Influence of Family History of Hypertension on the Relationships between Blood Pressure, Body Weight, Electrolyte Metabolism, Renin, Prolactin and Parathormone

1981 ◽  
Vol 61 (s7) ◽  
pp. 359s-362s ◽  
Author(s):  
F. Wessels ◽  
D. Hoffmann ◽  
H. Wagner ◽  
H. Zumkley

1. The influence of family history of hypertension on the relationships between blood pressure, relative body weight, sodium/creatinine ratio of the 24 h urine, plasma renin activity and the plasma concentration of prolactin and parathormone were examined in 102 healthy male students. 2. Grouping together results from all students showed significant positive correlations between systolic blood pressure and prolactin, parathormone as well as relative body weight, between plasma renin activity and prolactin and a significant negative correlation between plasma renin activity and sodium/creatinine ratio of the 24 h urine. 3. By dividing the students into two groups according to their family history of hypertension we could demonstrate in those with family history of hypertension a highly significant positive correlation between mean blood pressure and sodium/creatinine ratio of the 24 h urine and an improvement of the correlations between systolic blood pressure and prolactin and between sodium/creatinine ratio of the 24 h urine and plasma renin activity. In students without family history of hypertension these relationships were no longer detectable. In the students without family history of hypertension the correlations between systolic blood pressure and relative body weight as well as between plasma renin activity and prolactin gained substantially in significance. In students with positive family history of hypertension these correlations could no longer be demonstrated. The correlations between systolic blood pressure and parathormone remained unaffected by family history of hypertension. 4. The results suggest that a genetic predisposition to essential hypertension is able to intensify the blood pressure effect of Na intake and of prolactin, which, besides its function as a sex hormone, is presumed additionally to be able to retain salt. However, the positive relationship between body weight and blood pressure, as well as between plasma renin activity and prolactin, the significance of which increases greatly in subjects without family history of hypertension, appears to be lost as the result of the increased sensitivity to salt in positive family history of hypertension.

2005 ◽  
Vol 109 (3) ◽  
pp. 311-317 ◽  
Author(s):  
Hans Herlitz ◽  
Eva Palmgren ◽  
Bengt Widgren ◽  
Mattias Aurell

The renin–angiotensin system is implicated in the pathophysiology of hypertension. Renin release is regulated by a number of factors, including circulating Ang II (angiotensin II), the so-called short feedback loop. The aim of the present study was to investigate the responsiveness of circulating Ang II on PRA (plasma renin activity) in normotensive subjects with a PFH or NFH (positive or negative family history of hypertension respectively). PRA, renal haemodynamics and urinary sodium excretion were measured during infusion of Ang II without and with pretreatment with the AT1 (Ang II type 1) receptor blocker irbesartan. Normotensive men with a PFH (n=13) and NFH (n=10), with a mean age of 38 years, were given on different occasions intravenous Ang II infusions of 0.1, 0.5 and 1.0 ng·kg−1 of body weight·min−1 before and after pretreatment with 150 mg of irbesartan once a day for 5 consecutive days. RPF (renal plasma flow) and GFR (glomerular filtration rate) were also measured. Before Ang II infusion, the PFH and NFH groups did not differ with respect to BP (blood pressure), body mass index, PRA, RBF (renal blood flow) or urinary sodium. There was no difference in BP or renal haemodynamic response to the highest Ang II dose between the groups. PRA declined with the highest Ang II dose (P<0.01) in subjects with a NFH, but not in subjects with a PFH. After treatment with irbesartan when Ang II had no effect on BP in either group, Ang II also suppressed PRA in subjects with a PFH (P<0.01), and the difference between the groups at baseline was thus eliminated. In conclusion, these findings indicate that subjects with a PFH have a defective Ang II suppression of PRA, which is corrected by AT1 receptor blockade.


1988 ◽  
Vol 6 (6) ◽  
pp. 489-493 ◽  
Author(s):  
Yuhei Shibutani ◽  
Kunihiro Sakamoto ◽  
Shingo Katsuno ◽  
Sachiko Yoshimoto ◽  
Takamaro Matsuura

1986 ◽  
Vol 66 (3) ◽  
pp. 351-355 ◽  
Author(s):  
G. Clementi ◽  
E. Rapisarda ◽  
C.E. Fiore ◽  
A. Prato ◽  
M. Amico-Roxas ◽  
...  

1978 ◽  
Vol 55 (s4) ◽  
pp. 271s-274s
Author(s):  
W. H. L. Hoefnagels ◽  
J. I. M. Drayer ◽  
J. A. Hofman ◽  
A. G. H. Smals ◽  
TH. J. Benraad ◽  
...  

1. Pronounced hypoaldosteronism was found in five young women with low-renin hypertension and characteristic features of the mineralocorticoid hypertensive syndrome. 2. There was no overproduction of the mineralocorticoids 11-deoxycorticosterone and 18-OH-11-deoxycorticosterone. 3. Dexamethasone restored blood pressure to normal, decreased body weight, increased plasma potassium, and increased plasma renin activity and aldosterone excretion in all patients. 4. The data suggest overproduction of an unknown adrenocorticotrophic hormone-dependent mineralocorticoid maintaining hypertension in these patients.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Rajat Kalra ◽  
Lama Ghazi ◽  
David A Calhoun ◽  
Suzanne Oparil ◽  
Tanja Dudenbostel

Introduction: While primary aldosteronism (PA) is a recognized and relatively well-defined cause of resistant hypertension (RHTN), there is a relative paucity of data defining patients with hyperreninemic aldosteronism (HA) and RHTN. Hypothesis: We sought to identify characteristics of patients with HA and compare them to patients with and without PA within a large cohort of patients with RHTN. Methods: We analyzed 1236 RHTN patients who were referred to our Hypertension Clinic with and underwent complete biochemical work-up including plasma aldosterone concentration, plasma renin activity, and 24-hour urinary aldosterone. Demographics, antihypertensive drug regimen, comorbidities, biochemical parameters and evaluation for secondary RHTN, where indicated, were evaluated. Hyperreninemic aldosteronism was defined as plasma renin activity >1 ng/mL*hr, aldosterone-renin-ratio of ≈ 8 or more, and 24-hour urinary aldosterone >12 mcg/24h. Results: In 128 eligible patients with resistant hypertension and HA, the mean age was 52.9±12.1 years with 56% being males (Table). Systolic and diastolic blood pressures were 149.2±22.0 and 87.9±15.5 mm Hg, respectively. Significant numbers of HA patients had co-morbid obesity (63.3%) and obstructive sleep apnea (44.9%). Compared to patients with PA, patients with HA had statistically significant lower proportions of patients with African-American race and systolic blood pressure. Compared to all RHTN patients, HA patients had lower mean age and systolic blood pressure, but were more likely to be male and have obstructive sleep apnea. Conclusions: Resistant hypertension due to hyperreninemic aldosteronism appears to predominantly affect obese, middle-aged males. Patients with HA causing RHTN have distinct differences from PA patients with RHTN. More investigation is required to identify appropriate treatment protocols for this poorly defined subset of patients with RHTN.


2010 ◽  
Vol 28 ◽  
pp. e253-e254
Author(s):  
S Stabouli ◽  
V Kotsis ◽  
G Karafilis ◽  
S Papakatsika ◽  
K Papadopoulou ◽  
...  

1975 ◽  
Vol 48 (1) ◽  
pp. 17-26 ◽  
Author(s):  
F. H. H. Leenen ◽  
J. W. Scheeren ◽  
D. Omylanowski ◽  
J. D. Elema ◽  
B. Van Der Wal ◽  
...  

1. The relationships between the renin-angiotensin-aldosterone system, sodium and potassium balance and systolic blood pressure were studied during development of moderate (160–180 mmHg; clip i.d. 0.25 mm) and severe (200–230 mmHg; clip i.d. 0.20 mm) renal hypertension in rats with an undisturbed contralateral kidney. 2. In severely hypertensive rats renin activity in the peripheral plasma increased from day 9, by which time the systolic blood pressure was elevated to 160–180 mmHg. The rate of total corticosteroid and aldosterone production in vitro increased from day 14 and plasma renin substrate concentration increased from day 24. In moderately hypertensive rats, none of these changes occurred. 3. During the first 10 days after the application of 0.25 and 0.20 mm clips, sodium and potassium retention/g gain in body weight were higher than in sham-operated controls. During the next 10 days, the positive balance stabilized in animals with a 0.25 mm clip whereas, in animals with a 0.20 mm clip, sodium and potassium balance returned to the level of the sham-operated controls through increased renal losses. Despite these changes the systolic pressure rose further in animals with a 0.20 mm clip. 4. The initial sodium retention could be a factor in the early rise of blood pressure and could account for the delay in the rise of peripheral plasma renin activity. The subsequent loss of the retained sodium and potassium during the development of severe hypertension could have facilitated the rise in peripheral plasma renin activity, but did not initiate this rise.


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