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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↗

PubMed1979

Nylidrin: a potent anti-hypertensive agent in hypertensive rats.

Nylidrin HCl lowered the blood pressure and increased the heart rate of conscious, spontaneously hypertensive rats (SHR), Goldblatt hypertensive rats, and DOCA hypertensive rates. In SHR, the minimum effective dose was 0.5 mg/kg, s.c. At that dose, the anti-hypertensive activity of nylidrin lasted more than 3 hours. Propranolol reversed both effects on blood pressure and heart rate by nylidrin, whereas atenolol, a specific cardiac beta 1 blocker, only blocked or reversed the tachycardia caused by nylidrin but did not block the anti-hypertensive effect of the compound. In normotensive rats of Wistar/Kyoto strain (WKY) and Holtzman strain, nylidrin at 5 or 10 mg/kg, s.c., produced a transient hypotensive effect which lasted less than an hour and tachycardia that persisted for several hours. In WKY, atenolol prolonged the hypotensive activity of the compound by partially reversing the tachycardia. These observations indicate that SHR is more sensitive than WKY to the anti-hypertensive activity of nylidrin, which is probably caused by vasodilatation mediated by beta 2 receptors.

Animals↗

PubMed1979

Decrease of calcium binding by the red blood cell membrane in spontaneously hypertensive rats and in essential hypertension.

Ca binding in the red blood cell (RBC) membrane of spontaneously hypertensive rats (SHR) and of patients with essential hypertension was studied. Under conditions of physiological concentration of free Ca in the incubation medium of RBC the outer part of the membrane binds 393 +/- 32 and 435 +/- 30 nmole of Ca per ml of RBC in rats and humans, respectively, without essential differences in the amount of Ca in hypertensive individuals as compared to the normotensive controls. The membrane of red blood cell ghosts (RBCgh) at concentrations of free Ca corresponding to its intracellular concentration binds 4.28 +/- 0.39 and 3.53 +/- 0.15 nmole of Ca per mg of protein of RBCgh in rats and humans, respectively. This part of membrane-bound Ca pool (most probably related to the inner part of the red blood cell membrane) is reduced by 48% in SHR and by 28% in patients with essential hypertension as compared to normotensive controls. It is suggested that the decrease of Ca binding ability of the RBC membrane in both types of hypertension studied may be a pattern of a more widespread cell membrane defect.

Adolescent↗

PubMed1978

Morphological findings in spontaneously hypertensive rats in comparison with findings after experimental renal hypertension.

The morphological findings in spontaneously hypertensive rats (SHR) were compared with the findings after experimental renal hypertension. In addition the effect of an arteriosclerogenic diet was investigated. Cardiac hypertrophy occurred in all types of hypertension. During the course of renal hypertension there was also hypertrophy of the tunica media of the arterial vessels of the heart, kidneys, mesenterium, and orta. Degenerative changes in the vascular walls occurred when nephrectomized rats were given a diet containing 2% cholesterol and 1% cholic acid. This produced intima lipoidosis after seven to eleven weeks. The intensity seemed to be dependent on the degree of hypertension and the duration of the experiment.

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↗

PubMed1978

Vascular reactivity of isolated perfused kidneys from normotensive, renal hypertensive and spontaneously hypertensive rats.

By means of an isolated kidney perfusion technique, reactivities of renal body vessels to electrical stimulation of renal plexus and intravascular administrations of low dosed norepinephrine and epinephrine were determined in the spontaneously hypertensive rats of Wistar strain, normotensive Sprague-Dawley rats and Sprague-dawley rats with renal hypertension of the same sex and as equal as possible with respect to age and body weight. The basal vascular resistance as indicated by the perfusion pressure caused by the same rat of perfusion was significantly higher in the renal hypertensive group. Both electrical stimulation of the renal plexus and intravascular administrations of catecholamines caused a rise of perfusion pressure. Analysis of the dose-response relationship reveals that in the dose range used, the sensitivities to electrical stimulation and to norepinephrine are significantly higher in the normotensive than the hypertensive groups. The results indicate that structural change in the blood vessels is more important than the adrenergic actions of low intensity in the cause of high resistance of blood flow in hypertensive subjects at least in the kidney.

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↗

PubMed1977

Mild high-renin essential hypertension. Neurogenic human hypertension?

To determine whether the elevated plasma renin activity in some cases of mild essential hypertension expresses sympathetic-nervous-system over-activity, we compared indexes of sympathetic activity in 16 patients with mild high-renin essential hypertension, 15 hypertensive patients with normal plasma renin activity and 20 normal subjects. Patients with elevated activity exhibited a raised plasma norepinephrine concentration (P less than 0.05), a greater fall in cardiac output with cardiac beta-adrenergic blockade by intravenous propranolol (P less than 0.01), reduction in total peripheral vascular resistance with alpha-adrenergic blockade produced by intravenous phentolamine (P less than 0.01), and reduction to normal of blood pressure by "total" autonomic blockade (atropine, propranolol and phentolamine). On psychometric testing, patients with high-renin hypertension, but not those with normal plasma renin activity, exhibited suppressed hostility (P less than 0.01), a behavioral pattern linked to increased sympathetic activity. The hypertension in these patients with high renin activity is neurogenic and possibly psychosomatic in origin.

Adolescent↗

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↗

PubMed1978

Effect of renal denervation on the development of hypertension in spontaneously hypertensive rats.

The involvement of the renal nerves in the development of hypertension in Okamoto spontaneously hypertensive rats (SHR) was investigated by performing bilateral renal denervation in a group (n = 7) of SHR at 8 weeks of age. A sham-operated group (n = 7) of SHR served as surgical controls. Systolic arterial pressure was recorded twice a week until 14 weeks of age using a tail cuff method. Renal denervation significantly (P less than 0.01) altered the time course for development of hypertension, although both groups eventually developed hypertension. During the 6-week observation period, there were no significant differences in body weight, average 24-h food and fluid intake, urine output, or Na+ and K+ excretion between the two groups. At 20 weeks of age there were no significant differences in systolic pressure, average fluid intake, or urine output between the sham and denervated groups. These results suggest that the renal nerves may be involved in the early phase of development of hypertension in the SHR. The possibility that altered renal function may be the mechanism of the above effects is discussed.

Animals↗

PubMed1979

Plasma volume contraction: a significant factor in both pregnancy-associated hypertension (pre-eclampsia) and chronic hypertension in pregnancy.

The role of plasma volume in hypertension in pregnancy (pre-eclampsia) was investigated. Significant volume expansion from non-pregnant levels (16.5 +/- 1.60 ml/cm height) was present throughout pregnancy in 189 normal women, reaching 23.1 +/- 1.21 ml/cm at 33-36 weeks amenorrhoea. In another 40 initially normotensive pregnant women who developed hypertension, similar early volume expansion was followed by significant volume contraction in the third trimester, before evaluation of blood pressure in 29 (20.6 +/- 1.26 ml/cm), after it in 11 (18.6 +/- 1.27 ml/cm). Equivalent volume contraction was present in another 44 women studied only after hypertension developed in the third trimester. Oedema had no value as a clinical sign. In another 30 women with chronic hypertension, blood pressure was inversely related to plasma volume (r = 0.822) and to fetal growth (r = -0.710), which was directly related to plasma volume (r = 0.701). Plasma volume depletion plays a significant role in hypertension in pregnancy.

Blood Pressure↗

PubMed1978

[Cardiovascular radiography, changes in the thoracic aorta, ECG and clinical parameters in hypertension. 2. Changes in the thoracic aorta in hypertension].

In 142 hypertensives and a control group of 230 normotensives the measure of the aorta after Kreuzfuchs was estimated. In the two groups a significant increase of the width of the aorta was found with growing age. Whilst the width of the aorta concerning the degree of severity I of hypertension on an average were slightly below those of normotensives, they were increased in the degrees of severity II and III, but a further increase could not be ascertained at the transition from degree of severity II to III. On the other hand, the duration of hypertension is of particular importance when a dilation of the aorta is present. Also between deformation of the heart and measure of the aorta close relations which may conclude to a homogenous development are to be seen particularly in the younger patients. The influence of the sclerosis of the aorta in the sense of an additional dilation of the aorta could not be clearly confirmed on the basis of our material. On the other hand, the frequency of calcium depositions significantly increased with growing age in the region of the aortic arce and in the group of younger patients with the duration of hypertension, whereas the different degrees of severity II and III had a smaller influence. It is interesting that several patients showed normal widths of the aorta despite a duration of the hypertension of more than 5 years and a degree of severity III.

Aorta, Thoracic↗

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↗

PubMed1977

Diagnostic evaluation of hypertension: pilot study in a hypertension clinic.

Two hundred and eighty-two (282) patients suffering from hypertension were evaluated for the detection of secondary forms of hypertension. Apart from clinical and routine laboratroy investigation in each, straight film of abdomen, intravenous pyelography (IVP), isotope renography and aortography were done in 174, 51, 109 and 2 cases respectively. Evidences of secondary hypertension was present in 22(7.8%) of which renal aetiology was probable in all but 4. Of the 10 patients with a primary kidney condition, possible renal aetiology was unsuspected in only one patient with unilateral renal hypoplasia. In 8 patients with renal involvement due to systemic disease, or in 4 with non-renal causes, the aetiological diagnosis was suggested by the clinical situation. In view of low yield of curable hypertension and high cost, IVP and renography should only be employed selectively and not as routine investigations.

Adult↗

PubMed1979

Primary pulmonary hypertension presenting as portal hypertension.

A two and a half-year old child is described who presented with signs of portal hypertension (hematemesis, hepatosplenomegaly, ascites). Her subsequent work-up revealed that the "pressure-head" originated within the pulmonary arterial bed. Indeed, severe changes of primary pulmonary hypertension were found at autopsy. What is unique about this case is the absence of cardiopulmonary symptoms prior to the development of suprahepatic portal hypertension. In addition, the pulmonary disease developed in the absence of underlying chronic hepatic disease or extrahepatic portal vein thrombosis which, reportedly, can lead to pulmonary hypertension.

Autopsy↗

PubMed1976

Hypertension screening of 1 million Americans. Community Hypertension Evaluation Clinic (CHEC) program, 1973 through 1975.

During 1973 through 1975, more than 1 million persons were screened in the nationwide Community Hypertension Evaluation Clinic (CHEC) program at 1,171 sites. While those screened were not from defined populations, findings paralleled those of recent surveys of US population samples. First, CHEC confirmed the scope of the problem of elevated blood pressure in the United States. Of those screened, 247 of 1,000 had a diastolic reading of 90 mm Hg or higher; 116 of 1,000 had a reading of 95 mm Hg or greater. Prevalence of elevated blood pressure rose with age up to age 50 years, was higher in blacks than in whites, and was higher in men than in women. Second, CHEC data confirmed the challenge of undetected, untreated, and uncontrolled hypertension. Previously undetected hypertension was present in 27.7% of hypertensive people, detected but untreated in 10.7%, and treated but uncontrolled in 16.7%--totaling 55.1%.

Adult↗

PubMed1977

Propranolol in DOCA hypertensive rats: development of hypertension inhibited and pressor responsiveness enhanced.

D,L-Propranolol given in single doses by gavage or s.c. injection to awake rats, always slowed the heart without affecting blood pressure. Doses of 0.2 mg/100 g injected twice daily lowered systolic pressure after 3 days in DOCA hypertensive but not in normotensive or spontaneously hypertensive rats. When chronic treatment with propranolol preceded the induction of DOCA hypertension, the pressure elevation attained 14 weeks later was less in treated than in untreated rats. Pressor responses to injected norepinephrine and to posterior hypothalamic stimulation were significantly larger in DOCA hypertensive rats that had been treated chronically with propranolol than in those that had not. These results suggest that propranolol's antihypertensive effects are unimpressive because they are simultaneously opposed by an enhanced cardiovascular responsiveness to pressor stimuli.

Animals↗