Lipid Metabolism Alterations in Normotensive Subjects With Positive Family History of Hypertension

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

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Stimulatory effect of insulin on tubular sodium reabsorption in normotensive subjects with a positive family history of hypertension

Nephrology Dialysis Transplantation ◽

10.1093/ndt/11.1.47 ◽

1996 ◽

Vol 11 (1) ◽

pp. 47-54 ◽

Cited By ~ 7

Author(s):

H. Herlitz ◽

B. Widgren ◽

V. Urbanavicius ◽

S. Attvall ◽

B. Persson

Keyword(s):

Family History ◽

Positive Family History ◽

Sodium Reabsorption ◽

Tubular Sodium Reabsorption ◽

History Of ◽

Family History Of Hypertension ◽

Normotensive Subjects

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Different Haemodynamic Reaction Patterns during Noise Exposure in Normotensive Subjects with and without Heredity for Essential Hypertension

Clinical Science ◽

10.1042/cs063371s ◽

1982 ◽

Vol 63 (s8) ◽

pp. 371s-374s ◽

Cited By ~ 13

Author(s):

L. Andrén ◽

S. Piros ◽

L. Hansson ◽

H. Herlitz ◽

O. Jonsson

Keyword(s):

Blood Pressure ◽

Family History ◽

Noise Exposure ◽

Blood Pressure Response ◽

Positive Family History ◽

Peripheral Resistance ◽

Sodium Concentration ◽

History Of ◽

Family History Of Hypertension ◽

Normotensive Subjects

1. Stimulation with noise (100 dBA) for 10 min caused a significant increase in diastolic and mean arterial pressure in normotensive subjects with and without a positive family history of hypertension. 2. The blood pressure response in the group with a positive family history of hypertension was due to a significant increase in total peripheral resistance (9%, P < 0.05); no such change was seen in the group without heredity for hypertension. 3. Systolic blood pressure, heart rate, stroke volume and cardiac output did not change significantly during exposure to noise. 4. There was no difference between the groups in mean intracellular sodium concentration measured in erythrocytes.

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Blood Pressure and Intra-Erythrocyte Sodium during Normal and High Salt Intake in Middle-Aged Men: Relationship to Family History of Hypertension, and Neurogenic and Hormonal Variables

Clinical Science ◽

10.1042/cs0660427 ◽

1984 ◽

Vol 66 (4) ◽

pp. 427-433 ◽

Cited By ~ 8

Author(s):

Ottar Gudmundsson ◽

Hans Herlitz ◽

Olof Jonsson ◽

Thomas Hedner ◽

Ove Andersson ◽

...

Keyword(s):

Blood Pressure ◽

Family History ◽

Salt Intake ◽

Sodium Intake ◽

Positive Family History ◽

Sodium Content ◽

High Salt Intake ◽

History Of ◽

Family History Of Hypertension ◽

Erythrocyte Sodium

1. During 4 weeks 37 normotensive 50-year-old men identified by screening in a random population sample were given 12 g of NaCl daily, in addition to their usual dietary sodium intake. Blood pressure, heart rate, weight, urinary excretion of sodium, potassium and catecholamines, plasma aldosterone and noradrenaline and intra-erythrocyte sodium content were determined on normal and increased salt intake. The subjects were divided into those with a positive family history of hypertension (n = 11) and those without such a history (n = 26). 2. Systolic blood pressure and weight increased significantly irrespective of a positive family history of hypertension. 3. On normal salt intake intra-erythrocyte sodium content was significantly higher in those with a positive family history of hypertension. During high salt intake intra-erythrocyte sodium content decreased significantly in that group and the difference between the hereditary subgroups was no longer significant. 4. In the whole group urinary excretion of noradrenaline, adrenaline and dopamine increased whereas plasma aldosterone decreased during the increased salt intake. 5. Thus, in contrast to some earlier studies performed in young subjects, our results indicate that moderately increased sodium intake acts as a pressor agent in normotensive middle-aged men whether there was a positive family history of hypertension or not. We confirm that men with positive family history of hypertension have an increased intra-erythrocyte sodium content, and that an increase in salt intake seems to increase overall sympathetic activity.

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Altered baroreflex sensitivity in young women with a family history of hypertension

Journal of Neurophysiology ◽

10.1152/jn.00471.2018 ◽

2019 ◽

Vol 121 (3) ◽

pp. 1011-1017 ◽

Cited By ~ 2

Author(s):

Evan L. Matthews ◽

Kelly N. Sebzda ◽

Megan M. Wenner

Keyword(s):

Family History ◽

Young Women ◽

Baroreflex Sensitivity ◽

Valsalva Maneuver ◽

Muscle Sympathetic Nerve Activity ◽

Positive Family History ◽

The Future ◽

History Of ◽

Family History Of Hypertension ◽

Important Marker

A positive family history of hypertension (+FH) is a risk factor for the future development of hypertension. Hypertension is associated with reductions in baroreflex sensitivity (BRS). Therefore, we hypothesized that young women with a +FH [ n = 12, 22 ± 1 yr, body mass index (BMI) 21 ± 1 kg/m2, mean arterial pressure (MAP) 79 ± 1 mmHg] would have lower BRS compared with young women without a family history of hypertension (−FH) ( n = 13, 22 ± 1 yr, BMI 21 ± 1 kg/m2, MAP 77 ± 2 mmHg, all P > 0.05 between groups). Continuous measurements of muscle sympathetic nerve activity, blood pressure, and electrocardiogram derived R-R interval were recorded at rest and during a Valsalva maneuver. Both cardiovagal BRS and vascular sympathetic BRS were assessed. Resting cardiovagal BRS was reduced in the +FH women (all sequences: −FH 32.3 ± 3.7 vs. +FH 20.2 ± 2.9 ms/mmHg, P = 0.02). Cardiovagal BRS during phase IV (−FH 16.5 ± 2.7 vs. +FH 7.6 ± 1.3 ms/mmHg, P < 0.01) but not phase II (−FH 5.5 ± 0.9 vs. +FH 5.0 ± 0.8 ms/mmHg, P = 0.67) of the Valsalva maneuver was also lower in the +FH women. Vascular sympathetic BRS at rest (−FH −2.38 ± 0.7 vs. +FH −2.33 ± 0.3 bursts· min−1·mmHg−1, P = 0.58) and during the Valsalva (−FH −0.74 ± 0.23 vs. +FH −0.66 ± 0.18 bursts·15 s−1·mmHg−1, P = 0.79) were not different between groups. These data suggest that healthy young women with a positive family history of hypertension have reduced cardiovagal BRS. This may be one mechanism contributing to the increased incidence of hypertension in this population later in life. NEW & NOTEWORTHY Having a family history of hypertension increases the risk of developing future hypertension. Reductions in baroreflex function have been demonstrated in hypertension and are an important marker for future cardiovascular disease. We show that young women with a family history of hypertension have lower cardiovagal baroreflex sensitivity. This alteration in autonomic function may be one mechanism contributing to the future incidence of hypertension in this patient population.

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Failure of angiotensin II to suppress plasma renin activity in normotensive subjects with a positive family history of hypertension

Clinical Science ◽

10.1042/cs20050055 ◽

2005 ◽

Vol 109 (3) ◽

pp. 311-317 ◽

Cited By ~ 1

Author(s):

Hans Herlitz ◽

Eva Palmgren ◽

Bengt Widgren ◽

Mattias Aurell

Keyword(s):

Angiotensin Ii ◽

Family History ◽

Plasma Renin Activity ◽

Plasma Renin ◽

Urinary Sodium ◽

Renin Activity ◽

Ang Ii ◽

History Of ◽

Family History Of Hypertension ◽

Normotensive Subjects

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.

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Intracellular Na+ and Ca2+ Activities in Essential Hypertension

Clinical Science ◽

10.1042/cs063041s ◽

1982 ◽

Vol 63 (s8) ◽

pp. 41s-43s ◽

Cited By ~ 36

Author(s):

W. Zidek ◽

H. Vetter ◽

K.-G. Dorst ◽

H. Zumkley ◽

H. Losse

Keyword(s):

Essential Hypertension ◽

Family History ◽

Secondary Hypertension ◽

Genetic Trait ◽

Hypertensive Patients ◽

Intracellular Na Activity ◽

History Of ◽

Family History Of Hypertension ◽

Normotensive Subjects

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.

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