scholarly journals Elevated blood pressure: Our family’s fault? The genetics of essential hypertension

2014 ◽  
Vol 6 (5) ◽  
pp. 327 ◽  
Author(s):  
Aniket Natekar ◽  
Randi L Olds ◽  
Meghann W Lau ◽  
Kathleen Min ◽  
Karra Imoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Genetics Of Essential Hypertension

Nature of Elevated Blood Pressure in Normoalbuminuric Type I Diabetic Patients Essential Hypertension?

1993 ◽  
Vol 6 (10) ◽  
pp. 830-836 ◽  
Author(s):  
Kirsten Nørgaard ◽  
Else Rasmussen ◽  
Tonny Jensen ◽  
Jorn Giese ◽  
Bo Feldt-Rasmussen
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Elevated Blood Pressure ◽  
Diabetic Patients ◽  
Type I ◽  
Elevated Blood

Diagnosis, assessment, and treatment of essential hypertension

2010 ◽  
pp. 3039-3057
Author(s):  
Bryan Williams ◽  
John D. Firth
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Subsequent Treatment ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Assessment And Treatment

Essential hypertension is almost invariably symptomless, and usually detected by routine screening or opportunistic measurement of blood pressure. Key questions to answer in the assessment of a person presenting with an elevated blood pressure are: (1) Do they have hypertension, i.e. is the blood pressure persistently elevated? (2) Are there any associated clinical features that might warrant further evaluation to exclude secondary causes of hypertension? (3) Are there factors that might be contributing to an elevated blood pressure, including lifestyle or dietary factors or concomitant medication? (4) Is there any associated target organ damage or comorbidity that influences the overall cardiovascular disease risk and subsequent treatment of the patient?...

Plasma Dopamine β-Hydroxylase and Noradrenaline Amounts in Essential Hypertension

1973 ◽  
Vol 44 (6) ◽  
pp. 617-620 ◽  
Author(s):  
L. B. Geffen ◽  
R. A. Rush ◽  
W. J. Louis ◽  
A. E. Doyle
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Essential Hypertension ◽  
Sympathetic Nervous System ◽  
Diastolic Blood Pressure ◽  
Plasma Catecholamines ◽  
Plasma Noradrenaline ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Sympathetic Nervous

1. Plasma dopamine β-hydroxylase (DβH) amounts were measured by radioimmunoassay in twenty-eight patients, twenty of whom had essential hypertension. There was a positive correlation between resting diastolic blood pressure and plasma DβH concentration. 2. Plasma DβH amounts also correlated significantly with those of plasma noradrenaline (NA) in individual patients. 3. These findings provide further support for the conclusions drawn from studies of plasma catecholamines that the sympathetic nervous system contributes toward the maintenance of the elevated blood pressure in essential hypertension.

Low Urinary Kallikrein Excretion and Elevated Blood Pressure Normalized by Orally Applied Kallikrein in Essential Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 263s-265s ◽  
Author(s):  
A. Overlack ◽  
K. O. Stumpe ◽  
C. Ressel ◽  
F. Krück
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Elevated Blood Pressure ◽  
Urinary Kallikrein ◽  
Elevated Blood ◽  
Kinin System ◽  
Borderline Hypertension ◽  
Low Sodium Diet ◽  
Urinary Kallikrein Excretion ◽  
Normotensive Subjects

1. Urinary kallikrein was measured in 67 patients with essential hypertension and 25 normotensive subjects variously on unrestricted and low sodium diet. Also, the effect of orally applied hog pancreatic kallikrein on elevated blood pressure and kallikrein excretion was evaluated. 2. Urinary kallikrein was reduced in a large subgroup of patients with sustained essential hypertension. 3. With salt restriction, urinary kallikrein rose markedly in normotensive subjects and patients with borderline hypertension but not in those with sustained hypertension. 4. Oral kallikrein normalized reduced kallikrein excretion and lowered elevated blood pressure. 5. The rise in urinary kallikrein with oral kallikrein was due to an increased formation of endogenous enzyme. 6. A defective kallikrein—kinin system may be involved in both the low urinary kallikrein excretion and the hypertension.

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