female spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats were used to analyze expression patterns of 96 genes spanning inflammatory, metabolic, sympathetic, fibrotic, and renin-angiotensin (RAS) pathways in five organs, at five time points from the onset to established hypertension. We analyzed this multi-dimensional dataset containing ~15,000 data points and developed a data-driven dynamic network model that accounts for gene regulatory influences within and across visceral organs and multiple brainstem autonomic control regions. We integrated the data from female SHR and WKY with published multiorgan gene expression data from male SHR and WKY. In female SHR, catecholaminergic processes in the adrenal gland showed the earliest gene expression changes prior to inflammation-related gene expression changes in the kidney and liver. Hypertension pathogenesis in male SHR instead manifested early as catecholaminergic gene expression changes in brainstem and kidney, followed by an upregulation of inflammation-related genes in liver. RAS-related gene expression from the kidney-liver-lung axis was downregulated and intra-adrenal RAS was upregulated in female SHR, whereas the opposite pattern of gene regulation was observed in male SHR. We identified disease-specific and sex-specific differences in regulatory interactions within and across organs. The inferred multi-organ network model suggests a diminished influence of central autonomic neural circuits over multi-organ gene expression changes in female SHR. Our results point to the gene regulatory influence of the adrenal gland on spleen in female SHR, as compared to brainstem influence on kidney in male SHR. Our integrated molecular profiling and network modeling identified a stage-specific, sex-dependent, multi-organ cascade of gene regulation during the development of hypertension.

Animals↗
PubMed1978

Fetal hypertension and the development of increased pulmonary vascular smooth muscle: a possible mechanism for persistent pulmonary hypertension of the newborn infant.

Chronic pulmonary arterial hypertension was produced in six fetal lambs. In four (126 to 139 days' gestation) unilateral fetal renal artery constriction caused systemic arterial mean blood pressure elevations. In another fetus, constriction of the umbilical artery caused a systemic mean blood pressure elevation; in the sixth, partial occlusion of the ductus arteriosus caused isolated pulmonary arterial hypertension. The right lung of each fetus was perfused with fixative at the in vivo mean arterial pressure and the amount of smooth muscle in the fifth generation (resistance) vessels analyzed using the medial width/external diameter ratio. There was a significant increase in the medial width/external diameter ratio in the six experimental animals as compared to that in six normal fetuses. In separate fetuses the increased ratios were due to a decreased external diameter, increased smooth muscle, or both these factors. The total number of resistance vessels was counted in the right lung of each fetus and no significant difference from normal was observed. We postulate that either fetal systemic hypertension or constriction of the ductus arteriosus causes fetal pulmonary hypertension in utero and that this produces increased smooth muscle development in pulmonary arterial resistance vessels; this may be a pathogenic mechanism for the syndrome of persistent pulmonary hypertension of the newborn infant.

Animals↗
PubMed1975

Is low-renin hypertension a stage in the development of essential hypertension or a diagnostic entity?

A study of the frequency distribution of plasma-renin concentration in 81 patients with essential hypertension produced no evidence of a distinct sub-population with low renin levels. An arbitrary dividing line was used, therefore, to define low-renin hypertension (36% of patinets). Patients in this group were older than those with normal renin levels, and there was a significant negative correlation between renin and age among all patients. Low-renin hypertension was not characterized by increased exchangeable sodium, but exchaneable postassium was significantly lower than in patients with normal plasma-renin. This difference became insignificant when five patients in the low-renin group with persistent hypokalaemia were excluded. It is concluded that low-renin hypertension does not represent a separate diagnostic entity but that plasma-renin falls with age in essential hypertension.

Adult↗
PubMed1979

Risk factors for death in treated hypertensive patients. Report from the D.H.S.S. Hypertension Care Computing Project.

A prospective study was performed to determine factors at presentation influencing survival in 2587 treated hypertensive patients who were followed for an average of 4 years. 86% had been referred to hospital clinics with hypertension and 14% were seen solely by their general practitioners. Of the 156 deaths, 81% were from cardiovascular causes. Independent risk factors for cardiovascular death were age, impairment of renal function, smoking habits, and systolic blood-pressure before treatment. Other independent factors of importance were proteinuria, history of myocardial infarction, and retinal changes of accelerated hypertension. Increased weight, serum cholesterol, and serum uric acid were not independent risk factors. Although these results agree substantially with data for normal populations, notable exceptions were impairment of renal function, which was very important in hypertensives, and raised serum cholesterol, which was not an independent risk factor in this hypertensive population.

Age Factors↗
PubMedDate not supplied

Studies on the role of vasopressin in blood pressure control of spontaneously hypertensive rats with established hypertension (SHR, stroke-prone strain).

We investigated the role of arginine-vasopressin (AVP) in maintaining the blood pressure of spontaneously hypertensive (SH) rats (stroke-prone strain) with established hypertension (22--28 weeks of age). In comparison with normotensive Wistar Kyoto (WKY) rats, plasma AVP concentrations of SH rats with benign hypertension (BH) were elevated twofold and in rats with severe or malignant hypertension (S-MH), fourfold. The height of the blood pressure was quantitatively related to plasma AVP in both BH and S-MH rats, the overall correlation coefficient being 0.66 (p less than 0.001). The intravenous injection of a specific AVP antiserum into conscious and unrestrained rats lowered blood pressure in 4 BH rats by 48 +/- 14 mm Hg and in 4 S-MH rats by 78 +/- 10 mm Hg and had only a marginal effect in 4 normotensive WKY rats. Infusion of saralasin did not lower blood pressure in WKY and BH rats and reduced blood pressure in only 2 of 7 S-MH rats tetsted (by 15 and 20 mm Hg). During AVP infusion the blood pressure of SH rats increased more (p less than 0.001) and heart rate fell much less (p less than 0.001) than in WKY rats. It is concluded that in SH rats with established hypertension, plasma AVP plays an important role in the maintenance of high blood pressure, while the renin-angiotensin system plays a minor or no role.

Animals↗
PubMed1977

[Factor analysis in hypertension. Risks of coronary heart disease and hypertensive arteriolosclerosis (author's transl)].

Based upon factor analysis, initial findings of the risk factors for coronary heart disease are reported, following invesitgations performed on a large number of patho-anatomical cases which were selected for specified criteria. The so-called hypertensive form of arteriosclerosis was demonstrated in the spleen, pancreas, and adrenal gland. It was shown that diabetes mellitus is an influencing factor in arteriolosclerosis in the liver. Several types of arterial hypertension can be differentiated according to clinical features and findings in the heart. Renoparenchymatous and renovascular sclerosis, pyelonephritis, diabetes mellitus, and age are the factors correlated or associated with various types of hypertension. Primary (?) renal hypertension can be differentiated from the secondary (?) TYPE. The discussion suggests that the morphological findings of arteriosclerosis and its complications may be explained, to a certain extent, by the known risk factors of coronary diseases defined by the methods described.

Adrenal Glands↗