Sex-dependent relation between ionized calcium in serum and blood pressure.

1984 ◽  
Vol 30 (1) ◽  
pp. 116-118 ◽  
Author(s):  
N Fogh-Andersen ◽  
L Hedegaard ◽  
J Thode ◽  
O Siggaard-Andersen

Abstract In an epidemiological study of 977 45-year-olds, both the mean concentration of ionized calcium in serum, [Ca2+]7.4, and arterial blood pressure were higher in men than in women. Among the men, there was a weak positive correlation between [Ca2+]7.4 and the systolic blood pressure, but no other significant correlation was found within each separate sex. Postmenopausal women had slightly increased [Ca2+]7.4 but normal blood pressure. Patients taking thiazide diuretics or beta-adrenergic blocking agents had normal [Ca2+]7.4.

1952 ◽  
Vol 95 (6) ◽  
pp. 523-529 ◽  
Author(s):  
Joseph R. Kahn ◽  
Leonard T. Skeggs ◽  
Norman P. Shumway ◽  
Paul E. Wisenbaugh

Hypertensin has been assayed in the blood of patients with normal blood pressure and in those with essential hypertension in both the benign and malignant phases. 250 ml. samples of arterial blood were obtained, chemically purified, and concentrated to a volume of 1 ml. These extracts were then assayed in anesthetized rats. The concentrations of hypertensin in the blood of patients with the malignant phase of essential hypertension were found to be greatly increased. The concentrations of hypertensin found in patients with benign hypertension had a moderate degree of overlapping with those found in the normotensive group, but the mean concentration of hypertensin in the former group was twice that of the controls. Although these results are statistically significant, the amounts of hypertensin recovered in the benign group are so small that no conclusions can be drawn as to its effectiveness in producing vasoconstriction in these patients.


1975 ◽  
Vol 53 (5) ◽  
pp. 866-872 ◽  
Author(s):  
George Constantopoulos ◽  
Jacques Genest ◽  
Miyako Kusumoto ◽  
José-Manuel Rojo-Ortega

Deoxycorticosterone pivalate (2.5 mg/kg) given intramuscularly on four occasions 10–15 days apart over a period of 45 days to unilaterally nephrectomized adult male mongrel dogs, receiving as drinking solution 0.9% NaCl in 5% dextrose, resulted in an average sustained rise in the mean arterial blood pressure of 30 mm Hg (1 mm Hg = 133 N/m2) in 60% of the animals. Hypertensive dogs had in their arterial tissues generally more sodium, potassium, magnesium, and calcium than the similarly treated but non-hypertensive dogs, but compared to the tissues of operated untreated or unoperated normotensive dogs, only sodium and calcium were significantly higher. The dogs who were similarly treated but did not develop hypertension had in their arterial tissues less sodium, potassium, and magnesium than operated untreated or unoperated normotensive dogs. Norepinephrine content in the branches of mesenteric arteries of all deoxycorticosterone- and NaCl-treated animals, irrespective of their blood pressure, was significantly lower, and in the myocardium significantly higher, than either the unoperated normotensive or operated but not further treated dogs. It is concluded, therefore, that in deoxycorticosterone + NaCl treatment the dogs which developed hypertension had more arterial sodium, potassium, magnesium, and calcium than those who were similarly treated but remained within the limits of normal blood pressure, and that there was no difference between hypertensive and non-hypertensive dogs in regard to their cardiovascular norepinephrine content.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Eun Sun Yu ◽  
Kwan Hong ◽  
Byung Chul Chun

Abstract Background The study aimed to estimate the incidence of and period of progression to stage 2 hypertension from normal blood pressure. Methods We selected a total of 21,172 normotensive individuals between 2003 and 2004 from the National Health Insurance Service-Health Screening and followed them up until 2015. The criteria for blood pressure were based on the American College of Cardiology/American Heart Association 2017 guideline (normal BP: SBP < 120 and DBP < 80 mmHg, elevated BP: SBP 120–129 and DBP < 80 mmHg, stage 1 hypertension: SBP 130–139 or DBP 80–89 mmHg, stage 2 hypertension: SBP ≥140 or DBP ≥ 90 mmHg). We classified the participants into four courses (Course A: normal BP → elevated BP → stage 1 hypertension→ stage 2 hypertension, Course B: normal BP → elevated BP → stage 2 hypertension, Course C: normal BP → stage 1 hypertension → stage 2 hypertension, Course D: normal BP → stage 2 hypertension) according to their progression from normal blood pressure to stage 2 hypertension. Results During the median 12.23 years of follow-up period, 52.8% (n= 11,168) and 23.6% (n=5004) of the participants had stage 1 and stage 2 hypertension, respectively. In particular, over 60 years old had a 2.8-fold higher incidence of stage 2 hypertension than 40–49 years old. After the follow-up period, 77.5% (n=3879) of participants with stage 2 hypertension were found to be course C (n= 2378) and D (n=1501). After the follow-up period, 77.5% (n=3879) of participants with stage 2 hypertension were found to be course C (n= 2378) and D (n=1501). The mean years of progression from normal blood pressure to stage 2 hypertension were 8.7±2.6 years (course A), 6.1±2.9 years (course B), 7.5±2.8 years (course C) and 3.2±2.0 years, respectively. Conclusions This study found that the incidence of hypertension is associated with the progression at each stage. We suggest that the strategies necessary to prevent progression to stage 2 hypertension need to be set differently for each target course.


In August, 1903, I published a paper in the ‘Journal of Pathology’(1) in which I demonstrated a method experimentally producing uncompensated hear disease in an animal, which was compatible with life. This method consisted in diminishing the size of the pericardial sac by stitches, so that the diastolic filling of the heart was impeded. The main symptoms of this condition were dropsy and diminution in the amount of urine excreted. As the immediate result of this interference with the action of the heart, there occurred a rise of pressure throughout the whole systemic venous system extending as far back as the capillaries, and a fall of the mean arterial blood-pressure. Further, I found that the pressure in all the veins fell to the normal limit again within the space of about one hour, and that subsequently when dropsy was being produced, the vanous pressure in all parts of the body was normal, and the arterial pressure had almost recovered itself.


Sensors ◽  
2021 ◽  
Vol 21 (5) ◽  
pp. 1867
Author(s):  
Tasbiraha Athaya ◽  
Sunwoong Choi

Blood pressure (BP) monitoring has significant importance in the treatment of hypertension and different cardiovascular health diseases. As photoplethysmogram (PPG) signals can be recorded non-invasively, research has been highly conducted to measure BP using PPG recently. In this paper, we propose a U-net deep learning architecture that uses fingertip PPG signal as input to estimate arterial BP (ABP) waveform non-invasively. From this waveform, we have also measured systolic BP (SBP), diastolic BP (DBP), and mean arterial pressure (MAP). The proposed method was evaluated on a subset of 100 subjects from two publicly available databases: MIMIC and MIMIC-III. The predicted ABP waveforms correlated highly with the reference waveforms and we have obtained an average Pearson’s correlation coefficient of 0.993. The mean absolute error is 3.68 ± 4.42 mmHg for SBP, 1.97 ± 2.92 mmHg for DBP, and 2.17 ± 3.06 mmHg for MAP which satisfy the requirements of the Association for the Advancement of Medical Instrumentation (AAMI) standard and obtain grade A according to the British Hypertension Society (BHS) standard. The results show that the proposed method is an efficient process to estimate ABP waveform directly using fingertip PPG.


1963 ◽  
Vol 44 (3) ◽  
pp. 430-442 ◽  
Author(s):  
B. Arner ◽  
P. Hedner ◽  
T. Karlefors ◽  
H. Westling

ABSTRACT Observations were made on healthy volunteers during insulin induced hypoglycaemia (10 cases) and infusion of adrenaline (3 cases) or cortisol (1 case). In all cases a rise in the cardiac output was registered during insulin hypoglycaemia. The mean arterial blood pressure was relatively unchanged and the calculated peripheral vascular resistance decreased in all cases. A temporary rise in plasma corticosteroids was observed. After infusion of adrenaline similar circulatory changes were observed but no rise in plasma corticosteroids was found. Infusion of cortisol caused an increased plasma corticosteroid level but no circulatory changes. It is concluded that liberation of catechol amines and increased adrenocortical activity following hypoglycaemia are not necessarily interdependent.


PEDIATRICS ◽  
1983 ◽  
Vol 72 (4) ◽  
pp. 500-502
Author(s):  
Pablo Yagupsky ◽  
Rafael Gorodischer

The antihypertensive drug clonidine has a double and antagonistic effect on arterial blood pressure. As a result of activation of peripheral α-adrenergic receptors, it causes a transient increase in blood pressure; by a central action it decreases sympathetic tone which results in sustained bradycardia and hypotension. Both central and peripheral effects are experimentally blocked by tolazoline, an α-adrenergic blocking agent. The toxic symptoms seen in clonidine poisoning are usually produced by the central effect. A case of severe clonidine poisoning in a 9-month-old infant is reported. The clinical picture included coma, miosis, apneic spells, bradycardia, and hypertension. Rapid and complete recovery was obtained with supportive treatment that included assisted ventilation. No adrenergic blockers or antihypertensive drugs were given. Use of tolazoline in cases of clonidine overdose in children remains controversial. Supportive measures alone may be adequate for even the most severe cases.


1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.


Perfusion ◽  
1990 ◽  
Vol 5 (4) ◽  
pp. 261-266
Author(s):  
V. Vainionpää ◽  
A. Hollme'n ◽  
J. Timisjärvi

The occurrence of vasomotor waves during cardiopulmonary bypass (CPB) is a recognized phenomenon. The lesser known oscillation of arterial pressure after cessation of CPB was observed in 18 open-heart patients. The duration of an oscillatory wave was 13.5±5.0 seconds, the amplitude 6.1 ±2.6mmNg and the mean arterial pressure 76.5± 10.7mmHg. Inter-and also intraindividual variations in frequency and amplitude of the oscillation, however, did occur. In 13 patients, this oscillation occurred during ventricular epicardial pacing. The oscillation continued until the end of the operation in eight patients; in others, the oscillation was of shorter duration. An oscillation of pulmonary arterial pressure (PAP) was simultaneously observed in nine patients (eight with pacemaker) and central venous pressure (CVP) oscillation in eight patients (all with pacemaker). The duration of a wave was the same as in systemic arterial pressure and the amplitudes were 1.5-3.0mmHg in PAP and 1.0-2.0mmHg in CVP. These arterial vasomotor waves, seen here after CPB, largely resemble those observed during perfusion in man and also the Mayerwaves explored in experimental animals. The pacing rhythm seems to favourthe appearance of those blood pressure oscillations.


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