Urinary Dopamine Excretion in Normotensive Subjects wiht or without Family History of Hypertension

1986 ◽  
Vol 4 (1) ◽  
pp. 57-60 ◽  
Author(s):  
Ikuo Saito ◽  
Eiko Takeshita ◽  
Takao Saruta ◽  
Shiro Nagano ◽  
Toshio Sekihara
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.


1982 ◽  
Vol 63 (s8) ◽  
pp. 41s-43s ◽  
Author(s):  
W. Zidek ◽  
H. Vetter ◽  
K.-G. Dorst ◽  
H. Zumkley ◽  
H. Losse

1. The intracellular Na+ and Ca2+ activity and Na+ concentration were measured in erythrocytes of normotensive subjects, with and without a familial disposition to hypertension, in essential hypertensive patients with and without a family history of hypertension, and in patients with secondary hypertension. 2. In normotensive subjects without a genetic trait of hypertension intracellular Na+ activity and concentration were 7.00 ± 1.38 mmol/l and 5.67 ± 0.95 mmol/l respectively. The intracellular Ca2+ activity was 4.82 ± 4.49 μmol/l. In normotensive subjects with a familial hypertensive disposition intracellular Na+ activity and concentration were 9.74 ± 1.43 mmol/l (P < 0.01) and 6.63 ± 0.88 mmol/l (P < 0.05). Intracellular Ca2+ was 9.59 ± 9.71 μmol/l (P < 0.05). 3. Essential hypertensive patients without a familial genetic trait had an elevated intracellular Na+ activity (8.35 ± 2.08 mmol/l, P < 0.05). Intracellular Na+ concentration was 6.64 ± 0.79 mmol/l (P < 0.05). The intracellular Ca2+ activity was markedly elevated to 25.33 ± 19.03 μmol/l (P < 0.01). The essential hypertensive patients with a familial disposition had an elevated intracellular Na+ activity (17.19 ± 4.37 mmol/l, P < 0.001) and Ca2+ activity (32.8 ± 32.51 μmol/l, P < 0.01). The intracellular Na+ concentration was 6.25 ± 1.23 mmol/l. 4. The results indicate that in essential hypertension intracellular Na+ activity is increased, particularly in patients with a familial disposition for hypertension. Intracellular Ca2+ is increased in essential hypertension whether or not there was a family disposition to hypertension.


1999 ◽  
Vol 56 (5) ◽  
pp. 1838-1845 ◽  
Author(s):  
Hans Herlitz ◽  
Lennart U. Jungersten ◽  
John Wikstrand ◽  
Bengt R. Widgren

1994 ◽  
Vol 131 (2) ◽  
pp. 179-183 ◽  
Author(s):  
Hans Herlitz ◽  
Bengt Widgren ◽  
John Wikstrand ◽  
Mattias Aurell

Herlitz H, Widgren B, Wikstrand J, Aurell M, Abnormalities in the renin–angiotensin–aldosterone system in normotensive subjects with a positive family history of hypertension. Eur J Endocrinol 1994:131:179–83. ISSN 0804–4643 Non-hypertensive men with a positive family history of hypertension in two generations (N = 16) were compared with weight-matched (N = 13) and lean (N = 12) control groups with a negative family history of hypertension with respect to the activity of the renin–angiotensin–aldosterone system at baseline and during an oral glucose tolerance test. Blood pressure was measured phonographically after 30 min of semirecumbent rest and the oral glucose tolerance test was performed after a 10-h overnight fast with 100 g of glucose given orally. Blood samples were drawn from a peripheral catheter at baseline, 30 and 120 min after the glucose challenge. Systolic and diastolic blood pressures did not differ between subjects with a positive or a negative family history of hypertension. At baseline, blood glucose and plasma insulin were similar in the three groups while the group with a positive family history of hypertension had a significantly lower plasma renin activity (PRA) (0.85 ± 0.09 compared with the weight-matched but not with the lean control group (1.36 ± 0.13 and 1.06 ± 0.15 ng AI·ml−1 · h−1; p < 0.01 and NS, respectively). The PRA increased significantly after the glucose challenge in all groups (p < 0.01), while the plasma aldosterone concentration decreased after 30 min and then showed an increase at 120 min. The PRA response was less pronounced in the group with a positive family history of hypertension compared with the weight-matched and lean control groups (p < 0.05 and p < 0.01, respectively). Serum potassium did not change significantly in either group after the glucose challenge. Urinary sodium excretion was similar in the three groups. In conclusion, non-hypertensive subjects with a positive family history of hypertension are characterized by a lower activity of the renin–angiotensin–aldosterone system at baseline and a diminished PRA response during hyperinsulinemia compared with normotensive individuals without such heredity. Whether this is due to volume expansion or to a tendency to a higher blood pressure remains to be clarified. Hans Herlitz, Department of Nephrology, Sahlgrenska sjukhuset, S-413 45 Göteborg, Sweden


Hypertension ◽  
1997 ◽  
Vol 30 (3) ◽  
pp. 629-631 ◽  
Author(s):  
Heno Ferreira Lopes ◽  
Hélio Bernardes Silva ◽  
José Augusto Soares ◽  
Barreto Filho ◽  
Fernanda Marciano Consolim-Colombo ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document